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Lecture outline
• Structural organisation of hypothalamus– Localisation + nuclei– Input/output pathways
• Physiological function of hypothalamus
Overview of anatomy
chiasmatic tuberal posterior
anteriormedial view
Amygdala
Mamillo-thalamic tract
Dorsal hypothalamic area
Lateral hyothalamicarea Supraoptic nucleus
Optic tract
Ventromedial nucleus
Arcuatenucleus
Median eminence
Lateral tuberalnucleus
Fornix
Dorsomedial nucleus
Amygdala
Medial forebrain bundle
Third ventricle
Overview of anatomycoronal view
Overview of physiological functions
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Overview of physiological functions• Maintenance of milieu interne
• Behaviour
• Memory
Regulation of energy metabolism (food intake, metabolic rate, temperature regulation, growth)
Reproductive function (including milk production, social interactions)
Biological clock, sleep-wake cycles
Control of blood flow (cardiac output, blood osmolarityand renal clearance, thirst regulation)
Overview of physiological functions• Maintenance of milieu interne
• Behaviour
• Memory
Regulation of energy metabolism (food intake, metabolic rate, temperature regulation, growth)
Reproductive function (including milk production, social interactions)
Biological clock (sleep-wake cycles)
Control of blood flow (cardiac output, blood osmolarityand renal clearance, thirst regulation)
Overview of physiological functions
Regulation of the autonomic nervous system
Release of hormonesHypothalamic neurons can release hormones (neuro-endocrine)
Overview of physiological functions• Detection of (changes in)
Blood osmolarity
Blood nutrient levels
Blood hormone levels
Body temperature
Directly and indirectly
Overview of connections• Input from
Retina (retinohypothalamic tract – terminates in SCN)
Olfactory receptors (medial forebrain bundle)
Cutaneous receptors
Higher (limbic) system (hippocampal formation: fornix – to mammillary bodies; amygdala: stria terminalis – to medial hypothalamus)
Viscera
Overview of connections• Output to
Thalamus (via mammillothalamic tract (Papez circuit: cingulategyrus – hippocampal formation – mammillary bodies – anterior thalamic nucleus – cingulate gyrus)) (also mammillotegmental tract to midbrain tegmentum)
Amygdala (from medial hypothalamus)
Midbrain PAG (from medial hypothalamus) (aggression, rage, flight)
Frontal and parietal lobes, habenular nucleus, midbrain…
Blood stream (pituitary)
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Overview of basic functions• Feed-back system
– Hypothalamus corrects deviations from a given set-point:
• measures current value• compares current value
with supposed value• makes adjustments to
achieve supposed value
– helps maintain body homeostasis
Overview of basic functions• Feed-back system
– Hypothalamus corrects deviations from a given set-point:
• measures current value• compares current value
with supposed value• makes adjustments to
achieve supposed value
– helps maintain body homeostasis
• Feed-forward system
– Hypothalamus can over-ride feed-back under special conditions
• Stress responses• Fever (body T set point is
changed to higher T)
Overview of basic functions• Feed-back system
– Hypothalamus corrects deviations from a given set-point:
• measures current value• compares current value
with supposed value• makes adjustments to
achieve supposed value
– helps maintain body homeostasis
• Feed-forward system
– Hypothalamus can over-ride feed-back under special conditions
• Stress responses• Fever (body T set point is
changed to higher T)
• Anticipation
– Hypothalamus adjusts its output to meet future needs
• Insulin secretion prior to food intake
• Look at neuroendocrine functions of hypothalamus
• Look at regulation of non-endocrine functions (ANS) of hypothalamus
Neuroendocrine hypothalamus
• Hypothalamic neurons can act as neuroendocrinecells
• Neurotransmitter = (neuro)hormone is released directly into blood stream
• Site of hormone release is pituitary gland• 2 principal pathways for eliciting hormone release:
– Via the anterior pituitary (adenohypophysis)• 2-tiers process
– Via the posterior pituitary (neurohypophysis)• 1-step process
Neuroendocrine hypothalamus
• Via anterior pituitary(adenohypophysis)– Hypothalamic parvocellular
neurons release releasing or inhibiting hormones into hypothalamo-pituitary portal veins
– Hypothalmo-pituitary portal veins carry these hormones to anterior pituitary
– Anterior pituitary has cells responding to the different releasing or inhibiting hormones
– Responsive cells release or stop releasing hormones in response to binding of hypothalamic releasing or inhibiting hormones into systemic circulation
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Neuroendocrine hypothalamus
