PSY 312 Ch 12 pt 2
Re-examination of the LH as a "Feeding Center"
LH lesions produce many non-specific effects Severe motor disturbances Deficits in responses to sensory stimuli Interfere with food-seeking responses
satiety peptides: decrease appetite
Cholecystokinin (CCK) Leptin
hunger peptides: increase appetite
Neuropeptide Y Galanin Orexin-A Ghrelin
Bilateral electrolytic lesions of the VMH produce:
hyperphagia and extreme obesity in rats
Peptides
short chains of amino acids that function as hormones and neurotransmitters
Role of Hypothalamus in Feeding?
Complex effects on ingestive (consummatory) behavior Regulation of energy balance Regulation of energy metabolism Motor behaviors Critically intertwined with other brain regions
VMH Satiety Center
High food intake does not persist indefinitely, but there is maintenance of the new higher body weight Animals less willing to work for food or eat food that is unpalatable A "Satiety Center"
Cholecystokinin (CCK)
CCK injections cause rats to eat less
LO8: Discuss the role of the gastrointestinal tract in hunger and satiety.
Cannon and Washburn (1912) Stomach contractions led to hunger Stomach distension led to satiety Hunger is still experienced by those with no stomach (but rest of GI tract remaining) Koopmans Experiment Extra stomach and length of intestine transplanted into rats Joined to major arteries and veins Food in transplanted stomach decreased eating in proportion to its caloric content and volume Extra stomach had no functional nerves and nutrients were not absorbed from it Blood borne satiety signal(s)
LO7: Critically evaluate the concept of hypothalamic hunger and satiety centers.
Early studies suggested two hypothalamic centers for satiety and hunger -Ventromedial hypothalamus (VMH) - Satiety center -Lateral hypothalamus (LH) - Hunger center Identified on the basis of lesion studies -Electrolytic Lesions -Neurotoxic Lesions (See word page for the locations in the rat brain of the ventromedial hypothalamus and the lateral hypothalamus.)
LH Feeding Center
Even in VMH lesioned animals, this could occur with LH lesioning However, Also produces adipsia Animals can eventually be coaxed to eating palatable food A "Feeding Center"?
Re-examination of the VMH as a "Satiety Center"
Problems VMH lesions produce increases in insulin Increases in lipogenesis (fat deposition) Decreases in lipolysis (conversion of fat to energy) Because calories are converted to fat too quickly, must eat constantly to ensure enough calories for energy needs Lesions to other areas produce similar effects -The adjacent paraventricular nucleus was also being damaged in these studies -Fibers of passage: The ventral noradrenergic bundle
Leptin
Produced by adipocytes (fat cells) Inhibits feeding via CNS receptors
VMH Satiety Center Two Phases
Two Phases Dynamic phase: Several weeks of excessive eating and rapid weight gain Static phase: Consumption declines to a level that is just sufficient to maintain a stable level of obesity
Neuropeptide Y (NPY)
Widely distributed throughout CNS Promotes feeding via CNS receptors NPY injections into PVN of hypothalamus increase eating
Bilateral electrolytic lesions of the LH produces
aphagia
