Immunoreactive somatostatin in the hypothalamus and other regions of the rat brain: effects of insulin, glucose, alpha- or beta-blocker and L-dopa.
Effects of various hormonal and pharmacological manipulations on somatostatin distribution were investigated to elucidate the physiological significance of somatostatin in the hypothalamus and the other regions of the rat brain. Immunoreactive somatostatin (IRS) was measured by radioimmunoassay newly developed. Insulin induced an increase of hypothalamic IRS and a decrease of plasma RGH, while glucose administration resulted in the opposite responses, which were not significant. Insulin also increased IRS in the thalamus and the brain stem. The insulin-induced increase of hypothalamic IRS was reduced by hyperglycemia. Glucagon reduced IRS initially and then increased it with an elevation plasma RGH. L-dopa did not affect hypothalamic IRS, although it decreased plasma RPRL. Phentolamine slightly increased plasma RGH and decreased IRS in most regions of the rat brain, while propranolol increased IRS in these regions. Pretreatment with propranolol significantly increased plasma RGH 120 min after insulin administration, and hypothalamic IRS decreased initially by pretreatment with propranolol, and then it increased significantly. When pretreated with propranolol, glucagon markedly increased plasma RGH and decreased IRS significantly. From these findings it is concluded that hypothalamic IRS may participate in the hormonal regulatory system in correlation to plasma RGH, as observed in studies on plasma GH and hypothalamic IRS following insulin, glucose, propranolol or phentolamine administration, but IRS in other regions of the brain may have some other actions as a neurotransmitter or a modulator, because of no significant correlation between plasma GH or PRL and IRS in these regions following various stimuli. In addition, glucose homeostasis and adrenergic mechanism may be important factors in regulating IRS in the rat brain.
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology*; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000818:Animals; D001923:Brain Chemistry; D005947:Glucose / Q000494:pharmacology*; D013006:Growth Hormone / Q000097:blood; D007031:Hypothalamus / Q000032:analysis*; D007328:Insulin / Q000494:pharmacology*; D007980:Levodopa / Q000494:pharmacology*; D008297:Male; D010646:Phentolamine / Q000494:pharmacology; D011388:Prolactin / Q000097:blood; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D013004:Somatostatin / Q000032:analysis* / Q000276:immunology
D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D007328:Insulin; D007980:Levodopa; D013004:Somatostatin; D011388:Prolactin; D013006:Growth Hormone; D011433:Propranolol; D005947:Glucose; D010646:Phentolamine