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Neurochemical transmission, the conduction of electrical impulses between neurons mediated by neurotransmitters, plays a vital role in various physiological processes. Autonomic drugs exert their effects by modulating neurotransmission within the autonomic nervous system. For instance, drugs such as hemicholinium block the precursor uptake necessary for synthesizing acetylcholine, an essential autonomic neurotransmitter. Following synthesis, neurotransmitters are stored in vesicles. Metyrosine...
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Related Experiment Video

Updated: Nov 1, 2025

An Optical Assay for Synaptic Vesicle Recycling in Cultured Neurons Overexpressing Presynaptic Proteins
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BACE1 controls synaptic function through modulating release of synaptic vesicles.

Brati Das1, Neeraj Singh1, Annie Y Yao1

  • 1Department of Neuroscience, UConn Health, Farmington, CT, USA.

Molecular Psychiatry
|June 23, 2021
PubMed
Summary
This summary is machine-generated.

Beta-secretase 1 (BACE1) inhibitors reduce amyloid plaques in Alzheimer's disease (AD) but impair synaptic function. Combining BACE1 inhibitors with metabotropic glutamate receptor 1 (mGluR1) positive allosteric modulators (PAMs) may improve cognitive function in AD patients.

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Molecular Biology

Background:

  • Beta-secretase 1 (BACE1) initiates amyloid-beta peptide (Aβ) production, linked to Alzheimer's disease (AD) cognitive decline.
  • BACE1 inhibitors reduce Aβ but often fail to improve cognition due to BACE1's role in synaptic function.

Purpose of the Study:

  • To investigate the synaptic role of BACE1 and explore therapeutic strategies to counteract BACE1 inhibitor-induced deficits.
  • To evaluate the efficacy of targeting metabotropic glutamate receptor 1 (mGluR1) positive allosteric modulators (PAMs) to restore synaptic function in AD models.

Main Methods:

  • Utilized BACE1-null mice and BACE1 inhibitor treatments (Verubecestat, Lanabecestat).
  • Assessed synaptic vesicle release, hippocampal long-term potentiation (LTP), and learning behaviors.
  • Administered mGluR1 PAMs to BACE1-deficient or inhibited mice.

Main Results:

  • BACE1 deficiency or inhibition reduced synaptic vesicle docking and impaired hippocampal LTP and learning.
  • mGluR1 levels were decreased in BACE1-null mice.
  • mGluR1 PAM treatment significantly improved LTP and cognitive behaviors in BACE1-deficient or inhibited mice, mitigating synaptic deficits.

Conclusions:

  • BACE1 is crucial for optimal synaptic vesicle release and function.
  • Targeting mGluR1 with PAMs can counteract synaptic deficits caused by BACE1 inhibition.
  • A combination therapy of BACE1 inhibitors and mGluR1 PAMs shows promise for treating Alzheimer's disease by addressing both amyloid pathology and synaptic dysfunction.