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Biochemistry Objectives 44 1. Vasopressin: a. Gene coding and neurophysin II carrier: vasopressin is produced as preprovasopressin and subsequently cleaved into provasopressin (composed of vasopressin, neurophysin II, and a glycoprotein). b. Neurogenic and nephrogenic diabetes insipidus: both caused by a decreased response to ADH: a. Neurogenic (nonhereditary) diabetes insipidus: results from a problem in the neuronal pathway of vasopressin release. Can be caused by a problem in the supraoptic nucleus (defective preprovasopressin gene), blocked transit to the axon terminal, or blocked exocytosis. b. Nephrogenic (hereditary) diabetes insipidus: results from a problem in the nephron receptor response to vasopressin. Can be caused by a problem in V2 receptor sensitivity to ADH, aquaporin-2 channel production, or any point in the pathways converging to aquaporin integration into the apical membrane. c. Secretion control at the following levels: a. Physiological: secretion can be induced by three major mechanisms: increased plasma osmolarity sensed by osmoreceptors in the supraoptic nucleus, decreased volume sensed by volume receptors in the atrium, and decreased pressure sensed by baroreceptors in the carotid sinus/aortic arch. b. Biochemical: a neural impulse is given in response to physiological changes via acetylcholine. Acetylcholine increases intracellular Ca2+, and causes vesicles to release vasopressin and neurophysin II. d. Aquaporin-2 water channel regulation: vasopressin initiates Gs protein cascade cAMP PKA which phosphorylates aquaporin-2 channels. Phosphorylated aquaporin-2 channels integrate into the apical membrane to increase reabsorption of water in the distal nephron. 2. Hypothalamic releasing and inhibiting factors: a. TRH: acts on thyrotrophs to release TSH (Gq, IP3/DAG/Ca2+) b. GnRH: acts on gonadotrophs to release FSH and LH (Gq, IP3/DAG/Ca2+) c. CRH: acts on corticotrophs to release ACTH (Gs, increased cAMP) d. GHRH: acts on somatotrophs to release GH (Gs, increased cAMP) e. GHIH: acts on somatotrophs to inhibit GH release (Gi, decreased cAMP) 3. GnRH binding LH, FSH release: GnRH binds to a Gq protein linked receptor, causing an increase in PLC, Ca2+, and CaM-kinase. CaM-kinase phosphorylates enzymes, and in conjunction with Ca2+, induces FSH, and LH vesicles to fuse with the gonadotrope membrane. 4. Neuromodulator peptides induce desired behavior: a. CCK-PZ: satiety (no more food needs to be eaten when CCK-PZ is secreted to digest food) b. GLP-1: suppresses appetite (causes insulin release, no more food needs to be eaten when glucose is already being stored) c. GnRH: mating behavior (increases LH and FSH, increased procreative capability) d. Oxytocin: maternal behavior (causes labor and milk ejection) e. Vasopressin: memory and learning (causes water reabsorption, and memory of place where water was so dehydration is avoided)