Effects of D-AP5 and NMDA microiontophoresis on associative learning in the barrel cortex of awake ratsстатья
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Аннотация:Experiments involving single-unit recordings and microiontophoresis were carried out in the barrel cortex of awake, adult rats
subjected to whisker pairing, an associative learning paradigm where deflections of the recorded neuron’s principle vibrissa S2. are
repeatedly paired with those of a non-adjacent one S1.. Whisker pairing with a 300 ms interstimulus interval was applied to 61 cells. In
23 cases, there was no other manipulation whereas in the remaining 38, pairing occurred in the presence of one of three pharmacological
agents previously shown to modulate learning, receptive field plasticity and long-term potentiation: N-methyl-D-aspartic acid NMDA.
ns8., the NMDA receptor antagonist AP5 ns17. or the nitric oxide synthase inhibitor L-nitro-arginine-N-methyl-ester L-NAME.
ns13.. Non-associative unpaired. experiments ns14. and delivery of pharmacological agents without pairing ns14. served as
controls. Changes in neuronal responsiveness to S1 following one of these procedures were calculated and adjusted relative to changes in
the responses to S2. On average, whisker pairing alone yielded a 7% increase in the responses to S1. This enhancement differed
significantly from the 17% decrease obtained in the non-associative control condition and could not be attributed to variations in the state
of the animals because analysis of the cervical and facial muscle electromyograms revealed that periods of increased muscular activity,
reflecting heightened arousal, were infrequent less than 4% of a complete experiment on average. and occurred randomly. The
enhancement of the responses to S1 was further increased when whisker pairing was performed in the presence of L-NAME 27%. or
NMDA 35%. whereas AP5 reduced it to 1%. During the delivery period, NMDA enhanced both neuronal excitability and responsiveness
to S1 whereas AP5 depressed them. However, the effects of both substances disappeared immediately after administration had ended.
L-NAME did not affect the level of ongoing activity and responses to S1 significantly. From these data, we concluded that, since the
changes in the responses to S1 lasted longer than the periods of both whisker pairing and drug delivery, they were not residual excitatory
or inhibitory drug effects on neuronal excitability. Thus, our results indicate that, relative to the unpaired controls, whisker pairing led to a
24% increase in the responsiveness of barrel cortex neurons to peripheral stimulation and that these changes were modulated by the local
application of pharmacological agents that act upon NMDA receptors and pathways involving nitric oxide. We can infer that
somatosensory cerebral cortex is one site where plasticity emerges following whisker pairing. q1998 Elsevier Science B.V. All rights
reserved.