this lecture began our introduction to diagnosis of endocrine disorders, courtesy of dr. marcus miller.
the hypothalamus is the endocrine organ that receives information from the CNS and in turn stimulates the pituitary to release hormones. it carries a set of hormones as well, including TRH, CRH, GnRH, GHRH, somatostatin, ADH, oxytocin, and dopamine. [quick note: somatostatin acts as a GHRH antagonist, and dopamine acts as a prolactin antagonist] the hypothalamus is connected via nerves as well as blood to the pituitary, which is divided into 3 lobes, anterior (makes up 80%), intermediate, and posterior. the posterior pituitary acts as a storage for ADH and oxytocin, and the intermediate lobe also contains hormones such as the melanocyte stimulating hormone. because of the pituitary's location in the sella turcica, pituitary adenomas might lead to bitemporal hemianopsia due to the upward growth and subsequent impingement on the optic chiasm.
the anterior pituitary's general function is to stimulate peripheral endocrine organs such as the thyroid and regulate growth and lactation. it does this by release of a variety of hormones, including growth hormone, LH / FSH, TSH, prolactin, and ACTH. ACTH is responsible for stimulating cortisol production from the adrenals. LH stimulates ovulation and progesterone production in females and prolactin has the opposite effect, while also stimulating lactation.
the posterior pituitary is made up of modified nerve fibers, axons, and glial cells extending from the supraoptic and paraventricular nuclei from the hypothalamus. as mentioned before, the axons of the posterior pituitary store two hormones made in the hypothalamus, ADH and oxytocin. ADH's main action is in the kidney, stimulating water reabsorption in the distal tubules, while oxytocin stimulates lactation and uterine contraction, among other things.
hypopituitarism means decreased output of pituitary hormones and can be due to a variety of causes-- oftentimes the cause for panhypopituitarism (equal reduction in all AP hormones) is iatrogenic-- either through radiation to the head or surgery that reduces blood flow. other causes might include destructive processes such as inflammation or infection, hemochromatosis, malignancy. hypopituitarism can also result in dwarfism, which comes in several varieties as well- if resulting from panhypopituitarism, body proportions will be normal, while a selective GH deficiency might result in abnormal proportions. achondroplastic dwarfism is a third type that is not related to hypopituitarism (and therefore is unresponsive to GH supplication).
some pituitary pathologies: pituitary apoplexy is a hemorrhage into a pre-existing adenoma, resulting in a sudden onset headache and diplopia. severe cases might also lead to ischemic necrosis and may even result in death. the most common cause of ischemic necrosis is sheehan's syndrome, although patients with this syndrome may have a range of outcomes, ranging from asymptomatic to death. sheehan's syndrome is a situation where the already hypoxic pituitary in pregnant women (due to an increase in pituitary size without increased vasculature) is further compromised by obstetric hemorrhage, leading to vasospasm and ischemic necrosis.
pituitary adenomas are the most common cause of hyperpituitarism, although a good portion of pituitary adenomas are non functional and can remain undetected. they can be macro (greater than 1cm) or micro (less than 1cm) and comprise 10% of all intracranial neoplasms. functional adenomas are generally composed of one cell type and secrete a single hormone. the most common functional adenomas are: prolactinoma, ACTH producing, gonadotropin producing, and growth hormone producing.
the most common type of adenoma produces prolactin and is composed of weakly staining acidophilic cells-- within which prolactin can be detected in the secretory granules. in females, the effects of a prolactinoma are what one would expect from increased prolactin levels: amenorrhea, diminished libido, ovarian cysts (due to inhibition of ovulation), galactorrhea. in males, prolactinomas might manifest asymptomatically, or decreased libido. prolactinomas might be diagnosed by high serum prolactin levels, and an MRI will confirm the presence of one as small as 2mm.
growth hormone producing adenomas are the second most common type. they are measured / diagnosed primarily by increased IGF-1 levels, from increased hepatic production due to GH stimulation. GH excess can lead to a variety of signs/symptoms, including diabetes, HTN, hyperglycemia, CHF, gonadal dysfunction, and muscle weakness. if the adenoma is functional before growth plate closure, the result is pituitary giantism, in which body size is increased and arms / legs are disproportionately long. if the adenoma is function after growth plate closure, the result is acromegaly, which has its own characteristics: enlarged hands, feet, face (nose broadens, teeth get further apart, jaw protrudes), and organomegaly. GH producing adenomas are diagnosed via IGF-1 levels as well as the GH suppression test, in which GH levels do not drop as they should in response to glucose administration.
empty sella syndrome describes any condition in which the sella turcica is enlarged but not filled with pituitary tissue. risk factors include pregnancy, obesity, and hypertension. ESS is caused by increased intracranial pressure which leads to CSF entering the sella turcica, compressing the pituitary against its walls. presentation might be asymptomatic, or may have papilledema. ESS might also be due to a surgical procedure or radiation which has enlarged the sella turcica.
excess ADH production may be related to posterior pituitary dysfunction and can result in dysfunction in the water balance in the body. syndrome of inappropriate ADH describes such a condition, which can also be caused by ectopic sites, generally from cancer cells. the signs and symptoms might be limited to reduced urine, and the diagnosis might be made by highly concentrated urine, decreased plasma osmolality, and hyponatremia.
diabetes insipidus is a condition which results from ADH deficiency; either from an underproduction from the hypothalamus (central) or dysfunctional ADH receptors in the kidney (nephrogenic). DI results in polyuria and polydipsia, with the polyuria generally exceeding the polydipsia. central might be caused by surgery/trauma, tumors, infection, sheehan's syndrome, while nephrogenic might be caused by chronic renal disease, lithium, among other things. a useful test for distinguishing central, nephrogenic DI, and psychogenic polydipsia is the water deprivation test. after depriving water, patients with psychogenic polydipsia will have increased osmolality while the other two conditions will not. after administration of ADH, psychogenic polydipsia and central DI will increase urine osmolality (increased reabsorption produces more concentrated urine), whereas nephrogenic will remain the same.
questions
hypothalamus and pituitary...
1. what is the relative prevalence of endocrine issues related to the hypothalamus, pituitary, and thyroid?
2. what are the hormones released by the hypothalamus?
3. what is the effect of these hormones on the pituitary?
4. where is the pituitary gland located?
5. what is the pituitary gland covered by?
6. how might a pituitary adenoma lead to loss of peripheral vision?
7. what are the divisions of the pituitary? which division predominates?
8. describe the general function of the posterior pituitary.
