Fifty Two and Fifty Three Flashcards
Generally, where is the hypothalamus located and what is its function?
Located beneath the thalamus at the ventral surface of the diencephalon forming the walls
of the third cerebroventricle, the hypothalamus is small in size (about 4 grams in the
adult) but is a major crossroad for emotional, autonomic and endocrine circuitry in the
brain. Afferents to the hypothalamus provide exteroceptive and enteroceptive information
that is then processed into neural and humoral signals responsible for the maintenance of
normal cardiovascular, renal, visceral and endocrine function, as well as for the
expression of appropriate and conditioned behavioral responses to our environment.
What are the caudal, dorsal, ventral, and rostral borders of the hypothalamus?
Boundaries: Rostral – lamina terminalis
Caudal – posterior aspects of mamillary nuclei
Dorsal – hypothalamic sulcus (approximately a line connecting
the foramen of Monroe and the cerebral aqueduct)
Ventral – ventral surface of the diencephalon
What are the 4 principal areas of the hypothalamus and what are the key landmarks/nuclei in each slice?
Preoptic – preoptic area, substantia inominata, septal nuclei, anterior commissure
Suprachiasmatic – optic chiasm, supraoptic nuclei, paraventricular nuclei, anterior hypothalamic nuclei, lateral
hypothalamic area, fornix
Tuberal – infundibulum with arcuate nucleus and median eminence, ventromedial and dorsomedial hypothalamic
nuclei, fornix, lateral hypothalamic area
Mamillary – mamillary nuclei, posterior hypothalamic area, fornix, mamillothalamic tract
What is the arterial blood supply of the hypothalamus? What is the venous blood supply of the hypothalamus? Of the pituitary?
Arterial: Anteromedial arteries from anterior cerebral and anterior communicating
Posteromedial arteries from posterior cerebral and posterior communicating
Superior and inferior hypophysial arteries from internal carotids
Venous: Hypothalamus – basilar vein to great cerebral vein to straight sinus to transverse sinus to internal jugular
Pituitary – intercavernous sinus to transverse sinus to internal jugular
What are 4 neural afferent fibers to the hypothalamus? What is their origin? What is their termination?
Medial forebrain bundle (#13)
Origin: septal and olfactory regions
Termination: most hypothalamic nuclei and midbrain reticular formation
Stria terminalis (#3)
Origin: amygdala
Termination: preoptic and septal nuclei, anterior hypothalamic area, ventromedial hypothalamic nuclei
Fornix (#2)
Origin: hippocampus and subiculum
Termination: mamillary nuclei, septal nuclei, anterior hypothalamic area, ventromedial hypothalamic area
Ventral amygdalofugal bundle (#16)
Origin: amygdala
Termination: lateral preoptic areas, septal nuclei, substantia innominata
What are 4 efferent fibers from the hypothalamus? Origin/termination?
Mamillothalamic tract (#8)
Origin: mamillary nuclei
Termination: anterior thalamic nuclei
Periventricular fibers (Dorsal Longitudinal Fasciculus) (#9)
Origin: diffuse hypothalamus
Termination: brainstem parasympathetic nuclei, motor nuclei of the trigeminal, facial nuclei, nucleus ambiguus (IX, X, XI), and hypoglossal nuclei
medial forebrain bundle (see above)
Stria medullaris thalami (#4)
Origin: septal nuclei and preoptic area
Termination: habenula
What are 2 examples of hypothalamic neural input/neural output?
Hypothalamic control of autonomic function and hypothalamic control of temperature regulation
How are parasympathetics controlled by the hypothalamus? How is it manifest? Same questions for sympathetics.
Parasympathetics – stimulation of the anterior hypothalamus (preoptic and
suprachiasmatic regions) results in increased vagal and sacral parasympathetic activity (as manifested by reduced heart rate and increased visceral secretomotor function)
Sympathetics – stimulation of the lateral and posterior hypothalamus results in
increased sympathetic tone (as manifested by increased metabolic rate, increased heart
rate, increased vascular tone, increased rate and depth of respiration, and inhibition of
visceral secretomotor function….a.k.a. the stress reaction)
What areas of the Hypothal are responsible for heat dissipation? How does this occur? What do lesions in this area result in?
Heat dissipation – thermal sensors in the preoptic and anterior hypothalamic areas
detect increases in the temperature of the blood supply and set in motion reflexes that
result in heat loss. Stimulation of this area causes sweating and cutaneous vasodilation.
[N.B. Here is one place where the distinction between parasympathetic and sympatheticfunction is an exception.
Lesions in the Preoptic and Anterior Hypothalamic Area disrupt the heat loss
mechanism resulting in the inability of the patient to “lose heat” (a.k.a. hyperpyrexia
associated with tumors in the anterior hypothalamus).
What centers of the hypothal dectect drops in temp. of blood supply that lead to heat gain/conservation? How does this manifest? What do lesions there result in? Why?
