Neuronal responses to systemic nicotine in the solitary tract nucleus: origin and possible relation with nutritional effects of nicotine.

Single-unit activity was recorded extracellularly in the caudal part of the solitary tract nucleus of anesthetized rats. Of 60 recorded neurons, 44 (73.3%) responded to intravenous (I.V.) nicotine. The incidence of response was significantly greater in the cells sensitive to moderate changes in blood glucose level, suggesting that the effects of nicotine on food intake and body weight are partly mediated by the glycemia-sensitive neurons in the caudal nucleus tractus solitarius. Only one-fourth of the neurons affected by I.V. nicotine responded in the same direction to iontophoretic nicotine application, suggesting that sensitivity to systemic nicotine results mainly from an indirect mechanism. Based on the observed effects of nicotinic agonists and antagonists unable to cross the blood-brain barrier, a majority of indirect unit responses to I.V. nicotine might be mediated by peripheral receptors, while the remaining ones might involve central or both central and peripheral receptors.

Characteristics of glycemia-sensitive neurons in the nucleus tractus solitarii: possible involvement in nutritional regulation.

Single unit responses to moderate glycemic variations were extracellularly recorded in the caudal division of the nucleus tractus solitarii of rats anesthetized by i.v. infusion of ketamine. As previously observed, a majority of recorded neurons (70%) were either activated or depressed by moderate hyperglycemia. Responses were consistently reproducible and amplitude was dependent on the maximum level of hyperglycemia. All glycemia-sensitive neurons responded in opposite directions to induced hyperglycemia and hypoglycemia, and almost all displayed the same type of response to local and i.v. glucose administration. Most glycemia-sensitive neurons were depressed by iontophoresis of clonidine, suggesting that they were adrenergic or noradrenergic. Based on these findings, we speculate that glycemia-sensitive neurons in the caudal nucleus tractus solitarii may act as glucose sensors that transmit glycemic information corresponding to different nutritional states, as well as other relevant signals toward hypothalamic structures involved in feeding and metabolic regulation via ascending adrenergic and noradrenergic pathways.

Sensitivity of nucleus tractus solitarius neurons to induced moderate hyperglycemia, with special reference to catecholaminergic regions.

Extracellular single-unit recordings have been carried out in the caudal part of the nucleus tractus solitarius of male rats anesthetized by i.v. infusion with Ketamine. The sensitivity of 38 cells to 0.2 ml of 0.55 M glucose i.v. administration has been studied. The spike frequency of 75% of these cells was affected by the induced moderate hyperglycemia and a majority of them was activated. Immunohistochemical data on 9 glycemia-sensitive neurons showed that all recording sites were within TH-immunoreactive regions of the caudal part of the nucleus (either in the A2 noradrenergic group, or the C2 adrenergic group). These results confirm the existence of glycemia-sensitive neurons in the nucleus tractus solitarius, and suggest that these cells might mediate the effects of physiological fluctuations in blood glucose level on the control of food intake and metabolic regulations. The localization of these cells in catecholaminergic regions suggests that adrenaline and/or noradrenaline efferents might convey feeding relevant information concerning glycemic level or satiety signal from the nucleus tractus solitarius to forebrain structures involved in food intake, such as the perifornical lateral hypothalamic area and the paraventricular nucleus.