Daniel Feldman

Professor of Neurobiology
Department of Molecular and Cell Biology and Helen Wills Neuroscience Institute
University of California, Berkeley
(March 28, 2016)

Sensory Maps and Homeostasis in Whisker Somatosensory Cortex

Aside from being excellent tools for tickling humans, animal whiskers are highly sensitive to the sensory world. Sensory inputs from the whiskers can help an animal build a mental representation of their environment, allow such feats as squeezing through small holes and remembering where to find the yummiest foods. As Dr. Feldman discussed, the neurons of the rodent sensory cortex are arranged in layers of highly organized circuits. His lab examines how these layers interact to maintain homeostasis, or balance, in the face of a changing environment. How do the networks change and maintain their activity level through processes such as learning or sensory deprivation? Dr. Feldman highlighted the role of interneurons in maintaining homeostasis in whisker sensory networks.

How do neural circuits in cerebral cortex encode and process sensory information, and learn and adapt to patterns in the sensory world? My lab studies these questions in the whisker map in rodent somatosensory cortex (S1), with emphasis on layer (L) 2/3, which contains a sparse and highly plastic whisker representation. We recently quantified the topography of the whisker map in L2/3 at cellular resolution using calcium imaging. We found pronounced salt-and-pepper intermixing of neurons tuned to different whiskers, in contrast to the common model of a smooth whisker map with homogeneous local tuning. L2/3 pyramidal cells projecting to different targets differentially sample this salt-and-pepper map, with more somatotopically accurate  information being relayed to S2 (the likely pathway for form perception) than to M1. Some L2/3 neurons are tuned for complex multi-whisker stimuli, but how this is mapped in S1 remains unknown.

We also study circuit mechanisms for use-dependent map plasticity and homeostasis in S1. Cortical plasticity is a dynamic balance of Hebbian mechanisms that alter neural tuning in response to experience,
and homeostatic mechanisms that actively maintain cortical firing rates. Whisker deprivation induces rapid homeostatic plasticity that preserves sensory responsiveness and precedes classical changes in receptive fields and maps. The most rapid homeostasis occurs with one day of deprivation and is mediated by disinhibition of pyramidal cells. This occurs through rapid regulation of parvalbumin (PV) interneuron circuits, including both feedforward and recurrent inhibitory networks in L2/3. We identified several sites of plasticity within L2/3 PV networks that mediate homeostatic disinhibition following sustained whisker deprivation. In ongoing work, we show that the most rapid disinhibition is mediated by reduced intrinsic excitability of PV neurons.

These findings support a growing body of evidence that PV interneurons are a critical nexus for homeostatic plasticity in sensory cortex. This single site of plasticity can control average firing rate in local cortical networks, regulate sensory gain, and gate subsequent Hebbian plasticity for reorganization of the whisker map. We find that feedforward inhibition in L2/3 is strongly impaired in several genetically distinct transgenic mouse models of autism, suggesting that dysregulation of inhibitory homeostasis may be a common factor for this disorder.