No abstract

No abstract

No abstract

In order to examine possible neurophysiological changes during an immune response, we have recorded neural activity in a conscious animal bearing chronic recording electrodes in the preoptic area/anterior hypothalamus (PO/AH) and hypothalamic paraventricular nucleus (PVN). Male rats were sensitized with sheep red blood cells (SRBC) injected intraperitoneally. Basal PO/AH multiunit activity (MUA) was recorded as 14.7 +/- 2.1 Hz prior to sensitization and was seen to increase significantly to a maximum of 33.1 +/- 6.0 Hz (p less than 0.005) five days after SRBC injection. This increase correlated with the initial appearance of anti-SRBC serum antibodies at a mean antibody titer of 1:32. Also recorded were decreases in PO/AH MUA on days 3 and 8 after the sensitization (8.2 +/- 2.4 Hz, p less than 0.005); 7.1 +/- 3.3 Hz, p less than 0.005, respectively). Basal PVN MUA was recorded as 14.7 +/- 2.4 Hz. It decreased significantly for the first three days after immunization, and then returned to a basal rate before increasing to 25.9 +/- 8.4 Hz (p less than 0.005) on day 6. On the ninth and tenth days after SRBC injection PO/AH and PVN MUA levels returned to those recorded before immunization.

The direct involvement of the hypothalamic paraventricular nucleus (PVN) in the control of adrenocortical secretion is now generally accepted. In order to contribute to our understanding of the electrical activity of cells in this region during adrenocortical activation, we have recorded multiunit electrical activity (MUA) in response to acute neural stimuli in freely moving male rats and have examined the pathways involved. Photic, acoustic, olfactory, and sciatic nerve stimulation all increased PVN MUA by between 130% and 250%. These responses were selectively blocked, according to the stimulus modality tested, by radiofrequency lesions of central neural structures. Thus PVN responses to photic stimulation were blocked by lesions of the suprachiasmatic nuclei and reduced by mammillary peduncle lesions but were unaffected by lesions of the bed nuclei of the stria terminalis. Responses to acoustic stimulation were blocked by lesions of the mammillary peduncles but not by those placed in the suprachiasmatic nuclei, the septum, or the bed nuclei of the stria terminalis. Lesions of the septum blocked the response to sciatic nerve stimulation but did not affect the response to olfactory stimulation with amyl acetate fumes, which was blocked by lesions of the bed nuclei of the stria terminalis. The data confirm those obtained in endocrine studies concerning the neural pathways involved in the transmission of neural stimuli that produce adrenocortical activation.