420 



S. J. JABBUR AND A. L. TOWE 



Fig. 1. Cuneate neuron discharged by electrical stimulation of the ipsilateral 

 forepaw (a) and the contralateral motor cortex (b). Peripheral shock artifacts 

 are marked with dot. A short train of shocks applied to the ipsilateral motor cortex 

 would just discharge the neuron, a. Mean initial spike latency following forepaw 

 shocks, L = 5-77 msec; mean number of spikes per discharge, JfB = 3-82; 

 maximum frequency following, #= 312/sec. b. Following stimulation of contra- 

 lateral motor cortex, £ = 26-70 msec; JJcl = 3-12. 



of shocks to the cortex (Fig. 1b) ; a subsequent afferent volley finds the neuron 

 less responsive. The remaining two-thirds of the cuneate neurons are rendered 

 less excitable by such conditioning stimulation. As illustrated in Fig. 2, a 

 short train of shocks is usually required. The time course of this decrease in 

 excitability, shown in Fig. 3, is the same as that obtained by interacting two 

 cutaneous inputs; it is fully developed within 20 msec after the end of the 

 conditioning stimulus and the unit has fully recovered 100-200 msec later. 

 Like the monosynaptic inhibitory interaction shown in the Table on p. 415, 

 the response latency of the cortically inhibited cuneate neuron increases, and 

 the number of spikes decreases, until the peak depression is attained. Respon- 

 siveness then returns to normal. Conditioning stimulation apphed to either 

 hemisphere depresses the unit's responsiveness, but stimulation of the cortex 

 contralateral to the recording site is more efficacious (Fig. 4). The magnitude 

 of the depressive effect can be increased either by increasing the strength of 

 the cortical shock or by decreasing the strength of the forepaw shock. When 

 the conditioning stimulus consists of at least ten strong shocks with a fre- 

 quency of 300/sec, and the testing stimulus is reduced to near threshold 

 intensity, maximal inhibition is observed, Thus, the inhibition is milder than 



