This preview shows page 1. Sign up to view the full content.
Unformatted text preview: PSL302: Lecture 28, by Prof. MacKay! Monday, Nov. 22, 2010 Hypothalamus & Limbic System: Controller & Programmer of Autonomic Fxns
- Higher order homeostatic fxns of ANS, principally involving hypothalamus Micturition: urination; voiding the bladder - Partly under reflex control (involving parasympathetic system) + programmed control - At spinal cord: sacral reflex driven by bladder stretch receptors - Drives parasympathetic efferents (in intermediolateral section of sacral cord ! ! -> bladder muscles contract = urination - All there is in newborn infant/sp.c. Injuries = incontinence = no suppression - Control of reflex occurs at brainstem - At brainstem: Pontine centers organize reflex: oppose one another for control 1) Sequence of relaxation of external sphincter muscle + pelvic floor muscles - Time to pee: turn off (inhibit) Onuf's nucleus - Turn ON Barrington's nucleus (in Pons) = disinhibit & activate sacral reflex ! ! ! = promote urination 2) Continence: lateral Pons -> project into bladder motor nucleus - Also activate voluntary motor centers - I.e. Onuf's nucleus: innervates ext. sphincters -> closes urethra - Default: normally active -> tonically contracting ext. sphincters ! ! ! = suppress urination - At midbrain: PAG zone selects continence/micturition (autonomic programming area) - Controls which centers in pons are active - Relies on input from hypothalamus (medial preoptic n.), amygdala & limbic frontal lobe - Tells PAG when appropriate to urinate and when it's not mus & Limbic System November 22, 2010 Limbic System control: Pontine programing: micturition & continence centers Spinal R fl S i l Reflex: parasympathetic 1 of 7 PSL302: Lecture 28, by Prof. MacKay! Monday, Nov. 22, 2010 Homeostasis: definition - Maintenance of a stable, internal body envmt (`milieu interieur') - Product of many physiological control circuits (negative feedback loops) - Hypothalamus is major coordinator of homeostatic control - Hypothalamus is major regulator of core parameters - I.e. plasma glucose, osmolality;Systemtemperature Hypothalamus & Limbic body - Sensors w/i hypothalamus to detect changes in these parameters - Corrective mechs (programmed) initiated: autonomic endocrine + somatomotor Hypothalamus - Ideal location: interface w/ - Endocrine system (via pituitary) - Autonomic circuitry (in PAG) - Somatomotor systems (via reticular formation's postural centers) - Interacts w/ brainstem motor + autonomic centers (PAG) via axonal projections - Brainstem: modulatory centers - I.e. Raphe->serotonergic, locus ceruleus->noradrenergic = fxnally part of sympathetic system - Reticular formation: postural programming - Interacts w/ endocrine system via pituitary - On bottom -> hormone secretion Hypothalamus & Limbic System - Can coordinate complete physiological response to challenges to internal envmt Pituitary Body - Provides an interface btwn CNS and endocrine system - 2 modes of commc w/ hypothalamus: 1) Direct axonal projections: hormone release from terminals - Neuron produces ADH -> excitation = release at posterior pituitary provides an interface between CNS and - E.g. ADH, anti-diuretic hormone 2) `releasing hormone' intermediary: carried to endocrine system pituitary in portal system of - Secreted from median eminence (base 2 modes to communicate with hypothal.: hypothalamus) -> carried via portal system to anterior 1) axonal projections: release of hormone pituitary from terminals (e.g. ADH) ( g ) - E.g. CRH, corticotropin releasing hormone 2)`releasing hormone' intermediary; carried Ex 1. ADH neurons in supraoptic n. -> axonal projection to posterior hypothalamus -> release ADH into bloodstream to pituitary in portal system (e.g. CRH) Ex 2. Paraventricular neurons -> axonal projection to median eminance of hypothalamus -> release CRH into bloodstream via portal system -> carry signal to anterior pituitary -> release adrenocortocotropin hormone (ACTH) = affect adrenal glands Novembe No Pituitary Body Temperature regulation Thermoreceptors at base of hypothalamus 2 of 7 too cold skin vasoconstriction, piloerecki t i ti il e e tion, brown fat thermogenesis, decreased cardiac output, shift of fluid out of plasma, PSL302: Lecture 28, by Prof. MacKay! Monday, Nov. 22, 2010 Temperature regulation - Thermoreceptors at base of hypothalamus (although skin thermoreceptors project here: advance warning of temp, vs. core body temp) - Too cold: heat loss, generate heat in body - Skin vasoconstriction: heat loss from skin (sympathetic) - Piloerection: flow of air across skin = heat loss from skin (sympathetic) - Brown fat thermogenesis: generate heat thru fat breakdown - Hypothalamus -> Raphi nuclei -> serotonergic - cardiac output: circulation to skin (parasympathetic) - Shift of fluid out of plasma: overall blood volume - Shivering (somatomotor