Study Notes on Motivated Behavior and Hypothalamic Control

CHAPTER 16: Motivation

MOTIVATED BEHAVIOR

  • Overview of Content:

    • Hypothalamic control of motivated behavior

    • Long-term feeding

    • Short-term feeding

    • Thirst

    • Temperature regulation

    • Next class topics:

    • Serotonin and Dopamine in motivated behavior

    • “Going Beyond” (dopamine paper)

MOTIVATED BEHAVIOR DEFINED

  • Motivation:

    • Governs movements necessary to satisfy a need.

    • Acts as a driving force on behavior.

    • Dictates the probability and direction of behavior.

    • Can involve both unconscious reflexes and conscious (voluntary) movements that may be motivated.

HOMEOSTASIS

  • Definition and Function:

    • Homeostasis maintains the internal environment within a narrow physiological range.

  • Role of Hypothalamus:

    • Regulation of homeostasis includes a number of behaviors:

    • Hunger

    • Thirst

    • Body temperature

    • Sleep/circadian rhythms

    • Sex

    • Parenting and attachment

HYPOTHALAMUS

  • Neuronal Response Components Upon Homeostasis Disruption:

    • Humoral response: Release or inhibition of pituitary hormones into the bloodstream.

    • Visceromotor response: Adjustment of autonomic activity (sympathetic vs parasympathetic).

    • Somatic motor response: Induction of a somatic motor behavioral response (including motivated behavior) - primarily by the lateral hypothalamus.

HYPOTHALAMIC CONTROL OF MOTIVATED BEHAVIOR

  • Example: Response to a drop in core body temperature:

    • Humoral responses: Modulation of pituitary leading to mobilization of body fat reserves.

    • Visceromotor responses: Sympathetic activation leading to blood being shunted away from the body surface.

    • Somatic motor responses: Voluntary movements aimed at seeking or generating warmth.

REGULATION OF FEEDING BEHAVIOR

  • State Definitions:

    • Prandial State (just ate): Intestines full; anabolism refers to energy storage as glycogen and triglycerides.

    • Postabsorptive State (done digesting): Intestines empty; catabolism refers to the breakdown of complex macromolecules. Energy balance is crucial since the brain needs glucose.

ENERGY BALANCE

  • The balance can be depicted in different states:

    • Normal

    • Obesity

    • Starvation

  • Components involved include the energy intake versus expenditure.

BODY FAT AND FOOD CONSUMPTION

  • Lipostatic Hypothesis:

    • Suggests that the brain monitors adipose tissue and acts to defend against perturbations to this energy store.

    • The brain endeavors to return body weight to a “normal” level, as evidenced in studies conducted on rodents.

BODY FAT, LEPTIN, AND FOOD CONSUMPTION

  • Leptin:

    • A protein released by fat cells (adipocytes); it regulates body mass.

    • Effects of Leptin Levels:

    • Low Leptin: Increases appetite and initiates adaptive responses to combat starvation.

    • High Leptin: Decreases appetite and increases energy expenditure.

THE HYPOTHALAMUS AND FEEDING IN THE RAT

  • Lesion Studies by Hetherington and Ranson (1942):

    • Anorexia: Occurs with bilateral lesions of the lateral hypothalamus (LH); rats would not eat, indicating LH stimulates feeding.

    • Obesity: Results from bilateral lesions of the ventromedial hypothalamus (VMH); rats overeat, suggesting VMH reduces feeding.

    • An overly simplistic view, as both responses are tied to leptin signaling, which will be revisited in relation to sex behaviors.

NEW VIEW: THE HYPOTHALAMUS AND FEEDING

  • Key Hypothalamic Nuclei Important for Feeding Control:

    • Paraventricular Nucleus

    • Lateral Hypothalamus

    • Arcuate Nucleus

HYPOTHALAMIC RESPONSE TO ELEVATED LEPTIN

  • Mechanism:

    • Leptin binds to receptors on neurons in the Arcuate Nucleus.

    • This activation stimulates the release of:

    • αMSH (Alpha-melanocyte-stimulating hormone): An anorectic peptide that diminishes appetite.

