Abstract
Synaptic efficacy at the rat Ia–motoneuron synapse has been reported to increase in vivo, within 3 d of sectioning a single muscle nerve (Miyata and Yasuda, 1988). We provide an indirect test of the hypothesis that this increase is caused by altered probability of transmitter release of axotomized afferents. Experiments consisted of in vivo recording of maximal composite group I EPSPs evoked in intact rat medial gastrocnemius (MG) motoneurons by stimulation of the lateral gastrocnemius-soleus nerve (LG-S). We compared the maximal LG-S EPSP amplitude and the response to high-frequency stimulation (modulation) recorded in untreated rats, with the same measures recorded in rats that had the LG-S nerve axotomized 3 d before data collection. In confirmation of previous work, the mean amplitude of LG-S EPSPs evoked by stimulation of axotomized afferents was significantly larger than that measured in untreated rats (3.9 ± 0.34 and 2.3 ± 0.19 mV, respectively). The increase in EPSP amplitude was accompanied by significantly greater negative modulation (depression) of EPSP amplitude during high-frequency stimulation (−39 ± 4% and −53 ± 4%, untreated and treated, respectively). Modulation would not be expected to change if the increase in EPSP amplitude was attributable solely to a greater number of afferent connections (Koerber and Mendell, 1991). Therefore, the present results are consistent with the hypothesis that the initial axotomy-induced increase in synaptic efficacy occurs because of an increase in the probability of transmitter release. Furthermore, these results suggest that the probability of transmitter release at this synapse is regulated by either afferent activity and/or trophic communication with the target muscle.