system: dorsal hypothalamus -> raphe) - Too hot - Skin vasodilation: heat loss (sympathetic) - Sweating: evaporation heat loss (sympathetic) - ACh transmitter (not NA) to turn on sweat glands - Hypothalamus & Limbic System If NA, leak over = vasoconstriction! - cardiac output - Shift of fluid into plasma from ECF - ADH release = water retention - Coordinated at preoptic hypothalamus Diagram: At hypothalamus... - Preoptic area - Cooling (ADH release) - Dorsal posterior hypothalamus warming - Heat generation in body - Dorsomedial nucleus - Brown fat thermogenesis - Posterior nucleus cooling - Shivering * Both act thru Raphe nuclei - Suprachiasmatic nucleus - Retinal input=circadian rhythms - Paraventricular nucleus - CRH release -> ACTH release - -> adrenal glands - Supraoptic nucleus - Regulate plasma osmolality (ADH release) - Arcuate nucleus - Regulation of feeding ([glucose]plasma) Regulation of Feeding - Arcuate nucleus control: 2 opposing systems of neurons - NPY, neuropeptide-Y = drives feeding -> HUNGER (via paraventricular n., PVN) - Melanocortin = suppress feeding -> SATIETY - Neurons in ventromedial & arcuate nucleus act as glucoreceptors in hypothalamus Arcuate [glucose] firing of - Discharge in relation to ambient glucose lvls: nucleus control: 1 setrateneurons (NPY) drives feeding via paraventricular n.; other - Inhibit NPY cells = inhibit drive to feed neurons (melanocortin) suppress feeding - Leptin, secreted by adipose tissue = long-term suppression of feeding Neurons - Inhibit NPY cells + promote melanocortin in ventromedial (& arcuate) nucleus act as glucoreceptors; discharge in relation to ambient glucose levels, inhibit drive to eat 3 of Leptin, secreted by adipose tissue, provides long- 7 term suppression of feeding November 22 Regulation of Feeding PSL302: Lecture 28, by Prof. MacKay! Hypothalamus & Limbic System Monday, Nov. 22, 2010 November 22, 2 Diagram: Schematic cross-sec of hypothalamus - Arcuate nucleus: arcs around IIIrd ventricle (in midline -> extends up to thalamus) - Two opposing systems: mutually inhibitory - NPY neurons = HUNGER - Project into PVN - Melanocortin neurons = SATIETY - Inhibitory cxns w/ NPY cells - SATIETY HUNGER - [Glucose] -> bind to glucoreceptors in VM+arcuate n. = inhibit NPY cells - Leptin + insulin -> arcuate n. = promote melanocortin cells - PPY (released from gut) -> arcuate n. = inhibit NPY cells (-ve feedback) - Other gut hormones (i.e. CCK, OEA, GLP-1) influence localized vagal Hypothalamus & Limbic System afferents November 22, 2010 - HUNGER SATIETY - Ghrelin (released by empty stomach) -> arcuate n. = activate NPY cells
Hormonal and vagal feedback to control feeding Feedback from GI Tract Feedback from GI tract -Several hormones secreted by the gut feedback to hypothalamus and/or brainstem: Several hormones secreted by the gut feedback to -Ghrelin (empty stomach) = feeding hypothalamus and/or brainstem: -PYY (intestine) + insulin (pancreas) promotes feeding Ghrelin from empty stomach = feeding Hypothalamus & Limbic System -CCK, OEA, GLP-1 secreted by duodenum pancreas PYY from intestine and insulin from activate vagal afferents feeding inhibit -Via NTS =inhibit OEA, GLP-1 secreted by duodenum CCK, feeding CCK OEA GLP 1 t db d d
activate vagal afferents; via NTS inhibit feeding
Membrane tension sensitive ion channel November 22, 20 membrane is stressed by Plasma Osmolality swelling of cell - Osmoreceptors in supraoptic nucleus (osmoreceptor), the cation channel closes. - Secretory cell membrane has stretch-inactivated Plasma cation channels Osmolality - LOOSE -> channels OPEN Osmoreceptors in supraoptic nucleus; - STRETCHED -> channels pulled CLOSED secretory cell membrane has stretch- Regulates ADH release fro posterior pituitary inactivated cation channels - Setset pointis 295 mOsmol/l point is 295 mOsmol/l - cell shrinks cation channels ope >295:>295: Hypotonic, dehydration = [water] 95: ce s s c o c e s open - Cell shrinks: spikes increased ADH release membrane loose -> cation channels OPEN - Supraoptic n. firing <295: cell swells cation channels close -> ADH release = water retention few-spikes decreased ADH release <295: Hypertonic = [water] - Cell swells: membrane stretched -> cation channels CLOSE - Supraoptic n. firing -> ADH release ADH Model of stretch-inactivated membrane channel. When 8 Anti Diuretic Hormone, also known as Anti-Diuretic Hormone `vasopressin' 4 of 7 Hormone: increases water permeability of collecting ducts in kidney water retention Neurotransmitter in brainstem: facilitates Adrenal cortex PSL302: Lecture 28, by Prof. MacKay! Monday, Nov. activated in stressful situations by reticular 22, 2010 activating systems, etc. ADH - Anti-Diuretic Hormone: also known as vasopressin paraventricular n. CRH release into p ve cu . C e e se o - Hormone action: water permeability of collecting ducts in kidney = water retention - Neurotransmitter action in brainstem: facilitates learning + memory processes portal hypophysial vessels triggers ACTH release from anterior pituitary into HPA-Axis (endocrine parallel w/ sympathetic system) - Hypothalamus -> anterior Pituitary -> Adrenal cortex general circulation adrenal cortex - Hypothalamus: CRH release into portal hypophysical vessels