    • CART (Cocaine- and amphetamine-regulating transcript): Another peptide with a similar appetite-suppressing effect.

COORDINATED RESPONSES TO ELEVATED LEPTIN

  • Projection of Arcuate Neurons:

    • Coordinate humoral, visceromotor, and somatic responses:

    • Humoral response: Activates Paraventricular Nucleus.

    • Visceromotor response: Intermediolateral gray matter of spinal cord.

    • Somatic motor response: Lateral hypothalamus, inhibiting feeding behavior.

ARCUATE NUCLEUS RESPONSE TO ELEVATED LEPTIN → DECREASED FEEDING

  • Mechanism of Action:

    • Humoral Response: Stimulates ACTH and thyrotropin release from the anterior pituitary, increasing cellular metabolic rate (general stress response).

    • Visceromotor Response: Activates sympathetic nervous system via the Paraventricular Nucleus, which raises metabolic rate and body temperature.

    • Somatic Motor Response: Inhibition of feeding behavior through Lateral Hypothalamus.

HYPOTHALAMIC RESPONSE TO LOW LEPTIN

  • Activation of Arcuate neurons that release:

    • NPY (Neuropeptide Y) and AgRP (Agouti-related peptide) (potentially via ghrelin).

  • Effects on Energy Balance:

    • Orexigenic peptides increase appetite:

    • NPY and AgRP Effect:

      • Inhibit paraventricular secretion of TSH and ACTH (humoral response).

      • Activate parasympathetic division of autonomic nervous system (visceromotor response).

      • Stimulate feeding behavior (somatic motor response).

ARCUATE NUCLEUS RESPONSE TO DECREASED LEPTIN → INCREASED FEEDING

  • Actions Include:

    • NPY and AgRP release with inhibited PVN activity: lowering anterior pituitary ACTH and TSH (humoral response).

    • Activate parasympathetic division of ANS, inhibiting sympathetic responses and stimulating feeding behavior through Lateral Hypothalamus (somatic motor response).

MC4 RECEPTORS IN THE LATERAL HYPOTHALAMUS

  • Function: Opposes effects of Arcuate peptides in Lateral Hypothalamus.

    • Action at MC4 Receptor:

    • αMSH: Agonist that activates feeding inhibition.

    • AgRP: Antagonist that turns off feeding inhibition, leading to increased eating.

CONTROL OF FEEDING BY LATERAL HYPOTHALAMUS

  • Projection Pathways:

    • NPY/AgRP neurons from Arcuate Nucleus project to Lateral Hypothalamus, stimulating the release of:

    • Melanin-concentrating hormone (MCH) and Orexin.

    • Both create widespread cortical connections to initiate and prolong meals, effectively increasing appetite.

ANORECTIC AND OREXIGENIC PEPTIDES OF THE HYPOTHALAMUS: SUMMARY

  • Anorectic Peptides (Inhibit Feeding):

    • aMSH: Alpha-melanocyte-stimulating hormone

    • CART: Cocaine- and amphetamine-regulating transcript

  • Orexigenic Peptides (Stimulate Feeding):

    • NPY: Neuropeptide Y

    • AgRP: Agouti-related peptide

    • MCH: Melanin-concentrating hormone

    • Orexin: Released from Lateral hypothalamic area.

HOMEOSTATIC REGULATION OF BODY FAT AND FEEDING: SUMMARY

Condition

High Leptin

Low Leptin

Fat

Blood leptin level +

Lean

aMSH/CART neuron activity +

NPY/AgRP neuron activity +

Humoral Response

TSH and ACTH release +

TSH and ACTH release -

Sympathetic NS Activity

+

-

Feeding Behavior

-

+

THE SHORT-TERM REGULATION OF FEEDING BEHAVIOR

  • Three Phases:

    • Cephalic Phase: Hunger activated by the sight and smell of food engages the parasympathetic nervous system.

    • Gastric Phase: Stomach processes food through chewing, swallowing, and filling.

    • Substrate Phase: Absorption of nutrients from the intestine.

