Contribution of NMDA and non-NMDA receptors to synaptic transmission from the brachium of the inferior colliculus to the medial subdivision of the medial geniculate nucleus in the rabbit

Previous work from this laboratory has demonstrated that monosynaptic input s from the brachium of the inferior colliculus (BIC) to the medial subdivis ion of the medial geniculate nucleus (mMG) strengthen as a result of associ ative conditioning with an acoustic conditioned stimulus (i.e., fear condit ioning). One model that has been proposed to underlie certain types of neur onal plasticity involves the recruitment of N-methyl-D-aspartic acid (NMDA) -type glutamate receptors. The purpose of the present study was to examine the relative contributions of glutamatergic NMDA and non-NMDA receptors to synaptic transmission within this pathway. Individual contributions of the specific receptor types were assessed through the use of 2-amino-5-phosphon ovaleric acid (AP5), a selective NMDA receptor antagonist, and 6-cyano-5-ni troquinoxaline-2,3-dione (CNQX), a non-NMDA receptor antagonist. Bipolar st imulating electrodes were stereotaxically implanted in BIC and recording el ectrodes (attached to dual 32-gauge cannulae for delivery of drug) were pos itioned in mMG of New Zealand albino rabbits. Single pulses (150 mu s, 100- 350 mu A) delivered to BIC resulted in short-latency (<4 ms) responses in m MG. BIC-evoked single-unit activity was recorded from mMG before, during, a nd at several intervals after injection of AP5, CNQX, and/or artificial cer ebrospinal fluid (ACSF). Injection of either AP5 or CNQX, but not ACSF, sig nificantly attenuated the short-latency BIC-evoked responses in the vast ma jority of cells tested. These findings suggest that the monosynaptic pathwa y from BIC to mMG is glutamatergic and that this pathway frequently employs NMDA-type receptors during electrically stimulated synaptic transmission. Due to the NMDA receptors' proposed role in plasticity (e.g., long-term pot entiation), these results may have implications for understanding the mecha nisms of synaptic plasticity observed at this synapse during associative le arning.