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CHAPTER 16: Motivation

MOTIVATED BEHAVIOR

  • Definition of Motivation:
    • Governs movements necessary to satisfy a need.
    • Acts as a driving force behind behavior.
    • Dictates the probability and direction of behaviors.
    • Includes both unconscious reflexes and conscious (voluntary) movements.

HOMEOSTASIS

  • Definition:
    • The maintenance of the internal environment within a narrow physiological range.
  • Role of the Hypothalamus:
    • Regulates homeostasis and various behaviors, including:
    • Hunger
    • Thirst
    • Body temperature
    • Sleep/circadian rhythms
    • Sexual behavior
    • Parenting and attachment.

HYPOTHALAMUS

  • Three Components of Hypothalamic Neuronal Response:
    1. Humoral Response:
    • Involves the release or inhibition of pituitary hormones into the bloodstream.
    1. Visceromotor Response:
    • Adjustments of autonomic activity (sympathetic vs. parasympathetic).
    1. Somatic Motor Response:
    • Induction of a somatic motor behavioral response, including motivated behavior, notably linked to the lateral hypothalamus.
  • Hypothalamic Nuclei Important for Control of Feeding:
    • Paraventricular Nucleus
    • Lateral Hypothalamus
    • Arcuate Nucleus

REGULATION OF FEEDING BEHAVIOR

  • States of Feeding Behavior:
    • Prandial (just ate) State:
    • Intestines are full; involved in anabolism (energy storage as glycogen and triglycerides).
    • Postabsorptive (done digesting) State:
    • Intestines are empty; involved in catabolism (breakdown of complex macromolecules).
    • Energy Balance:
    • The brain requires glucose for functionality.

ENERGY BALANCE

  • Concept:
    • Energy balance can be affected by:
    • Normal intake/expenditure.
    • Excess intake leading to obesity.
    • Deficit leading to starvation.
  • Body Fat and Food Consumption:
    • Lipostatic Hypothesis:
    • The brain monitors body fat (adipose tissue) and acts to defend against any perturbation to this energy reserve.
    • The brain works to return body weight to a "normal" level, supported by evidence from rodent studies.

BODY FAT, LEPTIN, AND FOOD CONSUMPTION

  • Leptin:
    • A protein released by fat cells (adipocytes) that regulates body mass.
    • Low Leptin Levels:
      • Cause an increase in appetite.
      • Incites adaptive responses to combat starvation.
    • High Leptin Levels:
      • Cause a decrease in appetite.
      • Increase energy expenditure.

HYPOTHALAMIC LESION STUDIES

  • Studies by Hetherington and Ranson (1942):
    • Anorexia Induced:
    • Bilateral lesions of the lateral hypothalamus (LH) result in rats not eating, suggesting LH stimulates feeding.
    • Obesity Induced:
    • Bilateral lesions of the ventromedial hypothalamus (VMH) result in rats overeating, suggesting VMH suppresses feeding.
  • These responses are connected to leptin signaling, indicating more complexity than just lesion effects.

HYPOTHALAMIC RESPONSE TO LEPTIN

  • Elevated Leptin:
    • Leptin binds to receptors on neurons in the Arcuate Nucleus.
    • Stimulation leads to the release of αMSH and CART (anorectic peptides) that diminish appetite.
    • αMSH: Alpha-melanocyte-stimulating hormone.
    • CART: Cocaine- and amphetamine-regulated transcript.
  • Projecting Responses:
    • Arcuate neurons stimulate various brain regions, coordinating:
    1. Humoral Response: Paraventricular N. activation releasing ACTH and thyrotropin, raising metabolic rates.
    2. Visceromotor Response: Activation of sympathetic nervous system, raising metabolic rates/body temperature.
    3. Somatic Motor Response: Inhibition of feeding behavior via the Lateral Hypothalamus.

RESPONSE TO DECREASED LEPTIN

  • Activation of Arcuate Neurons:
    • Release of NPY (Neuropeptide Y) and AgRP (Agouti-related peptide).
    • These orexigenic peptides increase appetite, stimulating feeding behavior.
    • Inhibit paraventricular secretion of TSH and ACTH, which lowers metabolic rates and activates parasympathetic responses.
  • Increased Feeding Behaviors:
    • Result from inhibited thermogenic responses and stimulation of the lateral hypothalamus leading to a strong drive to eat.

MECHANISMS IN LATERAL HYPOTHALAMUS

  • Control of Feeding by Lateral Hypothalamus:
    • NPY/AgRP neurons project to lateral hypothalamus, stimulating the release of Melanin-concentrating hormone (MCH) and Orexin.
    • These factors have wide-ranging connections to the cortex and are critical in initiating and prolonging meals.

SUMMARY OF PEPTIDES IN THE HYPOTHALAMUS

  • Anorectic Peptides (Inhibit Feeding):
    • αMSH: Alpha-melanocyte-stimulating hormone.
    • CART: Cocaine- and amphetamine-regulated transcript.
  • Orexigenic Peptides (Stimulate Feeding):
    • NPY: Neuropeptide Y from the arcuate nucleus.
    • AgRP: Agouti-related peptide from the arcuate nucleus.
    • MCH: Melanin-concentrating hormone from the lateral hypothalamic area.
    • Orexin: Released from the lateral hypothalamic area.

