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1 Volen Center for Complex Systems, Brandeis University, Waltham,, MA, USA
2 Instituto de Neurociencias, Universidad Miguel Hernandez-CSIC, San Juan de Alicante, Spain
3 Department of Neurobiology, Yale University School of Medicine, New Haven, CT, USA
* To whom correspondence should be addressed. E-mail: xjwang{at}brandeis.edu.
Limiting redundancy in the real-world sensory inputs is of obvious benfit for effcient neural coding, but little is known about how this may be accomplished by biophysical neural mechanisms. One possible cellular mechanism is through adaptation to relatively constant inputs. Recent investigations in primary visual (V1) cortical neurons have demonstrated that adaptation to prolonged changes in stimulus contrast is mediated in part through intrinsic ionic currents, a Ca2+-activated K+ current (IKCa) and especially a Na+-activated K+ current (IKNa). The present study was designed to test the hypothesis that the activation of adaptation ionic currents may provide a cellular mechanism for temporal decorrelation in V1. A conductance-based neuron model was simulated, which included an IKCa and an IKNa. We show that the model neuron reproduces the adaptive behavior of V1 neurons in response to high contrast inputs. When the stimulus is stochastic with 1/f2 or 1/f-type temporal correlations, these autocorrelations are greatly reduced in the output spike train of the model neuron. The IKCa is effective at reducing positive temporal correlations at approximately 100 msec timescale, while a slower adaptation mediated by IKNa is effective in reducing temporal correlations over the range of 1-20 sec. Intracellular injection of stochastic currents into layer 2/3 and 4 (pyramidal and stellate) neurons in ferret primary visual cortical slices revealed neuronal responses that exhibited temporal decorrelation in similarity with the model. Enhancing the slow afterhyperpolarization resulted in a strengthening of the decorrelation effect. These results demonstrate that intrinsic membrane properties of neocortical neurons provide a mechanism for decorrelation of sensory inputs.
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