• Via anterior pituitary(adenohypophysis)– Hypothalamic parvocellular
neurons secrete releasing or inhibiting hormones into hypothalamo-pituitary portal veins
– Hypothalmo-pituitary portal veins carry these hormones to anterior pituitary
– Anterior pituitary has cells responding to the different releasing or inhibiting hormones
– Responsive cells release or stop releasing hormones in response to binding of hypothalamic releasing or inhibiting hormones into systemic circulation
R I
AnteriorPituitary
Hypothalamus
Neuroendocrine hypothalamus
• Via anterior pituitary(adenohypophysis)– Hypothalamic parvocellular
neurons secrete releasing or inhibiting hormones into hypothalamo-pituitary portal veins
– Hypothalamo-pituitary portal veins carry these hormones to anterior pituitary
– Anterior pituitary has cells responding to the different releasing or inhibiting hormones
– Responsive cells release or stop releasing hormones in response to binding of hypothalamic releasing or inhibiting hormones into systemic circulation
R I
AnteriorPituitary
Hypothalamus
Neuroendocrine hypothalamus
• Via anterior pituitary(adenohypophysis)– Hypothalamic parvocellular
neurons secrete releasing or inhibiting hormones into hypothalamo-pituitary portal veins
– Hypothalamo-pituitary portal veins carry these hormones to anterior pituitary
– Anterior pituitary has cells responding to the different releasing or inhibiting hormones
– Responsive cells release or stop releasing hormones in response to binding of hypothalamic releasing or inhibiting hormones into systemic circulation
R I
AnteriorPituitary
Hypothalamus
Neuroendocrine hypothalamus
• Via anterior pituitary(adenohypophysis)– Hypothalamic parvocellular
neurons secrete releasing or inhibiting hormones into hypothalamo-pituitary portal veins
– Hypothalamo-pituitary portal veins carry these hormones to anterior pituitary
– Anterior pituitary has cells responding to the different releasing or inhibiting hormones
– Responsive cells secrete or stop secreting hormones in response to binding of hypothalamic releasing or inhibiting hormones into systemic circulation
R I
AnteriorPituitary
Hypothalamus
GnRH gonadotrope FSH+LH gonads
CRH corticotrope ACTH
TRH thyrotrope TSH thyroid
GHRH somatotrope GH
Sost somatotrope GH
DA lactotrope prolactin
Rel./Inhib.hormone:
GnRH gonadotrope FSH+LH gonads
CRH corticotrope ACTH
TRH thyrotrope TSH thyroid
GHRH somatotrope GH
Sost somatotrope GH
DA lactotrope prolactin
Rel./Inhib.hormone:
Ant. Pit.target cell:
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GnRH gonadotrope FSH+LH gonads
CRH corticotrope ACTH
TRH thyrotrope TSH thyroid
GHRH somatotrope GH
Sost somatotrope GH
DA lactotrope prolactin
adrenalgland
mammaryglands
many cells(bones)
Rel./Inhib.hormone:
Ant. Pit.target cell:
Hormone: target:
GnRH gonadotrope FSH+LH gonads
CRH corticotrope ACTH
TRH thyrotrope TSH thyroid
GHRH somatotrope GH
Sost somatotrope GH
DA lactotrope prolactin
adrenalgland
mammaryglands
arcuate
arcuate
para-ventri-cular(PVN)
arcuate
anteriorHT
many cells(bones)
releasefrom:
Rel./Inhib.hormone:
Ant. Pit.target cell:
Hormone: target:
Neuroendocrine hypothalamus
• Via anterior pituitary– Hypothalamic parvocellular
neurons release releasing or inhibiting hormones into hypothalamo-pituitary portal veins
– Hypothalmo-pituitary portal veins carry these hormones to anterior pituitary
– Anterior pituitary has cells responding to the different releasing or inhibiting hormones
– Responsive cells release or stop releasing hormones in response to binding of hypothalamic releasing or inhibiting hormones into systemic circulation
• Via posterior pituitary(neurohypophysis)– Hypothalamic
magnocellular neuronsrelease hormones directly into systemic veins that drain into the systemic circulation
– Hypothalamo-hypophyseal tract (axons of neuroendocrinemagnocellular neurons)
Hypothalamus
medianeminence
posteriorpituitary
Neuroendocrine hypothalamus
• Via anterior pituitary– Hypothalamic parvocellular
neurons release releasing or inhibiting hormones into hypothalamo-pituitary portal veins
– Hypothalmo-pituitary portal veins carry these hormones to anterior pituitary
– Anterior pituitary has cells responding to the different releasing or inhibiting hormones
– Responsive cells release or stop releasing hormones in response to binding of hypothalamic releasing or inhibiting hormones into systemic circulation
• Via posterior pituitary(neurohypophysis)– Hypothalamic
magnocellular neuronsrelease hormones directly into systemic veins that drain into the systemic circulation
– Hypothalamo-hypophyseal tract(axons of neuroendocrinemagnocellular neurons)
Hypothalamus
medianeminence
posteriorpituitary
Neuroendocrine hypothalamus
ADH kidneys
oxytocin mammary gland+ uterus
bonding (autism?)
