Insights into brain function and breakdowns

Insights into brain function and breakdowns

Summary: The study identifies the protein synaptotagmin-3 (SYT3) as a key molecule that allows for synaptic transmission. The findings could aid in the development of treatments for various neurological disorders, including ASD and epilepsy.

Source: Oregon Health and Science University

Scientists at Oregon Health & Science University have identified a long-sought gene-encoded protein that enables the brain to communicate signals across gaps between neurons, known as synapses.

The discovery was published today in the journal the nature.

Known as synaptotagmin-3, or SYT3, the protein helps replenish the supply of chemical neurotransmitters that carry signals between neurons.

“When brain cells are active, they release neurotransmitters to communicate with their neighbors,” said senior author Skyler Jackman, PhD, assistant scientist at the OHSU Volum Institute. “If a cell is too active, it can deplete its supply of neurotransmitters, which can cause a breakdown in communication and brain dysfunction.

“It turns out that cells have a boost mode that replenishes their supply of neurotransmitters, but until now, we didn’t know the molecule responsible. We found that SYT3 is directly responsible for that neurotransmitter increase,” he said. “This gives us new insight into how the brain can break down and fail to process information correctly.”

The researchers created “knock-out” mice that lacked the SYT3 gene. They found that those mice lacked a stronger level of synaptic transmission than control mice with the gene.

It shows a brain
Known as synaptotagmin-3, or SYT3, the protein helps replenish the supply of chemical neurotransmitters that carry signals between neurons. Image is in public domain

Notably, mutations in the SYT3 gene have been implicated in human epilepsy and autism spectrum disorders. The research published today suggests the possibility of developing gene therapy or pharmaceutical approaches targeting SYT3, Jackman said.

“Imbalances in neurotransmitter release are the underlying cause of many neurological disorders,” said lead author Dennis Weingarten, PhD, a postdoctoral researcher in the Jackman Lab. In the future, he said, “understanding these molecular switches — like SYT3 — is an important step for us to fight these diseases.”

Jackman’s lab specializes in the study of synaptic transmission. The human brain has hundreds of trillions of synapses. Discovering these specialized structures and molecules with their unique properties is essential for understanding brain function and neurological disorders.

“Synaptic transmission is fundamental to perceiving our surroundings, making decisions, and almost every feature of our internal world,” Jackman said.

Financing: This work was supported by the Whitehall Foundation, the Medical Research Foundation and the National Institute of Health Imaging Core Facility, award P30NS061800.

With this news of neuroscience research, Dr

Author: Eric Robinson
Source: Oregon Health and Science University
Contact: Eric Robinson – Oregon Health & Science University
Image: Image is in public domain

Original Research: Closed access.
Synaptotagmin-3 is required for rapid redistribution of synaptic vesicles“By Skyler Jackman et al. the nature

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Synaptotagmin-3 is required for rapid redistribution of synaptic vesicles

Sustained neuronal activity demands rapid replenishment of synaptic vesicles to maintain reliable synaptic transmission. Refilling of such vesicles is accelerated by submicromolar presynaptic Ca2+ Signaling by an as yet unidentified high-affinity Ca2+ sensor.

Here we identify synaptotagmin-3 (SYT3) as the presynaptic high-affinity Ca2+ sensor, which drives vesicle replenishment and short-term synaptic plasticity. Synapses between Syt3 Knockout mice exhibited increased short-term depression, and recovery from depression was slow and insensitive to presynaptic residual Ca.2+.

During sustained neuronal firing, SYT3 accelerated vesicle replenishment and increased the size of the readily releasable pool. SYT3 mediated short-term facilitation under conditions of low release potential and another high-affinity synaptotagmin, SYT7 (ref.

Biophysical modeling predicts that SYT3 mediates both replenishment and facilitation by shifting loosely docked vesicles to a tightly docked, primed state.

Our results reveal an important role for presynaptic SYT3 in the maintenance of reliable high-frequency synaptic transmission. Furthermore, multiple forms of short-term plasticity may converge upon reversible processes, Ca2+– dependent vesicle docking.

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