Information flow in the central nervous system entails a wide variety of synaptic mechanisms encompassing both chemical and electrical synapses, both of which are subject to a great deal of plasticity. Electrical synapses, composed of gap junctions, are key components of neural circuitry throughout the CNS. Nowhere is this more apparent than in the vertebrate retina, where electrical synapses play critical roles in all classes of neurons. These roles include reducing noise at photoreceptor synapses, establishing receptive field sizes of many neurons, coordinating firing of spiking neurons, and establishing oscillations in neural networks. These functions are closely controlled during light adaptation, influencing the sensitivity and resolution of the retina, and accounting for a large part of the network plasticity. The primary focus of work in my lab is on revealing the molecular mechanisms that control network adaptation in the retina. This work includes deciphering the molecular properties of electrical synapses in retinal neurons and identifying the signaling pathways that regulate their function. We use mammalian and zebrafish model systems as well as expression systems to study these mechanisms. Our recent work has revealed complex GPCR and protein kinase/phosphatase signaling pathways that control photoreceptor coupling and AII amacrine cell coupling.
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