Depression of monosynaptic excitatory postsynaptic potentials by Mn2+ and Co2+ in cat spinal cord
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TL;DR
It is concluded that the monosynaptic excitatory postsynaptic potential evoked by Ia afferents in cat motoneurones is probably mediated by chemical transmission.
Abstract
In cats anesthetized with allobarbitone-urethane, Mn2+ and Co2+ (and occasionally La3+) were released extracellularly from micropipettes while recordings were made of monosynaptic excitatory postsynaptic potentials evoked in lumbosacral motoneurones by Ia afferent stimulation. These excitatory postsynaptic potentials consistently showed a marked depression in their rate of rise (by an average of 44%) and an increase in half-amplitude duration (by an average of 50%). There was a less pronounced reduction in peak amplitude and increase in time-to-peak. After applications of Mn2+ or Co2+, presynaptic potentials recorded in motoneurones showed no sign of any depression but the synaptic delay was clearly increased. It is concluded that the monosynaptic excitatory postsynaptic potential evoked by Ia afferents in cat motoneurones is probably mediated by chemical transmission.
