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Behavioral Genetics

Behavioral Genetics.

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Behavioral Genetics

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  1. Behavioral Genetics

  2. Temperament – that portion of a person’s personality that has an organic, and therefore genetic, basis. It is has been acknowledged for centuries that some portion of the personality has an organic basis, e.g. personality differences between men and women. It is obvious that some of these differences can be attributed to specific proteins, e.g. the hormones testosterone and estrogen.

  3. Chronic and Bipolar Depression • Genealogy of a family from the Central Valley of Costa Rica. Deceased persons are marked with a slash.

  4. It has been difficult to identify the specific genes behind bipolar depression because it is a polygenic trait, a trait caused by the joint action of multiple genes.

  5. The midbrain (mesencephalon): center for emotions and sex hypothalamus

  6. Synapses, neurotransmitters, and receptors

  7. Novelty- or Thrill-Seeking, and Addiction Dopamine synthesis

  8. People who psychologists would describe as thrill, or novelty seekers have been shown to have a mutation of the D4DR receptor allele, found on chromosome 11. • All addictions involve affecting the release, reuptake, or regulation of dopamine. • Reuptake: the transporting of a neurotransmitter back inside a dendrite by means of transporter protein.

  9. Dopamine and addiction

  10. Serotonin and Depression • Serotonin – Synthesized from the amino acid tryptophan. • Is involved in both relaxation and aggression. • Selective Serotonin Reuptake Inhibitors: Zoloft, Prozac.

  11. There is controversy about the role played by the serotonin transporter in chronic depression – whether it is too efficient at transporting serotonin (the majority opinion) or defective in transporting serotonin (Dean Hamer), in which case Prozac and Zoloft should be seen a synthetic serotonin transporter proteins.

  12. Appetite and Satiety The hypothalamus is the homeostatic center of the brain, linked to the endocrine system: Lateral part – start eating. Ventromedial region and paraventricular nucleus – stop eating. Vagus nerve – All important for communicating between brain, stomach, and intestines. Stimulates secretion of insulin. β3-adrenergic receptor – receptors located in cells of adipose tissue (fat). Interacts with norepinepherine to produce lyposis (conversion of fat into energy).

  13. Brain chemicals involved with different types of foods: Serotonin – inhibits consumption of carbohydrates. Norepinephrine – stimulates carbohydrate consumption and lyposis (conversion of fat into energy). It inhibits the release of insulin. Insulin – hormone produced in the pancreas that causes liver and muscle cells to take up glucose from the blood. Absence of insulin causes the body to burn fat. Glanine – increases fat intake.

  14. Chemicals that signal the brain to start or stop eating Start eating: ghrelin – produced by cells of the stomach and pancreas. Signal hunger. Neuropeptide Y (NPY)- produced in hypothalamus. Stimulates food intake in reaction to presence of leptin. Stop eating: Cholecystokinin (CKK) – peptide produced by the intestine that signals satiety. Glucagon-like Peptide 1(GLP-1) and Peptide YY (PYY) – produced in the intestines; stimulates the pancreas to release insulin. Up to 70 receptor sites in the hypothalamus interact with these chemicals. Mutations in these receptors may explain up to 25% of obesity cases.

  15. Long-term stop eating signal: Leptin: secreted by fat cells, signals the brain to stop eating and increases metabolism. Metabolism: burning of calories.

  16. Effect of different classes of food on metabolism • Carbohydrates – stimulates production of insulin which robs bloodsteam of all amino acids except tryptophan. Leads to heightened serotonin production. Relieves “psychological hunger.” • Proteins – blocks tryptophan and increases metabolism. Does the Atkins diet work?

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