paraventricular(PVN)
+supraoptic
(SON)
Hormonesreleased:
Hormonetargets:
Releasefrom:
Neuroendocrine hypothalamus
ADH kidneys
oxytocin mammary gland+ uterus
bonding (autism?)
paraventricular(PVN)
+supraoptic
(SON)
Hormonesreleased:
Hormonetargets:
Releasefrom:
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ADH-release
• ADH promotes water retention in kidneys• release is modified when blood osmolarity
changes by more than ~ 1% from set point (~ 280 mOsm/kg)
– Hypotonic conditions inhibit ADH release
– Hypertonic conditions stimulate ADH release
ADH-release
How do cells in supra-optic and paraventricularnuclei know that blood osmolarity has changed?
• Osmosensitive neurons• Intrinsically osmosensitive neurons in OVLT, SFO
and NTS• ADH releasing neurons are intrinsically
osmosensitiveFiring rate of ADH-releasing neurons integrates central and peripheral information and their own osmosensitivity
ADH-release
How do cells in supra-optic and paraventricularnuclei know that blood osmolarity has changed?
• Osmosensitive neurons• Intrinsically osmosensitive neurons in OVLT, SFO
and NTS that directly project to the supraoptic and paraventricular nuclei
Circumventricular organ: brain structure that is devoid of blood brain barrier
How can a cell be intrinsically osmosensitive?
Change in osmolarity will cause cell swelling or shrinking, resulting in increased or decreasedstretch of plasma membrane
Stretch of plasma membrane can gate ion channels
stretch-activated
tethered
indirectly gated
Lumpkin & CaterinaNature 445, 858-865 (2007)
cytoskeleton
cytoskeleton
extracellularmatrix
extracellularmatrix
mechano-sensitiveprotein
ADH-release
TRPV1opens in response to hypertonic stimulus
TRPV4opens in response to hypotonic stimulus
Which is (are) the candidate ion channel(s) involved in osmosensing?
ADH-release
TRPV1opens in response to hypertonic stimulus
TRPV4opens in response to hypotonic stimulus
Which is (are) the candidate ion channel(s) involved in osmosensing?Transient Receptor Potential channels of the Vanilloid family (TRPV channels)(non-selective cation channels)
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ADH-release
TRPV1opens in response to hypertonic stimulus
TRPV4opens in response to hypotonic stimulus
Which is (are) the candidate ion channel(s) involved in osmosensing?
N-terminal variant
indirect effect
Transient Receptor Potential channels of the Vanilloid family (TRPV channels)(non-selective cation channels)
cell volume(cell shrinking)
Sharif Naeini et al. Nat. Neurosci. 9, 93 - 98 (2006)
membraneconductance
(TRPV1-/-)
Sharif Naeini et al. Nat. Neurosci. 9: 93 - 98 (2006)
membraneconductance
TRPV1
(TRPV1-/-)
Sharif Naeini et al. Nat. Neurosci. 9: 93 - 98 (2006)
Action potential firing rate in response to hypertonic solution
TRPV1
Sharif Naeini et al. Nat. Neurosci. 9: 93 - 98 (2006)
Impaired ADH release in TRPV1 knock-out micein response to hypertonic solution
TRPV1
AVP = ADH
Liedtke & Friedman PNAS;100:13698-13703 (2003)TRPV4+/+ = wild type-/- = TRPV4 knock-out
TRPV4 knock-out mice drink significantly more when infused with ADH-analogue dDAVP (i.e. when water retention is increased, which should result in decreased water intake) than wildtype mice.
TRPV4 channelsopen in responseto cell swelling(indirect effect)in expression systems
ADH-releaseHow does it all come together?