HOMEOSTATIC REGULATION OF BODY FAT AND FEEDING: SUMMARY

  • High Leptin:
    • Leads to activation of aMSH/CART neuron activity in Arcuate nucleus, triggering:
    • Increased release of TSH and ACTH (humoral response), increased sympathetic nervous system activity (visceromotor response), and increased feeding inhibition (somatic motor response).
  • Low Leptin:
    • Leads to activation of NPY/AgRP neuron activity, resulting in:
    • Inhibition of anterior pituitary ACTH and TSH release, decreased metabolic rate, increased parasympathetic activity, and stimulation of feeding behavior.

SHORT-TERM REGULATION OF FEEDING BEHAVIOR

  • Three Phases of Short-Term Regulation:
    1. Cephalic Phase:
    • Activation of the parasympathetic nervous system triggered by the sight and smell of food.
    1. Gastric Phase:
    • The stomach responds to chewing, swallowing, and filling with food.
    1. Substrate Phase:
    • Nutrient absorbance from the intestine.
Short-Term Hunger and Satiety Signals
  • Hunger Signals:
    • Triggered by orexigenic signals.
  • Satiety Signals:
    • Triggered by food consumption leading to feelings of fullness.

MECHANISMS OF SHORT-TERM REGULATION

  • Cephalic Phase Mechanism:
    • Ghrelin is released when the stomach is empty, activating neurons for increased appetite.
  • Gastric Phase Mechanism:
    • Gastric distension activates mechanoreceptors, signaling satiety to the brain via the vagus nerve to the medulla.
  • Substrate Phase Mechanism:
    • Release of CCK (cholecystokinin) from intestines in reaction to certain foods, leading to insulin release and promoting glucose uptake into cells.
  • Insulin Release:
    • Occurs throughout all phases but peaks during the substrate phase, helping signal satiety.

OTHER MOTIVATED BEHAVIORS: DRINKING

  • Two signaling pathways motivate fluid consumption:
    1. Hypovolemic (Volumetric) Thirst:
    • Triggered by decreased blood volume.
    1. Osmotic Thirst:
    • Triggered by increased salt concentration.
Two Kinds of Thirst
  • Hypovolemic Thirst:
    • Caused by the loss of fluid volume (e.g., blood loss). Fluid intake may include electrolytic drinks for nutrient restoration.
  • Pathway for Hypovolemic Thirst:
    • Decrease in blood volume → release of vasopressin from the posterior pituitary → increases water retention by kidneys.
Osmotic Thirst Mechanism
  • Osmotic Thirst:
    • Triggered by hypertonicity due to increased solute concentration.
  • Mechanism:
    • Sensed by neurons in the OVLT, leading to vasopressin release and signaling thirst.

OTHER MOTIVATED BEHAVIORS: TEMPERATURE REGULATION

  • Hypothalamic Role in Temperature Regulation:
    • Temperature-sensitive neurons in the anterior hypothalamus respond to body temperature changes (normal is 37°C or 98.6ºF).
  • Response to Decreased Blood Temperature:
    • Humoral Response: Release of Thyroxin Stimulating Hormone (TSH) increases metabolic rate.
    • Visceromotor Response: Includes shivering and blood vessel constriction.
    • Somatic Motor Response: Seeking warmth both involuntarily (shivering) and voluntarily.

MOTIVATED BEHAVIORS: SUMMARY

  • Summary of hypothalamic responses involved in motivating behaviors:
    • Eating Signals:
    • Bloodborne signals such as Leptin influence responses from the Arcuate nucleus, leading to humoral, visceromotor, and somatic motor responses in feeding.
    • Drinking and Thermal Signals:
    • Angiotensin II and OVLT activity increase vasopressin production for water intake; likewise, temperature regulation involves increased sympathetic activity during heat and actions aimed at reducing body temperature.

ROLE OF DOPAMINE IN MOTIVATION

  • Old Belief vs. New Understanding:
    • Older view: Dopamine signals hedonic reward. New view: Dopamine signals prediction and prediction error (stimulus relevance).
  • Dopamine-depleted Animals:
    • Show a "liking" for food without the motivation to seek it. This indicates the drive reduction associated with dopamine does not necessarily reflect liking.
Reinforcement and Reward
  • Wanting vs. Liking:
    • Wanting is tied to drive reduction; liking is tied to hedonic pleasure.
  • Electrical Self-Stimulation Studies:
    • Rodents demonstrate reinforcement through intracranial self-stimulation (ICSS), prioritizing stimuli that provide greater reinforcement than natural rewards (quick learning).
Dopaminergic Pathways in Reinforcement
  • Dopaminergic Pathway Locations:
    • VTA to nucleus accumbens, known as the medial forebrain bundle, plays a key role in reinforcement effects. Drugs affecting dopamine receptors impact reinforcements.
Dopamine and Reward Behavior
  • Reward Engagement:
    • Dopamine release peaks when animals engage in reinforcing behaviors (e.g., feeding, sexual activity).
    • Highly addictive substances like nicotine and cocaine enhance dopamine activity in the nucleus accumbens.
DOPAMINE AND ADDICTION
  • While drugs of abuse increase dopamine levels, chronic use can lead to deficits in dopamine system functioning, affecting motivation and reward pathways.