At the cellular level, learning and memory are represented by changes in the efficacy of the neuronal communication. Many neurological disorders, such as epilepsy, schizophrenia, and Parkinson’s disease may result from subtle disruptions in the regulation of release of neuronal transmitters. Release of transmitters from synaptic terminals is highly dynamic and plastic, and synaptic efficacy can be modified in response to activity at both structural and functional levels. We employ a combination of physiological, genetic, and anatomical approaches to understand how structure and function of neuronal terminals can be regulated by activity.
Chronic pain is a burdensome disorder which affects millions of people in their daily lives. Scientific Research established that pathologic synaptic function and connectivity is the cause for this disorder and many other diseases like epilepsy, stroke, and Alzheimer. We study synaptic function and connectivity to elucidate the physiological and molecular mechanisms that go awry in an attempt to find ways to correct the malfunctions that occur in patients. For this purpose we apply a wide range of modern scientific techniques that include high resolution 3D confocal laser microscopy, genetic approaches, transgenic mouse models, electrophysiology, and electron microscopy
New synapses can be formed in response to intense activity, and impairments in this process are associated with a broad range of neurological disorders including neurodegeneration, mental retardation, and Huntington’s disease. However, the presynaptic mechanisms that govern synaptic restructuring remain obscure. For bringing more light to that problem, we employ a combination of techniques such as confocal microscopy, genetic approach and electrophysiology.