• Increased blood osmolarity causes osmosensitive OVLT neurons to shrink
• TRPV1 channels open, leading to depolarisation and eventually firing of OVLT neurons (graded response)
• OVLT neurons make monosynaptic glutamatergic contacts with supra-optic nuclei neurons
• This promotes firing of ADH-releasing neurons and hence ADH release• ADH releasing neurons are intrinsically osmosensitive
Firing rate of ADH-releasing neurons depends on central and peripheral inputs as well as their intrinsic osmosensitivity
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ADH-releaseHow does it all come together?
• Increased blood osmolarity causes osmosensitive (OVLT) neurons to shrink
• TRPV1 channels open, leading to depolarisation and eventually firing of (OVLT) neurons (graded response)
• (OVLT) neurons make monosynaptic glutamatergic contacts with supra-optic nuclei neurons
• This promotes firing of ADH-releasing neurons and hence ADH release• ADH releasing neurons are intrinsically osmosensitive
Firing rate of ADH-releasing neurons depends on central and peripheral inputs as well as their intrinsic osmosensitivity
ADH-releaseHow does it all come together?
• Increased blood osmolarity causes osmosensitive (OVLT) neurons to shrink
• TRPV1 channels open, leading to depolarisation and eventually firing of (OVLT) neurons (graded response)
• (OVLT) neurons make monosynaptic glutamatergic contacts with supra-optic nuclei neurons
• This promotes firing of ADH-releasing neurons and hence ADH release• ADH releasing neurons are intrinsically osmosensitive
Firing rate of ADH-releasing neurons depends on central and peripheral inputs (baroreceptors!) as well as their intrinsic osmosensitivity
– Central DI• failure to secrete
ADH, resulting in excess urine output and dehydration
• following pituitary stalk damage (accident)
• Brattleboro rat produces no ADH
Diabetes insipidus Summary of neuroendocrine hypothalamus
• Arcuate GnRH (FSH, LH); GHRH (GH);DA (prolactin)
Reproduction; growth
• PVN CRH (ACTH); TRH (TSH); ADH; oxytocin
Steroid hormone production, energy metabolism, water retention; social behaviours, reproduction
• Ant. HT Sost (GH)Growth
• SON ADH; oxytocinwater retention; social behaviours, reproduction
Summary of neuroendocrine hypothalamus
• Arcuate GnRH (FSH, LH); GHRH (GH);DA (prolactin)
reproduction; energy metabolism
• PVN CRH (ACTH); TRH (TSH); ADH; oxytocin
behaviours, energy metabolism, water retention (blood flow), reproduction
• Ant. HT Sost (GH)energy metabolism
• SON ADH; oxytocinwater retention (blood flow), behaviours, reproduction
Non-endocrine control via the hypothalamus
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Non-endocrine control via the hypothalamus
• Food and drink intake
• Thermoregulation
• Circadian rhythms
Parasympathetic and sympathetic control
Non-endocrine control via the hypothalamus
• Food and drink intake
• Thermoregulation
• Circadian rhythms
Parasympathetic and sympathetic control
Non-endocrine control via the hypothalamus
• Food and drink intake
• Thermoregulation
• Circadian rhythms
ANS control
Food intake
Food intake
• Lateral hypothalamic area– “Feeding centre” (bilateral lesions: aphagia)– Receives olfactory input via medial forebrain bundle
• Ventromedial nucleus– “Satiety centre” (bilateral lesions: hyperphagia)– Receptors for glucose and free fatty acids
• Arcuate nucleus– Receptors for leptin (adipose tissue) and insulin
Separate lecture on food intake
Food intake
• Lateral hypothalamic area– “Feeding centre” (bilateral lesions: aphagia)– Receives olfactory input via medial forebrain bundle
• Ventromedial nucleus– “Satiety centre” (bilateral lesions: hyperphagia)– Receptors for glucose and free fatty acids
• Arcuate nucleus– Receptors for leptin (adipose tissue) and insulin
Separate lecture on food intake
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Food intake
• Lateral hypothalamic area– “Feeding centre” (bilateral lesions: aphagia)– Receives olfactory input via medial forebrain bundle
• Ventromedial nucleus– “Satiety centre” (bilateral lesions: hyperphagia)– Receptors for glucose and free fatty acids
• Arcuate nucleus– Receptors for leptin (adipose tissue) and insulin
Separate lecture on food intake
Food intake
