The major objective of the present study was to characterize, in terms of α- and β-receptor mechanisms, the previously observed facilitating actions of norepinephrine (NE) on somatosensory cortical neuronal responses to excitatory synaptic inputs and iontophoretic administration of acetylcholine (ACh). In the forelimb region of rat somatosensory cortex (SI), excitatory single unit responses to natural stimulation of the contralateral forepaw or microiontophoretic pulses (10 sec duration at 45 sec intervals) of ACh were examined before, during and after iontophoretic administration of NE, phenylephrine (PE) and isoproterenol (ISO). Adrenergic agonist actions were quantitatively assessed by computer-based analysis of poststimulus time or cholinergic response histograms. At doses which suppressed or had no effect on the spontaneous discharge, the α agonist, phenylephrine, facilitated excitatory synaptic transmission in 12 of 14 cells and enhanced neuronal responsiveness to ACh in 15 of 24 cells. Thus, phenylephrine consistently mimicked the potentiative actions of NE. whereas the β agonist, isoproterenol, at similar doses, was ineffective in enhancing synaptic efficacy (n = 12) or ACh-induced excitation (n = 19). In addition, iontophoretic application of the α blocker, phentolamine. reversibly antagonized NE-induced potentiation of ACh responses in 6 out of 6 cases. In contrast, administration of the beta antagonist, sotalol, had no effect on NE-mediated enhancement of ACh in all three neurons tested. Overall, these results suggest that endogenously released NE may facilitate excitatory synaptic transmission within the somatosensory cortex by activation of postsynaptic adrenoceptors with α characteristics.
All Science Journal Classification (ASJC) codes
- Cellular and Molecular Neuroscience