9. describe the function of the intermediate pituitary.
10. dopamine exerts inhibitory control over which other hormone?
anterior pituitary...
11. what are the hormones released by the anterior pituitary?
12. what is a better marker for checking growth hormone activity than a simple serum growth hormone level test?
13. describe the general function of the hormones released by the anterior pituitary.
14. what does ACTH do?
15. what does LH do in males and females?
16. what does prolactin do?
posterior pituitary...
17. describe the structure / content of the posterior pituitary.
18. what are the two hormones that are stored in the axons of the posterior pituitary?
19. what does ADH do?
20. what does oxytocin do?
hypopituitarism and dwarfism...
21. most cases of hypopituitarism are the result of...
22. what are some other potential causes of hypopituitarism?
23. what are the two types of pituitary dwarfism?
24. what is achondoplastic dwarfism?
acute pituitary pathologies...
25. what is pituitary apoplexy?
26. what are the symptoms of a pituitary apoplexy?
27. what are the complications of a severe case of pituitary apoplexy?
28. sheehan's syndrome is the most common cause of...
29. describe the pathophysiology of sheehan's syndrome.
pituitary adenoma...
30. pituitary adenomas are the most common cause of...
31. pituitary adenomas are usually...
32. what percentage of intracranial neoplasms are pituitary adenomas?
33. what age range is most common for pituitary adenomas?
34. functional adenomas are usually...
35. what is the difference between a macro and microadenoma?
36. are males more likely to present with a macro or microadenoma?
37. what are the most common types of functional adenomas?
prolactinoma...
38. most prolactinomas are composed of...
39. prolactin can be detected within...
40. what are the signs and symptoms of a prolactinoma in females?
41. what percentage of secondary amenorrhea cases are due to prolactinomas?
42. what are the signs / symptoms of a prolactinoma in males?
43. what are some labs and imaging techniques useful in diagnosing prolactinomas?
44. what is a naturopathic treatment option for prolactinoma?
growth hormone producing adenoma...
45. persistent oversecretion of GH stimulates...
46. what are the signs and symptoms of a GH producing adenoma?
47. how is a GH producing adenoma classified if it is functional before vs. after growth plate closure?
48. describe the body proportions of a patient with pituitary gigantism.
49. what are the signs and symptoms of a patient with acromegaly?
50. what are the lab tests used to diagnose GH producing adenomas?
51. how can a GH producing adenoma be differentiated from hyperglycemia?
corticotroph adenoma...
52. what is a corticotroph adenoma?
53. what is the difference between cushing's syndrome and cushing's disease?
empty sella syndrome...
54. what is the empty sella syndrome?
55. what are the risk factors for ESS?
56. what is the etiology of ESS?
57. what are the signs/symptoms of ESS?
58. what is secondary ESS?
syndrome of inappropriate ADH...
59. what is SIADH?
60. what are some etiological factors that might lead to SIADH?
61. what are the signs / symptoms of SIADH?
62. what are the lab results for SIADH?
diabetes insipidus...
63. what are the two causes of diabetes insipidus?
64. what are the signs and symptoms of DI?
65. what are some etiologies of central DI?
66. what is a drug that might cause nephrogenic DI?
67. what is a test that can distinguish between central DI, nephrogenic DI, and psychogenic polydipsia?
68. what is one possible treatment for DI?
answers
1. hypothalamus problems are much rarer than pituitary and thyroid.
2. TRH
CRH
GnRH
GHRH
somatostatin
dopamine
ADH
oxytocin
3. stimulates pituitary, except for somatostatin and dopamine.
4. the sella turcica.
5. dura mater, except for the a thin opening which conveys a stalk from the hypothalamus.
6. the upward growth of a pituitary tumor will impinge on the optic chiasm, which will block the optic pathways responsible for peripheral vision bilaterally.
7. anterior, intermediate, posterior lobes. anterior is 80%.
8. storage unit for oxytocin and ADH.
9. also contains hormones or precursor to hormones such as melanocyte stimulating hormone and a hormone that increases aldosterone production.
10. prolactin.
11. growth hormone
LH and FSH
TSH
prolactin
ACTH.
[G L/F T P A] [go left, pa]
12. IGF-1 levels.
13. stimulates peripheral endocrine organs and regulates growth and lactation.
14. stimulates cortisol production in the adrenals.
15. stimulates ovulation and progesterone production in females, stimulates testosterone production in males.
16. promotes lactation and suppresses ovulation and fertility.
17. a modified neural network consisting of modified glial cells, nerve fibers, and axonal processes extending from the supraoptic and paraventricular nuclei of the hypothalamus.
18. ADH and oxytocin.
19. stimulates water reabsorption in distal tubules of nephron.
20. regulates lactation and uterine contraction.
21. radiation or surgery which reduce blood flow to the brain.
22. destructive lesions
destructive processes
impingement from malignancy
infection
hemochromatosis
sarcoidosis
23. resulting either from deficiency of all AP hormones or just GH, in which body proportions remain normal and abnormal, respectively.
24. genetic dysfunction of fibroblasts that results in abnormal cartilaginous development.
25. sudden hemorrhage into an existing pituitary adenoma.
26. sudden onset headache and diplopia.
27. ischemic necrosis, death.
28. ischemic necrosis of the pituitary.
29. in pregnant women, the anterior pituitary enlarges without corresponding vasculature increase. this hypoxic state combined with an obstetric hemorrhage can cause vasospasm of the blood supply and ultimately ischemia and necrosis.
30. hyperpituitarism.
31. non functional, isolated lesions with no associated neoplasms.
32. 10%.
33. 30-60.
34. made of one cell type that produces one hormone.
35. greater than or less than 1 cm.
36. macro because of the greater chance of adenoma remaining undetected due to the lack of hormonal feedback as compared to women.
37. prolactinoma, ACTH cell adenoma, gonadotropin adenoma, growth hormone adenoma
[pro act gon grow] [functionally proactive: go and grow!]
38. weakly staining acidophilic cells.
39. secretory granules within cytoplasm of cells.
40. diminished menses or amenorrhea
diminished libido
infertility
ovarian cysts
galactorrhea
[prolact amen libido infertility cysts galact] [amen; all infertile cysts in the galaxy now have libidos]
41. roughly 25%.
42. asymptomatic, or decreased libido / sperm count.
43. serum prolactin and MRI.
44. botanicals that have phytoestrogenic or progesterone agonist effects.