• Lateral hypothalamic area– “Feeding centre” (bilateral lesions: aphagia)– Receives olfactory input via medial forebrain bundle
• Ventromedial nucleus– “Satiety centre” (bilateral lesions: hyperphagia)– Receptors for glucose and free fatty acids
• Arcuate nucleus– Receptors for leptin (adipose tissue) and insulin
Separate lecture on food intake
Drink intake/Thirst Drink intake/Thirst
• Subfornical organ– contains osmosensitive neurons
– projects to PVN, SON and POA
– stimulation of drinking behaviour (thirst)
other cirumventricular organs also contribute
More in separate lecture
Thermoregulation Thermoregulation • Alert consciousness and normal patterned motor
activities only when CNS temperature ~ 36 - 39°C
• Hypothalamus can stimulate thermogenesis– shivering, piloerection, skin vasoconstriction– behaviours that increase body temperature (or minimise
heat loss)
• Hypothalamus can stimulate heat loss– sweating, skin vasodilation– behaviours that promote body temperature cooling
• Controlled elevation of body temperature (fever) reduces pathogen viability and boosts immune system function
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Thermoregulation • Anterior hypothalamus (POA)
– Lesions cause hyperthermia– Endogenous temperature sensors (warm-sensitive neurons)
• T set-point can be changed by pyrogens, causing elevated core temperature (PGE2 acting on EP3 receptors)
• Posterior hypothalamic area– Lesions cause hypothermia– Involved in sympathetic activation
• Dilation or contraction of cutaneous circulation and control of sweat glands
receive peripheral temperature information (TRPM8, TRPV3, TRPV4)
Thermoregulation • Anterior hypothalamus (POA)
– Lesions cause hyperthermia– Endogenous temperature sensors (warm-sensitive neurons)
• T set-point can be changed by pyrogens, causing elevated core temperature (PGE2 acting on EP3 receptors)
• Posterior hypothalamic area– Lesions cause hypothermia– Involved in sympathetic activation
• Dilation or contraction of cutaneous circulation and control of sweat glands
also receive peripheral temperature information (TRPM8, TRPV3, TRPV4)
• What is the central temperature sensor?
2 current models:1. Heat directly opens ion channel that then
depolarises neuron – AP firing
2. Heat indirectly promotes depolarisation of neuron – AP firing
Thermoregulation
• What is the central temperature sensor?
2 current models:
1. Heat directly opens ion channel that then depolarises neuron – AP firing
2. Heat indirectly promotes depolarisation of neuron – AP firing
Thermoregulation
TRPV1
– peripheral or central administration of TRPV1 agonist capsaicin induces hypothermia
– administration of TRPV1 antagonists induces hyperthermia (increased metabolism and reduced heat loss from body surface)
– TRPV1 is expressed in anterior hypothalamus
◄However: TRPV1 knock-out mice have no obvious deficit in body temperature control and TRPV1 channels in anterior hypothalamus are not activated by normal body temperature: TRPV1 is unlikely to be the hypothalamic thermosensor!
thought to be mediated by visceral TRPV1 channels that are tonically active
ThermoregulationTRPV1
– peripheral or central administration of TRPV1 agonistcapsaicin induces hypothermia
– administration of TRPV1 antagonists induces hyperthermia (increased metabolism and reduced heat loss from body surface)
– TRPV1 is expressed in anterior hypothalamus
◄However: TRPV1 knock-out mice have no obvious deficit in body temperature control and TRPV1 channels in anterior hypothalamus are not activated by normal body temperature: TRPV1 is unlikely to be the hypothalamic thermosensor!
thought to be mediated by visceral TRPV1 channels that are tonically active
Thermoregulation
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TRPV1
– peripheral or central administration of TRPV1 agonistcapsaicin induces hypothermia
– administration of TRPV1 antagonists induces hyperthermia (increased metabolism and reduced heat loss from body surface)
– TRPV1 is expressed in anterior hypothalamus
◄However: TRPV1 knock-out mice no obvious deficit in body temperature control; TRPV1 channels in anterior hypothalamus not activated by normal body temperature: TRPV1 unlikely to be hypothalamic thermosensor!
thought to be mediated by visceral TRPV1 channels that are tonically active
Thermoregulation
• What is the central temperature sensor?
