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A neural circuit that controls the gain of sensory responses and plasticity in mouse visual cortex

Abstract: The brainís response to sensory input is strikingly modulated by behavioral state. In the primary visual cortex (V1) of the mouse, responses are dramatically enhanced by locomotion (Niell & Stryker, Neuron 2010), a tractable and accessible example of a time-locked change in cortical state. Selectivity is unaltered, so that the change in cortical state is best described as an increase in the gain of visual responses like that produced by focal attention in primates. We have studied the neural circuits that transmit behavioral state to sensory cortex to produce this modulation. Optogenetic activation of the midbrain locomotor center below the threshold for inducing locomotion enhances V1 visual responses, suggesting that ascending connections to the basal forebrain are responsible (Lee et al., Neuron, in press, 2014). In the cortex, calcium imaging of behaving animals revealed that locomotion activates vasoactive intestinal peptide (VIP)-positive neurons in mouse V1 independent of visual stimulation and largely through nicotinic inputs from basal forebrain. Optogenetic activation of VIP neurons increased V1 visual responses in stationary awake mice, artificially mimicking the effect of locomotion, and photolytic damage of VIP neurons abolished the enhancement of V1 responses by locomotion (Fu et al, Cell 2014). These findings establish a cortical circuit for the enhancement of visual response by locomotion and provide a potential common circuit for the modulation of sensory processing by behavioral state. We wondered whether the enhanced activity produced by locomotion might also enhance plasticity in the adult cortex, where the recovery of V1 from early sensory deprivation is slow and incomplete. Indeed, visual stimulation during locomotion dramatically enhances recovery in the mouse (Kaneko & Stryker, eLife 2014). Excitatory neurons regained normal levels of response, while narrow-spiking (inhibitory) neurons remained less active. Visual stimulation or locomotion alone did not enhance recovery. Responses to the particular visual stimuli viewed by the animal during locomotion recovered, while those to another normally effective stimulus did not, suggesting that exercise promotes the recovery only of the neural circuits that are activated concurrent with the exercise. These findings suggest that the global state of cortical activity modulates plasticity. They may provide an avenue for improving recovery from amblyopia in humans.
Speaker: Michael Stryker - University of California San Francisco
Speaker Bio: After working on the mechanisms of cortical plasticity in cats and ferrets, Dr. Strykerís laboratory pioneered the modern use of the mouse visual cortex for the study of cortical function, development and plasticity. He and his students demonstrated rapid activity-dependent cortical plasticity in the mouse in response to monocular visual deprivation during a defined critical period in early life, delineated distinct molecular mechanisms responsible for temporally distinct phases of plasticity and recovery during the critical period, and carried out the first detailed study of visual cortical response properties in mouse V1. Many of the laboratories now working on mouse V1 (e.g., Scanziani, Dan, Adesnik, Carrandini, Janelia group) learned the techniques from visits to his lab, and others learned them from his former students. Stryker and colleagues discovered the mechanisms responsible for the formation of the V1 and superior colliculus azimuth maps and the connections between them. His laboratory made the fundamental discovery of the regulation of V1 cortical state by locomotion and delineated much of the neural circuitry responsible. He has trained graduate students and postdoctoral fellows with great success, 75% of them receiving tenured or tenure-track positions at major research universities or medical schools.
Poster Link: Poster
Presentation: Presentation on 6/27/2014 (PDF)