Heat gain/conservation – thermal sensors in the posterior hypothalamus detect
drops in the temperature of the blood supply and set in motion reflexes that result in heat
conservation or formation (largely sympathetic in nature including a shift of blood flow away from the skin, increased metabolic rate and shivering). Selective stimulation in these areas can result in heat gain.
However, since the descending efferents that arose in
the “heat loss” centers of the anterior hypothalamus pass through this same region, lesions of the posterior hypothalamus result in the inability of the patient to either gain heat (in a cold environment) or lose heat (in a hot environment). These patient’s body temperature therefore fluctuates with the temperature of their environment (a.k.a. poikilothermia associated with tumors or infarcts in the posterior hypothalamus).
What are some examples hypothalamic mixed neural input/mixed neural output?
Food Intake, Fluid Homeostasis
What are two different theories of how the hypothalamus uses blood-borne signals to control food intake? Explain them. Which of the four regions does this occur in? What is the neural input of the hypothal that detects fullness? Where does it come from?
Two prevalent theories of the control of food intake (eating) center on the
hypothalamus as a receptor for blood-borne signals that activate feeding behaviors. Both
theories rely on the perception by hypothalamic neurons of the absolute levels of these
signals and give rise to the lipostatic and the glucostatic theories of food intake. In the
lipostatic theory, a lipophylic peptide, LEPTIN, produced in adipocytes crosses into the
brain and signals the fullness of the body’s fat stores. In the glucostatic theory, it is the
absolute levels of glucose in the circulation that signal adequacy of the fuel supply for the
brain and the other organs. Both theories place the receptive elements in the tuberal
region of the hypothalamus where the “feeding” and “satiety” centers are located. Neural input to the hypothalamus reporting relative “fullness” of the stomach is conveyed via neurons originating in the nucleus tractus solitarius and vagal nuclei.
What centers are involved in the feeding center? What do bilateral lesions of this area result in? What centers are involved in the satiety center? What do bilateral lesions result in? What are these neurons actually responding to?
Feeding center – bilateral lesions in the lateral hypothalamic area of the tuberal hypothalamus result in hypophagia (decreased eating regardless of metabolic state and eventual wasting).
Satiety center – bilateral lesions of the ventromedial hypothalamic nuclei result in voracious appetite regardless of metabolic state (and in aggressive, often vicious behaviors).
Neurons responsive to both leptin and increased glucose concentrations (both of which inhibit feeding). Feeding center is activated by little glucose and inhibited by lots of leptin. Satiety center is activated by lots of glucose and leptin.
What is the neural output of the feeding/satiety centers? What is the humoral output?
The neural output of these centers is primarily to motivational centers in cortex and motor centers regulating the behaviors of food gathering and eating. Neural outflow also innervates parasympathetic centers in brain stem regulating salivary secretion and visceral secretomotor activity. Humoral output is via regulation of anterior pituitary lobe hormones related to metabolism (e.g. adrenocorticotropin, growth hormone, and thyroid stimulating hormone).
What happens when blood volume is increased? What is the pathway? What role does the hypothalamus play? What happens when blood volume is decreased? What is the pathway? What role does the hypothalamus play both neurally and humorally? What is AVP and what does it do? What tracts does the input to the hypothalamus run in?
Volume regulation – plasma volume is sensed primarily by baroreceptors located in the
aortic arch and carotid sinus. [Low pressure baroreceptors are also present in the heart
(atria) and the kidney.] Baroreceptor activity is determined by stretch (tension). When
volume status increases the sensory endings in the baroreceptors are depolarized and
afferent activity in the glossopharyngeal (IX) and vagus (X) nerves increases. That
activity exerts a negative effect in the brain stem (nucleus tractus solitarius) that is translated into a decrease in sympathetic outflow from the brain (and hence a slowing of the heart and vasorelaxation) and, via afferents to the hypothalamus (paraventricular and supraoptic nuclei), increased inhibition of VASOPRESSIN (AVP, a.k.a. ANTIDIURETIC HORMONE, ADH) release.
On the other hand when volume status decreases, the baroreceptor stretch is
relaxed (the receptors are “unloaded”) so less inhibitory activity arrives via IX and X and
sympathetic outflow increases (increased heart rate and vascular tone). Less inhibitory
input into hypothalamus results in AVP release. AVP stimulates the insertion of “pores
(aquaporins)” into the luminal membranes in the distal convoluted tubules and collecting
ducts of the kidney, resulting in a movement of free water down its concentration
gradient into the hypertonic interstitium of the renal medulla and therefore the “capture”
from the urine of water. Unloading of the baroreceptor (decreased plasma volume) also
signals via similar neuronal pathways the hypothalamic mechanisms regulating thirst,
resulting in increased fluid intake (to replace lost plasma volume). Thirst is a reflection of the neural output of the system, while AVP release represents the humoral mechanism.