45. hepatic secretion of IGF-1
46. hyperglycemia, DM, HTN, CHF, gonadal dysfunction, muscle weakness/arthritis. [sugar sugar blood blood nads muscles]
47. before: pituitary giant
after: acromegaly
48. bigger body size with disproportionately long arms and legs.
49. disproportionately large hands, feet, face
enlargement of heart, thyroid, liver, adrenals
jaw protrusion
spreading of teeth
broadening of nose
"spade like" hands
50. IGF-1 levels and the GH suppression test.
51. in the GH suppression test of a hyperglycemic patient, GH will be suppressed, but won't be in a patient with a GH producing adenoma.
52. an adenoma that produces ACTH, leading to adrenal hypersecretion of cortisol.
53. cushing's syndrome describes a state of hypercortisolism, of which cushing's disease is a specific type related to a corticotroph adenoma.
54. any condition that leads to an enlarged sella turcica not filled with pituitary tissue.
55. obese females
multiple pregnancies
hypertension
[fat fetus food]
56. increased intracranial pressure leads to CSF entering the sella turcica and compressing pituitary against wall.
57. asymptomatic, may see papilledema.
58. ESS due to surgical procedure or radiation that has enlarged the sella turcica.
59. excess secretion of ADH by ectopic sites.
60. cancer (lung, breast, prostate), head trauma, narcotics.
61. oliguria with no other signs.
62. highly concentrated urine, low plasma osmolality, hyponatremia.
63. deficiency of ADH either by hypothalamus underproduction or kidney unresponsiveness.
64. polyuria, polydipsia.
65. trauma
surgery
tumor
infection
sheehan's
66. lithium.
67. the water deprivation test.
68. oxytocin.
Showing posts with label hypothalamus. Show all posts
Showing posts with label hypothalamus. Show all posts
Monday, May 3, 2010
Monday, May 18, 2009
organ systems: limbic system part 1
the limbic system is a set of brain structures that are involved in a variety of neurological and physiological functions such as emotion and memory formation. the outer brain structures included in the limbic system include the parahippocampal cortices, cingulate gyrus, prefrontal cortex, entorhinal cortex, and the insula. the deeper brain structures include the amygdala, septum, the nucleus accumbens of the ventral striatum, and the hippocampus.
a sidebar on neuromodulatory pathways that are related to limbic functioning. the pathway involving norepinephrine begins in the locus ceruleus in the pons, and mediates attentional selection during stress, activating wide areas of the brain. the dopamine pathway starts at the ventral tegmentum in the midbrain and is involved in maintaining working memory and also reward seeking behavior via the mesolimbic system. the serotonin pathway begins in the raphe nucleus in the medulla, and regulates mood and the sleep/wake cycle. finally, the acetylcholine pathway begins in the diagonal band of broca, septum, and nucleus basalis, and is involved in memory formation and cognition.
the hippocampus is a structure in the limbic system that is centrally involved in formation of memories. it has an "archicortex" (a term that denotes a cortical area that has less than 6 layers) that bulges into the lateral ventricle. it receives sensory afferents from various areas of the brain; in particular, the septum and various cortical areas (sensory, premotor, association, cingulate), allowing it to form episodic memories-- the auto-noetic, contextual experiences of an event. this information is then projected to the hypothalamus for neuroendocrine function, as well as back to the cortical areas (prefrontal, cingulate, temporal) for storage of semantic memories: the abstracted, noetic, non-contextual knowledge which is parsed from episodic memories.
the next sections focused on the limbic system's role in mediating sleep / wake states. it introduced the EEG as a tool to measure synchronous brain activity, used as a tool to detect various brain states during different stages of sleep. during the night, humans alternate between stage 1-4 sleep and REM sleep, which have markedly different neurological and physiological features: stage 4 sleep has a high EEG amplitude and low frequency and thus is called slow wave sleep; it also features decreased afferent input to cortical areas, decreased metabolism, and sleepwalking / tossing. on the other hand, REM sleep is characterized by low amplitude, high frequency EEGs, paralysis of large muscles, and an extremely active mind- leading to dreaming and hallucinations.
the states of arousal and wakefulness are mediated by the thalamus, which receive afferents from the cholinergic pontine pathways which are active during waking and REM states, and then project to the cortex. when the pathways that stimulate the thalamus are activated, the thalamus is activated to send information to the cortex. the cortex receives afferents from monoaminergic pathways (norepinephrine, serotonin, dopamine), cholinergic pathways from the basal forebrain nucleus, and the orexin and hypocretin pathways (which are defective in narcolepsy). when these pathways are stimulated, the cortex is activated to process the input from the thalamus.
sleep regulation is mediated by the hypothalamus and SCN. the VLPO nucleus of the hypothalamus inhibits hypothalamic and brain stem nuclei involved in arousal via GABA and galanin, thus inducing drowsiness. the SCN, as covered in the optic system, receives light/dark information from the eyes and projects to the supraventricular zone and dorsal medial nuclei of the hypothalamus, which promotes wakefulness by inhibiting the VLPO nuclei of the hypothalamus via GABA as well as stimulating the orexin pathway via glutamate.
questions
anatomy and neuromodulators...
1. what are the cortical regions included in the limbic system?
2. what are the deeper brain regions included in the limbic system?
3. what are the brain areas involved in planning, cognition, stress, fear, and memory?
4. where does the neuromodulatory pathway for norepinephrine begin and what is it involved in?
5. where does the neuromodulatory pathway for dopamine begin and what is it involved in?
6. where does the neuromodulatory pathway for serotonin begin and what is it involved in?
7. where does the neuromodulatory pathway for acetylcholine begin and what is it involved in?
hippocampus and memory...
8. describe the structure and location of the hippocampus.
9. what are the structures that project afferents to the hippocampus?
10. describe the pathway of neural activity that leads in and out of the hippocampus.
11. where does the hippocampus project efferent neurons to?
12. what are the two types of explicit/declarative memory?
13. where are episodic memories processed and what are they?
14. where are semantic memories processed and what are they?
15. describe the encoding of episodic memories by the hippocampus.
16. describe the formation of semantic memory.
sleep: EEG's and REM...
17. what does an EEG measure?
18. what are the two stages of sleep that humans oscillate between? how often does this occur?
19. what happens to EEG waves when sleep progresses through stage 1 to stage 4?
20. describe the physiological and neurological state during stage 4 non-REM sleep.
21. describe the physiological and neurological state during REM sleep.
22. what types of sleep (REM vs. slow wave) are the first and second halves of sleep dominated by?
arousal pathways, regulation...
