Signaling and synaptic plasticity
The plasticity of neuronal signaling is crucial for mechanisms of learning and memory, and for the ability of animals and humans to adapt to changes in their environment. Neurotransmitter receptors in synapses are dynamically modulated and actively redistributed following nerve stimulation, strengthening or weakening synaptic connections. Neurotransmitters and neuromodulators activate cellular kinase pathways that change synaptic strength, nerve conduction properties and gene transcription profiles. Other signaling pathways mobilize intracellular calcium ions and lipid mediators that have profound effects on neuronal function. Pathological changes in cellular signaling pathways and synaptic plasticity is at the basis of many neurological conditions including depression, Parkinson’s disease, chronic pain and addiction. Faculty in the Department uses physiological, biochemical and behavioral approaches to investigate mechanisms of synaptic plasticity and signaling pathways in the brain and in peripheral nerves.
Signaling and Synaptic Plasticity Image Gallery

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Rat cerebellar slice [12 days PN] . Polyclonal antibody for type I InsP3 receptor, Llano and Ehrlich
Distribution of InsP3R type 1 and CGB in hippocamal slices showing that the distribution of the InsP3R type 1 is concentrated in CA1 when compared to CA3 (top panels) whereas the distribution of CGB is the opposite: high in CA3, low in CA1 (bottom panels). A similar pattern is seen in acute slides (left panels) and in slices maintained in culture for 10-15 days (right panels Excerpt from (Nicolay et al., 2007).
Calcium dependence of the type I InsP3 receptor. Bezprozvanny et al., Nature 351: 751‑754 , 1991
Physiological acoustic stimulation reduces the phosphorylation state of the Kv3.1 potassium channel in auditory brainstem neurons. Images show the levels of immunostaining for Kv3.1 specifically phosphorylated at serine 503 in two areas of the brainstem in an animal exposed to sound to one ear only. The nuclei at the top right and bottom left were stimulated by the sensory input and have lower levels of phosphorylated channels (from Song et al., Nature Neurosci., 8: 1335-1342, 2005)