MECHANISMS OF SHORT-TERM REGULATION OF FEEDING BEHAVIOR

  • Cephalic Phase:

    • Hunger: Ghrelin released as the stomach empties activates NPY and AgRP-containing neurons in the Arcuate Nucleus.

  • Gastric Phase:

    • Feeling Full: Gastric distension signals satiety to the brain via vagus nerve to the medulla.

  • Substrate Phase:

    • Feeling Full: Release of CCK (cholecystokinin) from intestines responds to certain foods; Insulin released by pancreas promotes glucose uptake into cells.

    • Insulin's role in anabolism vital for glucose uptake to liver, muscle, and adipose storage.

    • Insulin also released during the cephalic phase through parasympathetic stimulation of the pancreas.

  • Insulin has a consistent release pattern in all phases, reaching peak levels during the substrate phase when glucose and insulin levels trigger cessation of eating.

OTHER MOTIVATED BEHAVIORS: DRINKING

  • Two Signaling Pathways for Fluid Consumption:

    • Volumetric (Hypovolemic) Thirst: Triggered by decreased blood volume.

    • Osmotic Thirst: Triggered by increased concentration of solutes in blood, which is the more common motivation to maintain salt/water balance.

TWO KINDS OF THIRST:

  • Hypovolemic Thirst:

    • Results from loss of overall body fluid volume (e.g., blood loss or vomiting). The need to restore nutrients drives fluid intake (fluids other than water, e.g., Gatorade).

    • Example includes Chris Legh's dehydration incident during the Ironman Triathlon in 1997.

PATHWAYS TRIGGERING VOLUMETRIC THIRST

  • Hypovolemia: A decrease in blood volume leads to vasopressin release from the posterior pituitary.

    • Mechanisms:

    • Kidneys react to reduced blood volume with angiotensin II release, stimulating vasopressin via the subfornical organ.

    • Mechanoreceptors in blood vessel walls signal low volume, prompting vasopressin release via the nucleus of the solitary tract (medulla).

ON OSMOTIC THIRST

  • Cause: Increased concentration of solutes (e.g., salt) in body fluids leads to osmotic thirst.

  • Mechanisms: Hypertonicity causes the OVLT (Vascular Organ of the Lamina Terminalis) to release vasopressin, enhancing kidney water retention.

    • Neurons in OVLT fire action potentials when sensing water loss, promoting vasopressin secretion and activating the lateral hypothalamus to induce thirst and corresponding behaviors.

OTHER MOTIVATED BEHAVIORS: TEMPERATURE REGULATION

  • Mechanisms:

    • Neurons in the anterior hypothalamus are sensitive to temperature changes away from 37ºC (98.6ºF); these adjustments trigger humoral and visceromotor responses (general pituitary sympathetic/parasympathetic activity).

    • Neurons in the medial preoptic area also play a role, alongside the lateral hypothalamic area X for behavioral responses.

DROP IN BLOOD TEMPERATURE RESPONSE

  • Response Mechanisms:

    • Humoral response: Release of TSH to increase cellular metabolism.

    • Visceromotor response: Create physiological responses like goosebumps and blood vessel constriction.

    • Somatic motor response: Involves shivering (involuntary) and actively seeking warmth (voluntary).

RISE IN TEMPERATURE

  • Mechanisms to slow metabolism include reduced TSH release from the anterior pituitary, which decreases the release of thyroxin from the thyroid gland, ultimately reducing cellular metabolism.

SUMMARY OF MOTIVATED BEHAVIORS

  • Hypothalamic Responses to Stimuli:

    • Eating Signals: Bloodborne leptin affects the Arcuate nucleus leading to both humoral and somatic responses indicating feeding.

    • Drinking Signals: Bloodborne angiotensin II and tonic levels involved with vasopressin release drive drinking behaviors.

    • Temperature signals induce both sympathetic and parasympathetic responses leading to behavioral alterations for maintaining homeostasis.

CONCLUSION

  • Today's covered topics include hypothalamic control of motivated behavior, long-term and short-term regulation related to feeding behaviors, thirst, and temperature regulation. Upcoming class discussions will involve serotonin and dopamine's roles in motivated behaviors along with further discussions on dopamine-related materials.