23. what pathways are wakefulness and arousal mediated by?
24. what do pathways that activate the thalamus facilitate?
25. what are the specific pathways that activate the thalamus during wakefulness / arousal? when during the day or night are they the most active?
26. what do pathways that activate the cortex facilitate?
27. what are the specific pathways that activate the cortex during arousal / wakefulness?
28. which of these pathways degenerates during narcolepsy?
29. sleep is regulated by which brain structure?
30. describe the specific action of this brain structure in regulating sleep.
31. describe the regulation of sleep via circadian cycles.
answers
1. parahippocampal cortex, cingular cortex, prefrontal cortex, entorhinal cortex, insula.
2. amygdala, septum, ventral striatum / nucleus accumbens, hippocampus.
3. planning: frontal and cingulate cortices. cognition: cerebral cortex. stress: HPA axis, amygdala, hippocampus. fear: amygdala. memory: hippocampus, entorhinal cortex.
4. begins in locus ceruleus in pons, involved in attentional selectivity during stress and activating large areas of brain.
5. begins in the ventral tegmentum in midbrain, involved in facilitating working memory in prefrontal cortex, and reward seeking behavior via the mesolimbic dopamine system.
6. begins in raphe nucleus in medulla, involved in mood regulation and sleep-wake cycles.
7. begins in nucleus basalis, diagonal band of broca, septum, involved in memory formation and cognition.
8. has an archicortex that bulges into the temporal lobe / lateral ventricle.
9. the septum, and cortical regions such as prefrontal, association, sensory, cingulate cortices.
10. parahippocampal cortex, entorhinal cortex, hippocampus, amygdala.
11. from the fornix of the hippocampus to the hypothalamus for neuroendocrine function, and the prefrontal, cingulate, and temporal cortices for memory consolidation.
12. episodic and semantic.
13. processed in the hippocampus and hippocampal cortices; an auto-noetic, context based memory of the experience of an event.
14. non-contextual, noetic, long term representations based on knowledge of the world. encoded in the limbic cortices: anterolateral temporal and ventrolateral prefrontal.
15. sensory cortices project particular experiences, contexts, and relationships to the hippocampus to form the basis for episodic memory formation.
16. episodic memories are projected to the temporal and prefrontal cortices, where they are encoded into semantic memories; patterns and relationships are parsed from episodic memories and stored.
17. synchronous activity of large groupings of neurons which are producing EPSP's or IPSP's in unison.
18. REM sleep and non REM sleep, every 90 minutes.
19. amplitude of EEG waves increases and frequency gets slower.
20. decreased neural afferent input to cortices. decreased metabolism: heart rate, breathing rate, blood pressure. sleepwalking and tossing/turning. inactive mind, relatively active body.
21. decreased EEG amplitude/increased EEG frequency. rapid eye movements. increased metabolism. paralysis of large muscles. hallucinations and dreaming. active mind, inactive body.
22. first half dominated by slow wave sleep and second half dominated by REM sleep.
23. reticular pathways to the thalamus and cortex.
24. transmission of information from the thalamus to the cortex.
25. cholinergic pontine pathways: pedunculopontine and lateral dorsal tegmental nuclei- most active during waking and REM sleep.
26. processing of information from the thalamus.
27. monoaminergic pathways (norepinephrine, dopamine, serotonin pathway), cholinergic pathway from basal forebrain nucleus, orexin/hypocretin pathway from lateral hypothalamus. (base forbes, t rex hypocrit)
28. the orexin/hypocretin pathway.
29. VLPO nucleus of the hypothalamus.
30. inhibits hypothalamic and brain stem nuclei involved in arousal via GABA and galanin; thus inducing drowsiness.
31. the suprachiasmatic nucleus regulates sleep according to light-dark cycles- projecting neurons to supraventricular zone and dorsal medial nuclei of hypothalamus, which promotes wakefulness by inhibiting VLPO nuclei of hypothalamus via GABA, stimulates orexin via glutamate.
a sidebar on neuromodulatory pathways that are related to limbic functioning. the pathway involving norepinephrine begins in the locus ceruleus in the pons, and mediates attentional selection during stress, activating wide areas of the brain. the dopamine pathway starts at the ventral tegmentum in the midbrain and is involved in maintaining working memory and also reward seeking behavior via the mesolimbic system. the serotonin pathway begins in the raphe nucleus in the medulla, and regulates mood and the sleep/wake cycle. finally, the acetylcholine pathway begins in the diagonal band of broca, septum, and nucleus basalis, and is involved in memory formation and cognition.
the hippocampus is a structure in the limbic system that is centrally involved in formation of memories. it has an "archicortex" (a term that denotes a cortical area that has less than 6 layers) that bulges into the lateral ventricle. it receives sensory afferents from various areas of the brain; in particular, the septum and various cortical areas (sensory, premotor, association, cingulate), allowing it to form episodic memories-- the auto-noetic, contextual experiences of an event. this information is then projected to the hypothalamus for neuroendocrine function, as well as back to the cortical areas (prefrontal, cingulate, temporal) for storage of semantic memories: the abstracted, noetic, non-contextual knowledge which is parsed from episodic memories.
the next sections focused on the limbic system's role in mediating sleep / wake states. it introduced the EEG as a tool to measure synchronous brain activity, used as a tool to detect various brain states during different stages of sleep. during the night, humans alternate between stage 1-4 sleep and REM sleep, which have markedly different neurological and physiological features: stage 4 sleep has a high EEG amplitude and low frequency and thus is called slow wave sleep; it also features decreased afferent input to cortical areas, decreased metabolism, and sleepwalking / tossing. on the other hand, REM sleep is characterized by low amplitude, high frequency EEGs, paralysis of large muscles, and an extremely active mind- leading to dreaming and hallucinations.
the states of arousal and wakefulness are mediated by the thalamus, which receive afferents from the cholinergic pontine pathways which are active during waking and REM states, and then project to the cortex. when the pathways that stimulate the thalamus are activated, the thalamus is activated to send information to the cortex. the cortex receives afferents from monoaminergic pathways (norepinephrine, serotonin, dopamine), cholinergic pathways from the basal forebrain nucleus, and the orexin and hypocretin pathways (which are defective in narcolepsy). when these pathways are stimulated, the cortex is activated to process the input from the thalamus.
sleep regulation is mediated by the hypothalamus and SCN. the VLPO nucleus of the hypothalamus inhibits hypothalamic and brain stem nuclei involved in arousal via GABA and galanin, thus inducing drowsiness. the SCN, as covered in the optic system, receives light/dark information from the eyes and projects to the supraventricular zone and dorsal medial nuclei of the hypothalamus, which promotes wakefulness by inhibiting the VLPO nuclei of the hypothalamus via GABA as well as stimulating the orexin pathway via glutamate.
questions
anatomy and neuromodulators...