still unclear
Thermoregulation
Thermoregulation • Anterior hypothalamus (POA)
– Lesions cause hyperthermia– Endogenous temperature sensors (warm-sensitive neurons)
• T set-point can be changed by pyrogens, causing elevated core temperature (PGE2 acting on EP3 receptors)
• Posterior hypothalamic area– Lesions cause hypothermia– Involved in sympathetic activation
• Dilation or contraction of cutaneous circulation and control of sweat glands
also receive peripheral temperature information (TRPM8, TRPV3, TRPV4)
Thermoregulation • Anterior hypothalamus (POA)
– Lesions cause hyperthermia– Endogenous temperature sensors (warm-sensitive neurons)
• T set-point can be changed by pyrogens, causing elevated core temperature (PGE2 acting on EP3 receptors)
• Posterior hypothalamic area– Lesions cause hypothermia
• Dilation or contraction of cutaneous circulation and control of sweat glands
also receive peripheral temperature information (TRPM8, TRPV3, TRPV4)
Thermoregulation • Anterior hypothalamus (POA)
– Lesions cause hyperthermia– Endogenous temperature sensors (warm-sensitive neurons)
• T set-point can be changed by pyrogens, causing elevated core temperature (PGE2 acting on EP3 receptors)
• Posterior hypothalamic area– Lesions cause hypothermia
• Dilation or contraction of cutaneous circulation and control of sweat glands
also receive peripheral temperature information (TRPM8, TRPV3, TRPV4)
Thermoregulation • Anterior hypothalamus (POA)
– Lesions cause hyperthermia– Endogenous temperature sensors (warm-sensitive neurons)
• T set-point can be changed by pyrogens, causing elevated core temperature (PGE2 acting on EP3 receptors)
• Posterior hypothalamic area– Lesions cause hypothermia
• Dilation or contraction of cutaneous circulation and control of sweat glands
also receive cutaneous temperature information (TRPA1?, TRPM8, TRPV3, TRPV4)
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Circadian rhythms Circadian rhythms• Suprachiasmatic nucleus
– Sleep-wake cycle, feeding, temperature control, hormone release…..
– direct input from light-sensitive ganglion cells in retina (melanopsin)
(retinohypothalamic tract)
– phototransduction cascade similar to invertebrate one
• TRPC channels (originally cloned from drosophilaphotoreceptors)
• Separate lecture
Mammillary bodies
Mammillary bodies• Role in memory: Korsakoff’s syndrome
» alcohol-induced Vitamine B1 deficiency: damage to mammillary bodies (but also thalamus)
» Symptoms: anterograde and retrograde amnesia, confabulation
• Contain several nuclei with distinct connections
• Head direction cells (lateral nuclei) » fire selectively when animal faces specific direction
in horizontal plane; navigation
• Memory formation (medial nuclei)» connected with hippocampus via fornix and fire at
theta frequency (4-8Hz), which elicits long term potentiation in hippocampus
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Summary non-endocrine hypothalamus• Anterior HT ANS regulation;
endogenous T sensor; osmoregulation (energy metabolism, blood flow)
• SCN circadian rhythms
• Arcuate nucleus food intake
• Ventromedial nucleus “satiety” centre
• Lateral hypothalamus “hunger” centre
• Posterior HT ANS regulation(T sensor)
• Mammillary bodies memory (behaviours?)
Summary non-endocrine hypothalamus• Anterior HT ANS regulation;
endogenous T sensor; osmoregulation (energy metabolism, blood flow)
• SCN biological clock
• Arcuate nucleus food intake
• Ventromedial nucleus “satiety” centre
• Lateral hypothalamus “hunger” centre
• Posterior HT ANS regulation(T sensor)
• Mammillary bodies memory (behaviours?)
energymetabolism
Aggression and the hypothalamus• Neuronal subpopulations of ventromedial hypothalamus cause
aggressive behaviour (Lin et al. (2011) Nature 470:221-226)
“sexually experienced” male C57BL/6N mouse under investigation
Some cells are active duringnumber of different behaviourswhereas others (cell 4) are onlyactive during one particularbehaviour
“sexually experienced” male C57BL/6N mouse under investigation
Some cells are active duringnumber of different behaviourswhereas others (cell 4) are onlyactive during one particularbehaviour
Went on to selectively initiate behaviours by activating certain neurons and showed that neuronsactivated during an attack areinhibited during mating
Sex and the hypothalamus
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Sexual dimorphism of hypothalamusSexually dimorphic nucleus of preoptic area: Interstitial nucleus III
and also other hypothalamic regions
VERY controversial data/ woman
Sexual dimorphism of hypothalamusSexually dimorphic nucleus of preoptic area: Interstitial nucleus III
and also other hypothalamic regions
VERY controversial data/ woman