Abstract
The transmitter function of acetylcholine in the cerebral cortex has been the subject of many investigations. Application to the cortex of the drugs that influence cholinergic synapses gave results that are often contradictory and difficult to interpret, Chatfield and Purpura (1). In recent years, however, new techniques yielded fresh insight into the transmitter role of acetylcholine in the cerebral cortex. The release of acetylcholine from the surface of the brain was first demonstrated by Macintosh and Oborin (2) and later Collier and Mitchell (3, 4) and Mitchell (5) showed that afferent stimulation increases the output of acetylcholine from the somatosensory cortex. Recent experiments have proved that some nerve cells in the mammalian cortex can be excited by acetylcholine applied directly from micropipettes (6-9).
Another approach to the cortical cholinergic mechanism has been made by studying the effect of topically applied cholinomimetic drugs on the somatosensory evoked potentials (10). Cortical application of cerebro-spinal fluid (CSF) containing various concentrations of acetylcholine or eserine has been shown to increase the amplitude of the repetitive after discharges of the somatosensory evoked potentials. It was suggested that the afferent pathways responsible for the primary complex are not cholinergic, whereas those responsible for the repetitive after discharges are cholinergic in nature.