1. what are the cortical regions included in the limbic system?
2. what are the deeper brain regions included in the limbic system?
3. what are the brain areas involved in planning, cognition, stress, fear, and memory?
4. where does the neuromodulatory pathway for norepinephrine begin and what is it involved in?
5. where does the neuromodulatory pathway for dopamine begin and what is it involved in?
6. where does the neuromodulatory pathway for serotonin begin and what is it involved in?
7. where does the neuromodulatory pathway for acetylcholine begin and what is it involved in?
hippocampus and memory...
8. describe the structure and location of the hippocampus.
9. what are the structures that project afferents to the hippocampus?
10. describe the pathway of neural activity that leads in and out of the hippocampus.
11. where does the hippocampus project efferent neurons to?
12. what are the two types of explicit/declarative memory?
13. where are episodic memories processed and what are they?
14. where are semantic memories processed and what are they?
15. describe the encoding of episodic memories by the hippocampus.
16. describe the formation of semantic memory.
sleep: EEG's and REM...
17. what does an EEG measure?
18. what are the two stages of sleep that humans oscillate between? how often does this occur?
19. what happens to EEG waves when sleep progresses through stage 1 to stage 4?
20. describe the physiological and neurological state during stage 4 non-REM sleep.
21. describe the physiological and neurological state during REM sleep.
22. what types of sleep (REM vs. slow wave) are the first and second halves of sleep dominated by?
arousal pathways, regulation...
23. what pathways are wakefulness and arousal mediated by?
24. what do pathways that activate the thalamus facilitate?
25. what are the specific pathways that activate the thalamus during wakefulness / arousal? when during the day or night are they the most active?
26. what do pathways that activate the cortex facilitate?
27. what are the specific pathways that activate the cortex during arousal / wakefulness?
28. which of these pathways degenerates during narcolepsy?
29. sleep is regulated by which brain structure?
30. describe the specific action of this brain structure in regulating sleep.
31. describe the regulation of sleep via circadian cycles.
answers
1. parahippocampal cortex, cingular cortex, prefrontal cortex, entorhinal cortex, insula.
2. amygdala, septum, ventral striatum / nucleus accumbens, hippocampus.
3. planning: frontal and cingulate cortices. cognition: cerebral cortex. stress: HPA axis, amygdala, hippocampus. fear: amygdala. memory: hippocampus, entorhinal cortex.
4. begins in locus ceruleus in pons, involved in attentional selectivity during stress and activating large areas of brain.
5. begins in the ventral tegmentum in midbrain, involved in facilitating working memory in prefrontal cortex, and reward seeking behavior via the mesolimbic dopamine system.
6. begins in raphe nucleus in medulla, involved in mood regulation and sleep-wake cycles.
7. begins in nucleus basalis, diagonal band of broca, septum, involved in memory formation and cognition.
8. has an archicortex that bulges into the temporal lobe / lateral ventricle.
9. the septum, and cortical regions such as prefrontal, association, sensory, cingulate cortices.
10. parahippocampal cortex, entorhinal cortex, hippocampus, amygdala.
11. from the fornix of the hippocampus to the hypothalamus for neuroendocrine function, and the prefrontal, cingulate, and temporal cortices for memory consolidation.
12. episodic and semantic.
13. processed in the hippocampus and hippocampal cortices; an auto-noetic, context based memory of the experience of an event.
14. non-contextual, noetic, long term representations based on knowledge of the world. encoded in the limbic cortices: anterolateral temporal and ventrolateral prefrontal.
15. sensory cortices project particular experiences, contexts, and relationships to the hippocampus to form the basis for episodic memory formation.
16. episodic memories are projected to the temporal and prefrontal cortices, where they are encoded into semantic memories; patterns and relationships are parsed from episodic memories and stored.
17. synchronous activity of large groupings of neurons which are producing EPSP's or IPSP's in unison.
18. REM sleep and non REM sleep, every 90 minutes.
19. amplitude of EEG waves increases and frequency gets slower.
20. decreased neural afferent input to cortices. decreased metabolism: heart rate, breathing rate, blood pressure. sleepwalking and tossing/turning. inactive mind, relatively active body.
21. decreased EEG amplitude/increased EEG frequency. rapid eye movements. increased metabolism. paralysis of large muscles. hallucinations and dreaming. active mind, inactive body.
22. first half dominated by slow wave sleep and second half dominated by REM sleep.
23. reticular pathways to the thalamus and cortex.
24. transmission of information from the thalamus to the cortex.
25. cholinergic pontine pathways: pedunculopontine and lateral dorsal tegmental nuclei- most active during waking and REM sleep.
26. processing of information from the thalamus.
27. monoaminergic pathways (norepinephrine, dopamine, serotonin pathway), cholinergic pathway from basal forebrain nucleus, orexin/hypocretin pathway from lateral hypothalamus. (base forbes, t rex hypocrit)
28. the orexin/hypocretin pathway.
29. VLPO nucleus of the hypothalamus.
30. inhibits hypothalamic and brain stem nuclei involved in arousal via GABA and galanin; thus inducing drowsiness.
31. the suprachiasmatic nucleus regulates sleep according to light-dark cycles- projecting neurons to supraventricular zone and dorsal medial nuclei of hypothalamus, which promotes wakefulness by inhibiting VLPO nuclei of hypothalamus via GABA, stimulates orexin via glutamate.