- Ant. Pituitary: triggers ACTH release into general circulation - Adrenal cortex: triggers glucocorticoid release - Paraventricular n. activated in stressful situations by reticular activating systems,etc. - Net excitatory effect from amygdala (basal ganglion for limbic system) - Net inhibitory effect from hippocampus - Negative feedback: - [Glucocorticoids]plasma to certain lvl -> PVN = CRH release - Slow + fast feedback: - Fast: use endocannabinoids - Slow: block gene transcription of CRH + ACTH Glucocorticoid Regulation
HPA-axis regulates release of adrenal glucocorticoids Negative feedback of cortisol: blocks action of CRH on pituitary, release of CRH, and transcription of ACTH gene 5 of 7 PSL302: Lecture 28, by Prof. MacKay! Endocannabinoids (eCB) Monday, Nov. 22, 2010 Endocannabinoids (eCB) - Neurotransmitter released from CRH neurons = suppress HPA axis - Mimics active ingredient in marijuana (relaxant) - Cortisol feedback triggers eCB release - Diffuses thru near vicinity: binds to receptors on excitatory boutons along CRH neurons from amygdala (releasing glutamate) - eCB pre-synaptically inhibits CRH neurons = excitatory input - Retrograde transmission across synapse: signal in opposite direction Cortisol feedback triggers eCB release from CRH neurons; eCB then prepre synaptically inhibits excitatory input to CRH neurons Hypothalamus & Limbic System J.Neurosci. 30(45): 14980-14986 (2010) November 22 - Hypothalamus (PAG) controlled from limbic parts of NS (up in cerebrum) - Amygdala is part of limbic center Amygdala - Part of basal ganglia controlling autonomic behaviours - Location: deep inside temporal lobe, at end of tail of caudate nucleus (of thalamus) - Input from limbic cortex + autonomic brainstem - Output generally inhibitory on PAG-hypothalamus - Recall: pallidum is exclusively inhibitory - Amygdala is not -> excites HPA axis! - Lesions can result in uncontrolled autonomic behaviours (e.g. `sham rage', hypersexuality) - Cats: complete rage response but no rage - Primates: hypersexuality - Responses to lesions are species-specific Amygdala Part of basal ganglia controlling autonomic behaviors input from `limbic' cortex, autonomic brainstem output generally inhibitory on PAGp g y y G hypothalamus Emotion-related memory lesions can result in uncontrolled autonomic - Memories related to emotional experiences, esp fearful behaviors strengthen cxns btwn ones, rely on amygdala for consolidation (potentiate synapses -> (e.g. `sham rage', hypersexuality)
neurons = lay down memory) - Again, the amygdala is not the site of memory storage - That is distributed in association and limbic cortex: signal other parts of limbic system to store the memory = coordinate memory storage Emotion-related memory Memories related to emotional experiences, experiences Limbic cortex especially fearful ones, rely on the - Location: Border regions of cerebral cortex at edge of hemisphere amygdala for consolidation - Phylogenetically old part of cortex - Subserves emotional experience, motivation + memory consolidation is not the site of again, the amygdala - Principle parts around edges: memory storage; that is distributed in - Cingulate gyrus: medial edge btwn frontal + parietal lobesand limbic cortex association - Hippocampal region: lateral edge of temporal lobe - Insula: bottom of lateral fissure - Projects strongly to rest of limbic system -> hypothalamus, PAG, amygdala 6 of 7 PSL302: Lecture 28, by Prof. MacKay! Monday, Nov. 22, 2010 Diagram: Cross-sec of L cerebral hemisphere -Midline to right, edges of cerebral cortex to left -Medial edge of temporal lobe: hippocampus (curled up) -Adjacent parahippocampal gyrus -Medial edge of frontal + parietal lobes: cingulate gyrus -Bottom of lateral fissure: insula -In primitive cerebral cortex: zones would be continuous -Make up entire cortical sheet, i.e. nsula: sensory region -As neocortex developed, bulged out + pushed original portions apart > edge regions retained for cingulate System + hippocampus...ut insula gyrus Hypothalamus & Limbic isolated in middle + pushed down November 22, 2010 Diagram: Medial view of limbic cortex from midline (view of hemisphere) - Cingulate gyrus swings around in circle 13 - Meets up w/ parahippocampal gyrus - Hippocampus curlicue at bottom - Add in insula (on other side at bottom of lateral fissure) 14 7 of 7 ...
View Full Document
This note was uploaded on 03/27/2012 for the course PSL PSL300 taught by Professor Mackayfrench during the Fall '11 term at University of Toronto- Toronto.
- Fall '11