Different control of the adrenocorticotropin-corticosterone response and of prolactin secretion during cold stress, anesthesia, surgery, and nicotine injection in the rat: involvement of capsaicin-sensitive sensory neurons.

The release of ACTH, corticosterone, and PRL was compared in capsaicin-pretreated rats, which lack afferent C-fibers, and their controls under somatosensory (cold, surgery) and central (restraint) forms of stress. Cold stress induced the release of ACTH and consequently that of corticosterone in the controls, but not in the capsaicin-pretreated rats. Intravenous injection of ACTH1-24 was equally effective in releasing corticosterone in both groups. Whereas PRL was not released in response to cold stress, restraint stress did induce the release of both ACTH and PRL, in the capsaicin-pretreated as well as in the control group. Pentobarbital anesthesia alone elicited PRL, but no ACTH release. ACTH release was evoked by surgery under pentobarbital anesthesia but was abolished by capsaicin pretreatment. PRL levels were not further increased by surgery. Nicotine in a small dose (5 micrograms intra-arterially) evoked stimulation of afferent C-fibers as observed on a depressor reflex. Intraperitoneal injection of nicotine (250 micrograms/kg) caused a marked rise in plasma ACTH both in the capsaicin-pretreated conscious rats and in their controls, probably resulting from central stimulation as this effect was shown to be inhibited during pentobarbital anesthesia. A moderate rise of PRL by nicotine was seen in conscious rats. The stimuli used, regarded as experimental models of stress, show essential differences in their ability to evoke the release of ACTH, corticosterone, and PRL. Those stimuli which cause the release of ACTH and corticosterone via afferent C-fiber stimulation do not release PRL, whereas emotional and cognitive stress causes the release of both ACTH and PRL.