Tuesday, March 10, 2009
ms anatomy II: neurocranium part II
[picture courtesy of erica zelfand]
this is the second lecture in the series on the "neurocranium" and dealt with a variety of topics such as structure of the brain, functions of each lobe, blood supply, spinal cord, meninges, glial cells, and the blood brain barrier.
the cerebral portion of the brain is divided up into different lobes, which have been shown to have distinct cognitive and emotional correlates. for example, the frontal lobe is the primary motor area, and is also involved in speech and behavior. the parietal lobes are involved in somatosensory input, prioprioception, sense of self. the temporal lobes are involved in audition, olfaction, and memory. the occipital lobes are involved in vision. cerebellum, midbrain, medulla, are underneath the cerebral portion and are involved more in basic physiological processes. for example, the medulla is involved in autonomic regulation of the cardiovascular system and respiration. the hypothalamus is involved in autonomic, affective, and hormonal activity. the midbrain is involved in motor control. the cerebellum is involved in motor coordination and timing.
the blood supply to the brain comes ultimately from the brachiocephalic branch of the aorta, which branches into the common carotid and the subclavian. the vertebral arteries branch off of the subclavian, travel in the transverse foramen of C1-C6,
and penetrate the atlanto-occipital membrane. from there they ascend on the ventral surface of the brainstem and combine to form the basilar artery, from which other arteries branch out (see diagram) such as the pontine and cerebellar arteries. the common carotid artery, on the other hand, branches into the internal and external common carotid; the internal common carotid branches into the anterior and middle cerebral arteries, which supply blood to the lateral and medial cerebral cortex, internal capsule, basal ganglia, and cingulate gyrus. the occlusions in each of these small branches can produce different effects (see diagram).
a few details about the spinal cord: it extends down to L1, beyond which the dura extends until S2. the spinal cord ends at the conus medullaris, a tapering down of the cord which ends in the caudus equinus, which is a splaying out of a horse tail-like arrangement of nerve rootlets. around the spinal cord, there are the three meninge layers: pia, arachnoid, dura mater. denticulate ligaments are pial "projections" into the arachnoid and dura mater which serve to anchor the spinal cord. the filum terminale is the pial strand that connects from the end of the spinal cord (L1) to the end of the dural sac (S2).
a few notes about glial cells and the blood brain barrier. glial cells were covered briefly in histology as the cells that "support" the neurons. in the central nervous system these cells are astrocytes, oligodendrocytes. oligodendrocytes are the cells that produce the myelin sheath that increases the rate of neuronal conduction. whereas schwann cells can only wrap around 1 axon, a single oligodendrocytes can wrap up to 50 different axons. astrocytes provide electrical insulation between neurons, secrete neuronal growth factors and cytokines, and absorb neurotransmitters. they can be further divided into protoplasmic and fibrous- fibrous astrocytes are involved in repairing damaged neuronal tissue. astrocytes also aid in the maintenance of the blood brain barrier, which is made up of astrocyte foot processes, basal lamina, pericytes, and endothelium.
questions
general anatomy and fissures...
1. cerebral hemispheres include...
2. the cerebral cortex is the site for...
3. what are gyri and sulci/fissures?
4. what are the three main fissures in the brain?
5. what does the longitudinal fissure separate?
6. what does the lateral fissure separate?
7. what does the central fissure separate?
functions of...
8. frontal lobe
9. parietal lobe
10. occipital lobe
11. temporal lobe
12. medulla
13. cerebellum
14. pons
15. midbrain
16. thalamus
17. hypothalamus
cerebral arteries...
18. where does the common carotid artery branch off from?
19. where does the common carotid artery split?
20. what does the internal carotid artery split into?
21. what does the internal carotid artery supply blood to?
22. what is the difference between an ischemic and hemorrhagic stroke?
23. where does the middle cerebral artery run?
24. what do the cortical branches supply blood to and what occurs during a stroke of these arteries?
25. what do the lateral striate branches supply blood to and what occurs during a stroke of these arteries?
26. what does the anterior cerebral artery supply blood to?
27. what happens after stroke in the anterior cerebral artery?
basivertebral arteries...
28. describe the passage of the vertebral artery.
29. vertebral arteries unite to form...
30. where is the path of the basilar artery? what does it branch into?
31. what does occlusion in the anterior and posterior spinal branch lead to?
32. what does occlusion in the posterior inferior cerebellar branch lead to?
33. what does occlusion in the anterior inferior and superior cerebellar branch lead to?
34. what does occlusion in the pontine arteries lead to?
35. what does occlusion in the labyrinthine branch lead to?
36. how do occlusions of the vertebral basilar arteries result in deficits in vision?
37. how do occlusions of the vertebral basilar arteries result in problems with balance?
posterior cerebral and circle of willis...
38. where does the posterior cerebral artery project to?
39. what happens when the posterior cerebral artery is occluded?
40. what is the circle of willis?
41. what does the anterior communicating artery connect?
42. what does the posterior communicating artery connect?
spinal cord...
43. how far down does the spinal cord extend?
44. how far down does the spinal dura extend?
45. what is the conus medullaris?
46. what is the cauda equina?
47. where is the junctional zone between the central and peripheral nervous systems?
48. what does the dura turn into at this point?
meninges and spinal veins...
49. how far down does the dura mater extend?
50. what is in the epidural space?
51. what is arachnoid mater?
52. what are denticulate ligaments?
53. what is the filum terminale?
54. where would one extract CSF from the spinal cord?
55. what are the two ways of administering anesthetic to the spinal cord?
56. what does the basivertebral vein do?
57. what is the connection between the basivertebral veins and prostate cancer?
58. describe the vertebral vein's use as a shunt.
glial cells and blood brain barrier...
59. what are oligodendrocytes and what do they do?
60. "unlike schwann cells, oligodendrocytes do not..."
61. what do astrocytes do?
62. what is the difference between protoplasmic and fibrous astrocytes?
63. what are microglia and what do they do?
64. what cell types line the ventricles?
65. what makes up the blood brain barrier?
66. what is the blood brain barrier maintained and induced by?
67. describe the transport of glucose, amino acids, and gases through the blood brain barrier.
68. which brain regions is there no blood brain barrier?
answers
1. white matter, basal ganglia, cerebral cortex.
2. sensorimotor integration, perceptive quality of our experiences
3. gyri are convolutions of the cortex and sulci are divisions or gaps between the gyri.
4. longitudinal, lateral, central.
5. the left and right hemispheres.
6. the frontal and temporal lobes.
7. the frontal and parietal lobes.
8. primary motor area, speech, behavior
9. sensorimotor, prioprioception, association of sensorimotor-audition-vision, formation of egocentric space, sense of self
10. vision
11. audition, olfaction, memory
12. autonomic control over respiration, cardiovascular systems
13. motor coordination and timing
14. cerebellar connection
15. motor control
16. sensorimotor information to cerebral cortex
17. autonomic, hormonal, affective activity
18. the brachiocephalic branch of the aortic arch.
19. at the carotid sinus into the internal and external carotid arteries.
20. anterior and middle cerebral arteries
21. most of the cerebral hemispheres.
