In big brown bats, tone-specific plastic changes [best frequency (BF) shifts] of cortical and collicular neurons can be evoked by auditory fear conditioning, repetitive acoustic stimuli or cortical electric stimulation. It has been shown that acetylcholine (ACh) plays an important role in evoking large long-term cortical BF shifts. However, the role of N-methyl-d-aspartate (NMDA) receptors in evoking BF shifts has not yet been studied. We found 1) NMDA applied to the auditory cortex (AC) or inferior colliculus (IC) augmented the auditory responses, as ACh did, whereas 2-amino-5-phosphovalerate (APV), an antagonist of NMDA receptors, reduced the auditory responses, as atropine did; 2) although any of these four drugs did not evoke BF shifts, they influenced the development of the long-term cortical and short-term collicular BF shifts elicited by conditioning; 3) like ACh, NMDA augmented the cortical and collicular BF shifts regardless of whether it was applied to the AC or IC; 4) endogenous ACh of the AC and IC is necessary to produce the long-term cortical and short-term collicular BF shifts; 5) blockade of collicular NMDA receptors by APV abolished the development of the collicular BF shift and made the cortical BF shift small and short-term; 6) blockade of cortical NMDA receptors by APV reduced the cortical and collicular BF shifts and made the cortical BF shift short-term; and 7) conditioning with NMDA + atropine applied to the AC evoked the small, short-term cortical BF shift, whereas conditioning with APV + ACh applied to the AC evoked the small, but long-term cortical BF shift.
Disruption of Long-Term Alcohol-Related Memory Reconsolidation: Role of β-Adrenoceptors and NMDA Receptors
