|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 University of Barcelona, School of Pharmacy
2 Drexel University Coll Med
* To whom correspondence should be addressed. E-mail: mcastro{at}drexelmed.edu.
By the time neural responses driven by vibrissa stimuli reach the barrel cortex, they have undergone significant spatial and temporal transformations within subcortical relays. A major regulator of these transformations is thought to be subcortical GABA-mediated inhibition, but the actual degree of this influence is unknown. We used disinhibition produced by GABA receptor antagonists to unmask the excitatory sensory responses that are normally suppressed by inhibition in the main subcortical sensory relays to barrel cortex; principal trigeminal (Pr5) and primary thalamic (VPM) nuclei. We found that subcortical disinhibition had strong effects within the subcortical relays, particularly, on long-latency receptive fields. However, few of these subcortical effects were reflected in the barrel cortex. The most robust effect of subcortical inhibition on barrel cortex responses is to transiently suppress high frequency sensory stimuli delivered to the center and/or surround receptive field. The transient high frequency adaptation caused by subcortical inhibition recovers after a few stimuli and gives way to a steady-state adaptation that is independent of subcortical inhibition.
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |