Transient and long-lasting effects of iontophoretically administered norepinephrine on somatosensory cortical neurons in halothane-anesthetized cats.
We examined the modulatory effects of iontophoretically administered norepinephrine (NE) on the excitability of 117 neurons in cat somatosensory cortex. NE was released in the vicinity of neurons with receptive fields (31/117) while they were excited by somatic stimuli and near neurons without receptive fields (86/117) while they were excited by glutamate. In 54% of the neurons (n = 63) the effects were inhibitory, decreasing both the spontaneous and the driven activity. Most of these cells were found in the middle layers of cortex. In 36% of the neurons (n = 42), mostly located in either the upper or lower layers, the effects were excitatory, enhancing either or both driven and spontaneous activity, but 52% (n = 22) of this group displayed a transient phase of inhibition. NE usually had a proportionately greater effect on the spontaneous activity than on the evoked activity. Effects of specific NE agonists and antagonists indicated that alpha 2- and beta-receptors mediated the inhibition, but that alpha 1-receptors mediated the excitation. We hypothesize that when NE is released in cat somatosensory cortex, it modulates neuronal responses to afferent activity by generally reducing the excitability of cells in the middle layers and by increasing their signal-to-noise ratios. However, in the upper and lower layers NE will enhance neuronal activity, encouraging exchanges with other cortical areas. In addition, we tested and confirmed the hypothesis that short treatments with NE can modify the excitability of neurons in adult cat somatosensory cortex for long periods of time. Of 69 cells, 59% showed effects of NE lasting for more than 5 min. Response enhancement lasting for the duration of the recording session (5 to 36 min) occurred in 82% (18/22) of silent cells without a receptive field and in 63% (17/27) of spontaneously active cells without a receptive field, but only in 14% (2/14) of cells with a receptive field, suggesting an inverse relationship between cell excitability and this effect of NE. The magnitude of the enhancement followed the same relationship, being greatest for silent cells and least for cells with receptive fields (125, 58, and 49%, respectively). The long-lasting enhancement was blocked by an alpha 1-receptor antagonist in 6 of 9 neurons tested, while the administration of alpha 2- and beta-receptor agonists never produced a long-lasting effect, suggesting that the effect is mediated by alpha 1-adrenoceptors.
Warren
R A
RA
Department of Neurology and Neurosurgery, McGill University, Montréal, Canada.
Dykes
R W
RW
D000818:Animals; D002415:Cats; D002452:Cell Count / Q000187:drug effects*; D005260:Female; D006221:Halothane / Q000494:pharmacology*; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D009473:Neuronal Plasticity / Q000187:drug effects*; D009638:Norepinephrine / Q000494:pharmacology*; D013003:Somatosensory Cortex / Q000187:drug effects*; D013997:Time Factors
D006221:Halothane; D009638:Norepinephrine