|Abstract View |
|INACTIVATION OF RAT AUDITORY CORTEX: EFFECT
ON UNIT ACTIVITY IN VENTRAL MEDIAL GENICULATE |
Wittig Jr; S.K.
|Dept Neurosci, Univ Pennsylvania, Philadelphia,
|Acute inactivation of rat auditory cortex (AI)
by the GABA-A agonist muscimol leads to profound impairment in
pitch discrimination and tone detection (Talwar et al., 2001).
This suggests that AI is normally essential for basic auditory
functions although its detailed contribution remains unclear.
The muscimol observations contrast with numerous former
reports that animals with ablated AI perform pitch
discrimination at normal thresholds. However, in those
experiments the animals had a surgical recovery and retraining
period so that plastic reorganization could take part in
maintaining auditory function. |
AI sends massive feedback
to the ventral medial geniculate (MGBv). The role of cortex
could be only to maintain thalamic activity by tonic
excitation rather than carrying out any computations. To
investigate the feedback, we recorded evoked responses of MGBv
neurons in anesthetized rats during inactivation of AI by
muscimol applied on the cortical surface. In parallel auditory
evoked potentials (AEP) were recorded from the AI surface.
After inactivation of cortical activity all MGB neurons still
responded to clicks and tones although firing rates of some
neurons dropped by about 50%. The neurons maintained their
response latencies and tuning properties with BF unchanged.
Our finding suggests that AI functions in simple auditory
tasks either by performing computations and/or conveying
information to higher cortical areas. It is likely that there
are alternate pathways to higher centers that are inaccessible
during acute AI inactivation but may be recruited by plastic
reorganization during recovery after ablation.
by: NIH DC 01249, MH 46428
P.G. Musial, J.H. Wittig Jr,
S.K. Talwar, G.L. Gerstein. INACTIVATION OF RAT AUDITORY
CORTEX: EFFECT ON UNIT ACTIVITY IN VENTRAL MEDIAL GENICULATE
Program No. 354.6. 2002 Abstract Viewer/Itinerary
Planner. Washington, DC: Society for Neuroscience, 2002.