Feature selectivity and interneuronal cooperation in the thalamocortical system.
Action potentials are a universal currency for fast information transfer in the nervous system, yet few studies address how some spikes carry more information than others. We focused on the transformation of sensory representations in the lemniscal (high-fidelity) auditory thalamocortical network. While stimulating with a complex sound, we recorded simultaneously from functionally connected cell pairs in the ventral medial geniculate body and primary auditory cortex. Thalamic action potentials that immediately preceded or potentially caused a cortical spike were more selective than the average thalamic spike for spectrotemporal stimulus features. This net improvement of thalamic signaling indicates that for some thalamic cells, spikes are not propagated through cortex independently but interact with other inputs onto the same target cell. We then developed a method to identify the spectrotemporal nature of these interactions and found that they could be cooperative or antagonistic to the average receptive field of the thalamic cell. The degree of cooperativity with the thalamic cell determined the increase in feature selectivity for potentially causal thalamic spikes. We therefore show how some thalamic spikes carry more receptive field information than average and how other inputs cooperate to constrain the information communicated through a cortical cell.
Miller
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LM
W. M. Keck Center for Integrative Neuroscience and University of California San Francisco/Berkeley Bioengineering Group, San Francisco, California 94143, USA. lmiller@socrates.berkeley.edu
Escabí
M A
MA
Schreiner
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CE
D000161:Acoustic Stimulation; D000200:Action Potentials / Q000502:physiology*; D000818:Animals; D001303:Auditory Cortex / Q000502:physiology*; D001306:Auditory Pathways / Q000502:physiology*; D002415:Cats; D005829:Geniculate Bodies / Q000502:physiology; D007395:Interneurons / Q000502:physiology*; D011930:Reaction Time / Q000502:physiology; D013788:Thalamus / Q000502:physiology*