From Medical Xpress:

Presynaptic deletion of the two G-protein-coupled receptor kinase-interacting proteins (GITs), GIT1 and GIT2, at the mouse calyx of Held, leads to a large increase in the action potential (AP)-evoked release, resulting in increase of synaptic strength. Credit: Mónica S. Montesinos and Samuel M. Young Jr./Max Planck Florida Institute for Neuroscience.

Researchers at the Max Planck Florida Institute for Neuroscience have uncovered a critical molecule that regulates synaptic transmission.

Neurons communicate with each other through specialized structures called synapses. The information is transmitted in the form of that contain specific chemical messengers called neurotransmitters The amount and coordinated release of neurotransmitters regulates synaptic strength which is critical to maintain proper communication between neurons. To better understand and address a number of neurological disorders, we need a better understanding of the molecular mechanisms that regulate neuronal communication. A new study has revealed an important function of a class of presynaptic proteins previously implicated in neurological disorders in the regulation of synaptic strength.

Synaptic proteins and neuronal transmission

A synapse consists of a presynaptic terminal of one neuron and a postsynaptic terminal of another. The presynaptic terminal stores vesicles containing neurotransmitters, while the postsynaptic terminal contains neurotransmitter receptors. A dense collection of proteins is present in these terminals, however the functional role of many of these proteins remains unknown.

In particular, the G--coupled receptor kinase-interacting proteins (GITs) exert a critical control in , since deletions of these proteins are lethal or cause sensory deficits and cognitive impairments in…

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