Effects of iontophoretically administered norepinephrine in cat somatosensory cortex : modulation of neuronal responses to cutaneous input and prolonged increases of glutamate-induced excitations

This work describes the neuromodulatory effects of norepinephrine (NE) on single neurons isolated in the somatosensory cortex of halothane-anaesthetized cats. In 46 animals, a sample of 465 isolated neurons were characterized according to the presence or absence of peripheral input, of spontaneous activity and sensitivity to glutamate. The effects of NE were examined in 117 cases using two different paradigms; either the receptive fields of neurons displaying peripheral inputs were stimulated mechanically during NE administration or the effects of NE were studied on the response to iontophoretically-administered glutamate on neurons lacking a receptive field.In the presence of NE, 54% (63/117) of the neurons were inhibited. 36% (42/117) displayed some increase in neuronal activity and 10% (12/117) were unaffected. Often, the inhibitory effects of NE were more important on the spontaneous activity than on the induced activity producing an increase in the signal-to-noise ratio in 74% (28/38) of neurons. In contrast, when NE produced some excitation, the signal-to-noise ratio was increased in only 38% (11/29) of those cases. Inhibited neurons were located predominantly in the middle layers of the cortex while excited neurons were found in upper and lower layers. These results suggest that NE has different functions in different layers of the somatosensory cortex.After the cessation of NE administration, the response to a peripheral stimulus was increased for more than 5 min in 22% (2/9) of neurons. In contrast, long-lasting increases in the response to glutamate followed NE administration in 70% (31/44) of cases. In this latter group, NE also produced long-lasting decreases in the ongoing activity in 39% (9/23) of neurons and long-lasting increases in the signal-to-noise ratio in 59% (13/23).Pharmacological evidence suggests that the inhibitions were mediated by $ alpha sb{2}$- and $ beta$-receptors while the excitations and the long-lasting increases in neuronal activity were mediated by $ alpha sb1$-receptors