22. ischemic is blockage of the cerebral artery via a thrombus or embolus which leads to necrosis. hemorrhagic is rupture of the artery which causes a hematoma, which leads to necrosis.
23. in the lateral fissure; along the lateral surface of the cerebral cortex.
24. lateral surface of cortex. stroke causes sensory, motor, language deficits.
25. internal capsule and basal ganglia. stroke causes hemiplegia.
26. medial surface of cerebral cortex, including cingulated gyrus.
27. sensory, motor, emotional deficits.
28. branches off the subclavian artery, passes through transverse foramina of C1-C6, and penetrates the atlanto occipital membrane.
29. basilar artery on ventral medulla.
30. the ventral surface of the brainstem; branches into cerebellar, pontine, posterior cerebral arteries.
31. loss of spinal cord function
32. Wallenberg syndrome: loss of sensation of pain, heat, muscle coordination.
33. loss of muscle coordination.
34. cranial nerve dysfunction.
35. deafness and vertigo.
36. torsion/compression of vertebral basilar arteries can reduce blood flow to brain stem, cerebellum, occipital lobe- anoxia in the occipital lobe causes loss of vision.
37. anoxia in cerebellum or inner ear can cause problems with balance.
38. temporal and occipital lobes.
39. visual deficits.
40. the anterior and posterior communicating arteries.
41. anterior cerebral arteries.
42. middle and posterior cerebral arteries.
43. down to L1.
44. down to S2.
45. tapered end of the spinal cord.
46. the “horse’s tail”, the end of the spinal cord which branches into nerve roots that extend to lumbar and sacral foramina.
47. the intervertebral foramina
48. the epineurium that covers the dorsal and ventral rami and ganglia.
49. S2
50. veins and fat.
51. the meninge layer in between the dura and pia mater, with trabeculae inside the subarachnoid space.
52. pial connective tissue that suspends spinal cord to the inside of arachnoid / dura mater.
53. a pial strand that connects down to the end of the dural sac.
54. from the subarachnoid space.
55. to the epidural and subdural spaces.
56. drains vertebral bodies.
57. prostate cancer can metastasize into vertebrae through the basivertebral veins.
58. blood shunts from caval veins into vertebral veins if IVC constricted (while coughing, for example)
59. cells in the CNS that myelinate up to 50 axons.
60. "cover unmyelinated axons, which lay bare in the CNS"
61. electrically insulate neurons from each other, uptake neurotransmitters and ions, and secrete neuronal growth factors and cytokines.
62. protoplasmic interconnect neurons, induce early growth and development of the blood/brain barrier, whereas fibrous form astrocytic scars after brain tissue destruction.
63. phagocytic cells related to monocyte/macrophages which consume debris and secrete cytokines during inflammation.
64. ependymal cells.
65. endothelium, pericytes, basal lamina, astrocyte foot processes.
66. maintained by astrocytes.
67. glucose and amino acids pass through BBB via transport proteins, and gases diffuse through lipid membrane.
68. hypothalamus, area postrema, other periventricular regions.
this is the second lecture in the series on the "neurocranium" and dealt with a variety of topics such as structure of the brain, functions of each lobe, blood supply, spinal cord, meninges, glial cells, and the blood brain barrier.
the cerebral portion of the brain is divided up into different lobes, which have been shown to have distinct cognitive and emotional correlates. for example, the frontal lobe is the primary motor area, and is also involved in speech and behavior. the parietal lobes are involved in somatosensory input, prioprioception, sense of self. the temporal lobes are involved in audition, olfaction, and memory. the occipital lobes are involved in vision. cerebellum, midbrain, medulla, are underneath the cerebral portion and are involved more in basic physiological processes. for example, the medulla is involved in autonomic regulation of the cardiovascular system and respiration. the hypothalamus is involved in autonomic, affective, and hormonal activity. the midbrain is involved in motor control. the cerebellum is involved in motor coordination and timing.
the blood supply to the brain comes ultimately from the brachiocephalic branch of the aorta, which branches into the common carotid and the subclavian. the vertebral arteries branch off of the subclavian, travel in the transverse foramen of C1-C6,
and penetrate the atlanto-occipital membrane. from there they ascend on the ventral surface of the brainstem and combine to form the basilar artery, from which other arteries branch out (see diagram) such as the pontine and cerebellar arteries. the common carotid artery, on the other hand, branches into the internal and external common carotid; the internal common carotid branches into the anterior and middle cerebral arteries, which supply blood to the lateral and medial cerebral cortex, internal capsule, basal ganglia, and cingulate gyrus. the occlusions in each of these small branches can produce different effects (see diagram).a few details about the spinal cord: it extends down to L1, beyond which the dura extends until S2. the spinal cord ends at the conus medullaris, a tapering down of the cord which ends in the caudus equinus, which is a splaying out of a horse tail-like arrangement of nerve rootlets. around the spinal cord, there are the three meninge layers: pia, arachnoid, dura mater. denticulate ligaments are pial "projections" into the arachnoid and dura mater which serve to anchor the spinal cord. the filum terminale is the pial strand that connects from the end of the spinal cord (L1) to the end of the dural sac (S2).
a few notes about glial cells and the blood brain barrier. glial cells were covered briefly in histology as the cells that "support" the neurons. in the central nervous system these cells are astrocytes, oligodendrocytes. oligodendrocytes are the cells that produce the myelin sheath that increases the rate of neuronal conduction. whereas schwann cells can only wrap around 1 axon, a single oligodendrocytes can wrap up to 50 different axons. astrocytes provide electrical insulation between neurons, secrete neuronal growth factors and cytokines, and absorb neurotransmitters. they can be further divided into protoplasmic and fibrous- fibrous astrocytes are involved in repairing damaged neuronal tissue. astrocytes also aid in the maintenance of the blood brain barrier, which is made up of astrocyte foot processes, basal lamina, pericytes, and endothelium.
questions
general anatomy and fissures...
1. cerebral hemispheres include...
2. the cerebral cortex is the site for...
3. what are gyri and sulci/fissures?
4. what are the three main fissures in the brain?
5. what does the longitudinal fissure separate?
6. what does the lateral fissure separate?
7. what does the central fissure separate?
functions of...
8. frontal lobe
9. parietal lobe
10. occipital lobe
11. temporal lobe
12. medulla
13. cerebellum
14. pons
15. midbrain
16. thalamus
17. hypothalamus
cerebral arteries...
18. where does the common carotid artery branch off from?
19. where does the common carotid artery split?
20. what does the internal carotid artery split into?
