Electrophysiological studies of acetylcholine and the role of the basal forebrain in the somatosensory cortex of the cat. I. Cortical neurons excited by glutamate.

1. Microelectrodes attached to iontophoretic pipettes were used to isolate 410 single neurons in the primary somatosensory cortex of halothane-anesthetized cats. Basal forebrain (BF) stimulation, when paired with pulses of iontophoretically administered glutamate, affected the responsiveness in 24 (54%) of 39 neurons; 17 were facilitated, and seven were inhibited. Five minutes after BF stimulation the average response for a sample of 20 cells was enhanced by 45% (+/- 19). All but one of the effects lasted as long as the cell was studied, often greater than 1 h. 2. When atropine was administered while the BF was stimulated during glutamate excitation, 7 of 16 cells were enhanced, but the average increase was only 16% (+/- 15) for a sample of 15 cells. After the atropine had dissipated, four cells were enhanced by the BF stimulus. In three of these the enhancement had been blocked previously by atropine. 3. BF stimulation had effects similar to iontophoretically administered acetylcholine (ACh), but the effects appeared more frequently with BF stimulation than they had with acetylcholine administration. 4. We propose that the enhanced neuronal responsiveness is due to the release of acetylcholine by cortical terminals of cholinergic neurons located in the BF. The BF stimulus may be more effective than acetylcholine administration because corticopetal cholinergic fibers may end in the immediate vicinity of receptors responsible for long-term changes in membrane permeability.