[NO-dependent mechanisms of the amygdalofugal modulation of the hypothalamus vegetative neurons].
In neurophysiological and histochemical experiments on rats, amygdalo-fugal modulation of cells within NO-producing areas of the hypothalamus was studied. Electrical stimulation of the medial area of the central nucleus caused obvious excitatory neuronal reactions within the medial part of the paraventricular nucleus and rostral portion of the lateral hypothalamic area. The observed amygdala-induced neuronal responses were enhanced after i.v. N-nitro-1-arginine methyl ester (L-NAME, 10 mg/kg). The nistochemical study revealed that the central nucleus stimulation caused an increase in number and optical density of the NADPH-d-positive cells within the parvicellular zone of the paraventricular nucleus and in the medial part of the lateral hypothalamic area. The NO-producing cells within the ventrolateral part of the lateral hypothalamic area were inhibited. The described phenomenon may underlie the amygdalo-fugae modulation of autonomic outflow.
Liubashina
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Itsev
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D000679:Amygdala / Q000502:physiology*; D000818:Animals; D004558:Electric Stimulation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005071:Evoked Potentials; D007026:Hypothalamic Area, Lateral / Q000201:enzymology / Q000502:physiology*; D008297:Male; D009252:NADPH Dehydrogenase / Q000378:metabolism; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000502:physiology*; D010286:Paraventricular Hypothalamic Nucleus / Q000201:enzymology / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar
D004791:Enzyme Inhibitors; D009569:Nitric Oxide; D009252:NADPH Dehydrogenase; D019331:NG-Nitroarginine Methyl Ester