Abstract
<p>This study examined changes of synaptic efficacy in the medial subnucleus of the medial geniculate nucleus (mMG) resulting from classical heart rate (HR) conditioning with an auditory conditioned stimulus (CS). Conditioning-induced changes of synaptic efficacy were measured in awake animals by examining short latency ($<$3.0 ms) mMG single unit responses evoked by stimulation of one of two areas which send auditory-CS and non-auditory information monosynaptically to mMG, the brachium of the inferior colliculus (BIC) and the superior colliculus (SC), respectively. Synaptic efficacy was measured immediately before, immediately after, and 1 hour after one session of classical HR conditioning with a tone-CS and a corneal airpuff unconditioned stimulus. In order to determine if conditioning produced changes of synaptic efficacy on the auditory-BIC inputs to mMG cells, and not general changes of cellular excitability, analyses of synaptic efficacy were performed on the mMG units that could be evoked by both BIC and SC stimulation. Analyses revealed that the BIC- but not SC-test stimulus-evoked unit activity from the same neurons exhibited the following changes immediately after conditioning: decreases in unit response latency, increases in unit response reliability, and increases in spike frequency. However, BIC- and SC-evoked unit responses immediately following pseudoconditioning did not exhibit these changes in unit responding. These results suggests that the synapses carrying CS-auditory information to mMG neurons increase in strength as the result of associative HR conditioning with an acoustic CS. Most of the changes of synaptic efficacy diminished 1 hour following training.Several tests were performed which suggest that the increases of synaptic efficacy occurred at the auditory inputs to mMG neurons, and that these inputs may have been monosynaptic. These changes of synaptic efficacy in mMG are consistent with a Hebbian model of associative learning- related synaptic plasticity. Specifically, neurons in mMG and other areas of the HR conditioning circuitry which receive convergent and coactive CS and US inputs during learning are capable of associative learning-related changes of synaptic plasticity.</p>