Long-term cholinergic enhancement of evoked potentials in rat hindlimb somatosensory cortex displays characteristics of long-term potentiation.

Pairing a cutaneous electrical stimulus of the hind-paw with stimulation of the basal forebrain produces long-term cholinergic enhancement of the responsiveness to a tactile stimulus. A short period of pairing (20 trials) increased the area of the two main components of the evoked potential by 37.1 +/- 13.5% (+/- SEM) and 37.9 +/- 6.8%, respectively. The effects lasted for the duration of the experiment (> 2 h). The enhancement could be blocked by either MK-801, an NMDA receptor antagonist or by L-NAME, a nitric-oxide-synthase inhibitor when they were given prior to pairing. Control experiments with skin stimulation alone and basal forebrain stimulation alone had only small long-term effects (approximately 10%) on the size of the evoked potential. Thus, long-term cholinergic enhancement, attributable to disinhibition and increased release of acetylcholine in the cortex during neuronal excitation by other sources, and so named because it is blocked by atropine, may be a form of long-term potentiation. The existence of such a mechanism for the control of cortical neuronal plasticity identifies the basal forebrain as a powerful modulator of long-lasting changes in cortical neuronal excitability.