21. what does the internal carotid artery supply blood to?
22. what is the difference between an ischemic and hemorrhagic stroke?
23. where does the middle cerebral artery run?
24. what do the cortical branches supply blood to and what occurs during a stroke of these arteries?
25. what do the lateral striate branches supply blood to and what occurs during a stroke of these arteries?
26. what does the anterior cerebral artery supply blood to?
27. what happens after stroke in the anterior cerebral artery?
basivertebral arteries...
28. describe the passage of the vertebral artery.
29. vertebral arteries unite to form...
30. where is the path of the basilar artery? what does it branch into?
31. what does occlusion in the anterior and posterior spinal branch lead to?
32. what does occlusion in the posterior inferior cerebellar branch lead to?
33. what does occlusion in the anterior inferior and superior cerebellar branch lead to?
34. what does occlusion in the pontine arteries lead to?
35. what does occlusion in the labyrinthine branch lead to?
36. how do occlusions of the vertebral basilar arteries result in deficits in vision?
37. how do occlusions of the vertebral basilar arteries result in problems with balance?
posterior cerebral and circle of willis...
38. where does the posterior cerebral artery project to?
39. what happens when the posterior cerebral artery is occluded?
40. what is the circle of willis?
41. what does the anterior communicating artery connect?
42. what does the posterior communicating artery connect?
spinal cord...
43. how far down does the spinal cord extend?
44. how far down does the spinal dura extend?
45. what is the conus medullaris?
46. what is the cauda equina?
47. where is the junctional zone between the central and peripheral nervous systems?
48. what does the dura turn into at this point?
meninges and spinal veins...
49. how far down does the dura mater extend?
50. what is in the epidural space?
51. what is arachnoid mater?
52. what are denticulate ligaments?
53. what is the filum terminale?
54. where would one extract CSF from the spinal cord?
55. what are the two ways of administering anesthetic to the spinal cord?
56. what does the basivertebral vein do?
57. what is the connection between the basivertebral veins and prostate cancer?
58. describe the vertebral vein's use as a shunt.
glial cells and blood brain barrier...
59. what are oligodendrocytes and what do they do?
60. "unlike schwann cells, oligodendrocytes do not..."
61. what do astrocytes do?
62. what is the difference between protoplasmic and fibrous astrocytes?
63. what are microglia and what do they do?
64. what cell types line the ventricles?
65. what makes up the blood brain barrier?
66. what is the blood brain barrier maintained and induced by?
67. describe the transport of glucose, amino acids, and gases through the blood brain barrier.
68. which brain regions is there no blood brain barrier?
answers
1. white matter, basal ganglia, cerebral cortex.
2. sensorimotor integration, perceptive quality of our experiences
3. gyri are convolutions of the cortex and sulci are divisions or gaps between the gyri.
4. longitudinal, lateral, central.
5. the left and right hemispheres.
6. the frontal and temporal lobes.
7. the frontal and parietal lobes.
8. primary motor area, speech, behavior
9. sensorimotor, prioprioception, association of sensorimotor-audition-vision, formation of egocentric space, sense of self
10. vision
11. audition, olfaction, memory
12. autonomic control over respiration, cardiovascular systems
13. motor coordination and timing
14. cerebellar connection
15. motor control
16. sensorimotor information to cerebral cortex
17. autonomic, hormonal, affective activity
18. the brachiocephalic branch of the aortic arch.
19. at the carotid sinus into the internal and external carotid arteries.
20. anterior and middle cerebral arteries
21. most of the cerebral hemispheres.
22. ischemic is blockage of the cerebral artery via a thrombus or embolus which leads to necrosis. hemorrhagic is rupture of the artery which causes a hematoma, which leads to necrosis.
23. in the lateral fissure; along the lateral surface of the cerebral cortex.
24. lateral surface of cortex. stroke causes sensory, motor, language deficits.
25. internal capsule and basal ganglia. stroke causes hemiplegia.
26. medial surface of cerebral cortex, including cingulated gyrus.
27. sensory, motor, emotional deficits.
28. branches off the subclavian artery, passes through transverse foramina of C1-C6, and penetrates the atlanto occipital membrane.
29. basilar artery on ventral medulla.
30. the ventral surface of the brainstem; branches into cerebellar, pontine, posterior cerebral arteries.
31. loss of spinal cord function
32. Wallenberg syndrome: loss of sensation of pain, heat, muscle coordination.
33. loss of muscle coordination.
34. cranial nerve dysfunction.
35. deafness and vertigo.
36. torsion/compression of vertebral basilar arteries can reduce blood flow to brain stem, cerebellum, occipital lobe- anoxia in the occipital lobe causes loss of vision.
37. anoxia in cerebellum or inner ear can cause problems with balance.
38. temporal and occipital lobes.
39. visual deficits.
40. the anterior and posterior communicating arteries.
41. anterior cerebral arteries.
42. middle and posterior cerebral arteries.
43. down to L1.
44. down to S2.
45. tapered end of the spinal cord.
46. the “horse’s tail”, the end of the spinal cord which branches into nerve roots that extend to lumbar and sacral foramina.
47. the intervertebral foramina
48. the epineurium that covers the dorsal and ventral rami and ganglia.
49. S2
50. veins and fat.
51. the meninge layer in between the dura and pia mater, with trabeculae inside the subarachnoid space.
52. pial connective tissue that suspends spinal cord to the inside of arachnoid / dura mater.
53. a pial strand that connects down to the end of the dural sac.
54. from the subarachnoid space.
55. to the epidural and subdural spaces.
56. drains vertebral bodies.
57. prostate cancer can metastasize into vertebrae through the basivertebral veins.
58. blood shunts from caval veins into vertebral veins if IVC constricted (while coughing, for example)
59. cells in the CNS that myelinate up to 50 axons.
60. "cover unmyelinated axons, which lay bare in the CNS"
61. electrically insulate neurons from each other, uptake neurotransmitters and ions, and secrete neuronal growth factors and cytokines.
62. protoplasmic interconnect neurons, induce early growth and development of the blood/brain barrier, whereas fibrous form astrocytic scars after brain tissue destruction.
63. phagocytic cells related to monocyte/macrophages which consume debris and secrete cytokines during inflammation.
64. ependymal cells.
65. endothelium, pericytes, basal lamina, astrocyte foot processes.
66. maintained by astrocytes.
67. glucose and amino acids pass through BBB via transport proteins, and gases diffuse through lipid membrane.
68. hypothalamus, area postrema, other periventricular regions.
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