Scientists at the Max Planck Florida Institute for Neuroscience have discovered a crucial switch for understanding how cells in the nervous system communicate. The ground-breaking research could aid in the understanding of nervous system function and also help pinpoint what goes wrong in neurological conditions such as Huntington’s disease. The report, titled “Presynaptic Deletion of GIT Proteins Results in Increased Synaptic Strength at a Mammalian Central Synapse,” appeared on Dec. 2, 2015, in the journal Neuron.
In Huntington’s, a hereditary illness, the loss of brain cell connections occur in regions that process movement, called the basal ganglia and cortex, early in the disease. These lost connections inhibit other neurons that process movement, leading to such early symptoms as jerky, involuntary twitching. Understanding how to block the excitability of specific nerve cell connections may aid in the development of treatments. (Currently, Huntington’s has no cure and no effective treatments that can delay the disease.)
The new study identified previously undiscovered proteins that may influence the process of neuronal transmission of information. Cells of the functional nervous system (neurons) communicate with each other via special gaps between cells known as synapses. Neurons release chemicals there, called neurotransmitters, that then are picked up by receptors in other neurons, triggering electrochemical communication.
In the report, Drs. Samuel Young Jr., Mónica S. Montesinos and collaborators describe G-protein-coupled receptor kinase-interacting proteins (GITs) as critical modulators of neuron activity. Using mice as experimental animals, they found that removing GITs (known as GIT1 and GIT2) in neurons acting at the “giving” end of synapses greatly increased the electrochemical activity of the “receiving neuron.” The protein seemed to be able to control the neurotransmitter that was being released via a “squeezing out” process from the cell called exocytosis.
The scientists noted, “Thus, our data uncover distinct roles for GIT1 and GIT2 in regulating neurotransmitter release strength, with GIT1 as a specific regulator of presynaptic release probability.”
This research has identified previously unknown roles for GIT1 and GIT2, making it the first study of its kind. The work could pave the way for more research into how these proteins work, and opens up the possibility that they may be targeted as treatments for neurological diseases characterized by synaptic over-activity, such as Huntington’s disease.
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