A model system consisting of two rat strains bred for nervous system excitability in response to electric shocks was used to study changes in the number density of neurons in hippocampal field CA3 at 24 h, two weeks, and two and six months after prolonged emotional-pain stress (PEPS). Neuron density in hippocampal field CA3 decreased after completion of PEPS. These changes arose at different time points in the different rat strains (one day for low-excitability rats, two months for high-excitability rats) and persisted to six months. Thus, this is the first demonstration that persistent differential effects of stress on the number density of neurons in hippocampal field CA3, which plays an important role in learning and memory processes, depend on genetically determined constitutive characteristics of the nervous system.

The effects of densensitization of capsaicin-sensitive afferent neurons on the microcirculation in the stomach were studied before and after administration of indomethacin at an ulcerogenic dose in adrenalectomized rats receiving and not receiving replacement therapy with corticosterone and in sham-operated animals. Measures of the microcirculation consisted of blood flow rates in microvessels in the submucous layer of the stomach and the diameter and permeability of microvessels in the mucosa. Desensitization of capsaicin-sensitive afferent neurons was performed by administration of capsaicin at a dose of 100 mg/kg for two weeks and adrenalectomy one week before the experiment. Blood flow rates in microvessels and microvessel diameters were assessed in non-anesthetized rats by direct video recording methods using a special optical system with a contact dark-field epiobjective. Administration of indomethacin at an ulcerogenic dose led to decreases in blood flow rate in microvessels in the submucous layer, dilation of superficial microvessels in the mucosa of the stomach, and an increase in their permeability. Desensitization of capsaicin-sensitive neurons potentiated indomethacin-induced impairments to the microcirculation in the submucous layer and the mucosa of the stomach. These effects of densensitization were significantly enhanced in conditions of glucocorticoid hormone deficiency. Thus, glucocorticoid hormones have favorable effects on the gastric microcirculation in rats with desensitization of capsaicin-sensitive afferent neurons.