NROC61 - Lecture 8 Hypothalamus and Motivation 2

Regulation of meal size

Meal initiation = external and internal factors

Meal termination = biological

Phases of Short term regulation

Cephalic, Gastric, Substrate

Cephalic

Anticipatory activation of autonomic system (saliva, gastric juices)

Gastric

Increased intensity of responses when eating starts

Substrate (intesntinal)

Absorption of food begins

External Initiation factors

emotions, time of day, availability of foods, palatability of foods

Internal Initiation factors

Orexigenic signal (ghrelin in the stomach)

Meal termination

Onset of satiety

Decerebrate rats show brainstem circuitry alone is sufficient to regulate meal size

Short term satiety signals

Gastric distension, Cholecystokinin (CCK)

Gastric Distension

Mechanoreceptors monitoring stomach fullness through vagus nerve

Cholecystokinin (CCK)

Hormone released from duodenal mucosal cells when eating fat and protein

signal transmitted via vagus nerve to nucleus tractus solitarius (NTS) in brainstem

What more does CCK mediate?

Mediates pre-absorptive satiating effect of fat

High fat breakfasts produce greater feelings of satiety and elevated CCK levels

CCK-A receptor knock down

Rats developed hyperphagia (overeating), hyperinsulinemia (high insulin), and obesity

Overriding satiety

New tastes available = more consumption

Emotional/social factors (group eating)

Hedonics (pleasure of eating)

Hedonic property of food

Hedonic response to food heightened in state of depletion than satiation

Cafeteria diet results

Highly palatable food transmits info to reward circuitry, upregulates endocannabinoids (hunger signals like NPY, Orexin, AgRP)

Leptin signaling diminished (blunted satiety signal)

Evidence of other regions involved in eating

PET scans showed amygdala and ObFC more blood flow when shown menus with tasty food to override satiety

Need for Water and Fluids

Body mostly water

Volume of fluid important for blood pressure, osmolarity, plasma osmotic pressure (290-300 mOsm/L)

Osmosis

Movement of water through selectively permeable membrane to equalize concentrations

Levels of solutes in a cell

Isotonic, Hypertonic, Hypotonic

Isotonic

Solutes inside cell = outside cell

No movement of water

Hypertonic

Solutes in cell less than outside

Water moves out of cell, becomes dehydrated

Hypotonic

Solutes in cell more than outside

Water moves into cell, cell may burst

Types of Thirst

Osmotic thirst & Volumetric thirst

Osmotic thirst

Increase in osmotic pressure of extracellular fluid relative to intracellular (e.g. hypertonicity)

Volumetric thirst

Triggered by drop in blood volume (Hypovolemia)

OVLT (Vascular Organ of the Lamina Terminalis)

Osmoreceptors detects changes in osmolarity, elicits drinking behaviour

Osmoreceptor locations

OVLT

Median preoptic nucleus (MnPO)

Subfornical organ (SFO)

OVLT to PVN

Controls release of Antidiuretic hormone (ADH) from pituitary gland

Hypertonic condtions

Stimulate ADH release

Hypotonic conditions

Inhibit ADH release

MnPO and SFO project to?

LH to initiate drinking

Cellular pathway for Hypertonicity

Hypertonicity -> Osmoreceptors shrink -> Firing of OVLT neurons -> excitation of SON and PVN neurons -> ADH release

Cellular pathway for Hypotonicity

Hypotonicity -> Osmoreceptors swell -> Inhibition of OVLT neurons -> No firing of SON and PVN

What does ADH do?

Kidneys begin conserving water

Diabetes Insipidus

Failure to secrete ADH = excess urine + dehydration

Thirst and polyuria

No hyperglycemia

How does hypovolemia central thirst circuits to restore extracellular fluid volume?

Hypovolemia → kidneys detect low perfusion and release renin.

Renin converts angiotensinogen → angiotensin II (Ang II).

Angiotensin II actions

Vasoconstriction → raises blood pressure.

Adrenal cortex → releases aldosterone → kidneys retain water.

Brain access (OVLT & subfornical organ) → activates median preoptic nucleus (MnPO).

MnPO outputs

Lateral hypothalamus → triggers thirst → drinking.

Supraoptic nucleus & PVN → release vasopressin → kidneys conserve water.

Atrial Baroreceptors

Inform brain of drop in blood volume to initiate thirst to replace lost water and salt

Termination of drinking

Water in duodenum osmoreceptors stops drinking

Thermoregulation

Normal CNS temp between 36-39 Celsius

Hypothalamus in Thermoregulation

Stimulate thermogenesis

Stimulate heat loss

Thermogenesis

Temp outside very cold

Endocrine hormones increase

Sympathetic outflow (stop sweating, vasoconstriction)

Behaviourally wear clothes and ingest warm fluids

Behavioural Thermoregulation in rats

Cooling anterior hypothalamic preoptic area elicited lever pressing for external heat

Thermoreceptor TRP channels in skin

TRPM8 responsive to menthol (cool)

TRPV1 responsive to capsaicin (heat)

Hypothalamus and thermogenesis

Humoral responses through medial preoptic area (MPOA)

Medial Preoptic Area

Lesions caused hyperthermia

Normal function inhibits thermogenesis