On the current that flow during the strychnine spike

Abstract

Patterns of net vertical current flow and current source density during the normal primary evoked response and the strychnine spike induced by topical application were measured using single first-order and second-order differences of voltages occurring in depth and time in the cat's pericruciate cerebral cortex. Net vertical current flow during the primary response was dominated by a large downward current in layers II and III, 12–24 msec in time after a stimulus to the contralateral forepaw. Smaller, net upward currents occurred in layer V, 14–28 msec, and in layer II, 20–30 msec after the stimulus. Topical strychnine resulted in a pattern of net current flow that was an intensified and prolonged version of that for the normal evoked response. The great intensification occurred in layers II and III, with small changes occurring in layer V. No changes in the patterns of net vertical current flow during responses to stimulation of the other 3 paws were caused by strychnine. These patterns of current flow, and the changes that occurred in them after strychnine, can be understood in terms of the known synaptic interactions between sets of cortical neurons and the direct effect of strychnine on superficial, small receptive field neurons, with indirect involvement of deeper, large receptive field neurons. Current source density analysis showed a source/sink couplet in layers II and III, 11–15 msec after the contralateral forepaw stimulus. Sink/source couplets also were found at the same depth at 20–30 msec, and in layer V at 12–24 msec. The current source density pattern after strychnine was also an intensified and prolonged version of that occurring before strychnine, the greatest intensification being evident in layers II and III. Rates of ascent through the cortex of various components of the voltage, current, and source density patterns, and alternation of the strychnine spike with a near-normal primary response at stimulus rates of 3–4/sec, suggest that the strychnine spike results from two causes: (i) an enhancement of a normal process and (ii) the appearance of a new process. It is suggested that the former cause involves enlarged EPSPs, while the latter involves generation of Ca 2+ spikes by the enlarged EPSPs. It is also suggested that the effect of strychnine and other topical convulsants in exerted on thalamocortical afferents fibers in layer I, setting up antidromic spikes that influence layer III neurons by collaterals of the same thalamocortical fibers into this layer, with upward spread into layer II.