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The synaptic blocker botulinum toxin A decreases the density and complexity of oligodendrocyte precursor cells in the adult mouse hippocampus
Author(s) -
ChaconDeLaRocha Irene,
Fryatt Gemma L.,
Rivera Andrea D.,
Restani Laura,
Caleo Matteo,
GomezNicola Diego,
Butt Arthur M.
Publication year - 2021
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.24856
Subject(s) - neuroscience , synaptic plasticity , neurotransmission , hippocampus , oligodendrocyte , biology , neurotoxin , neural stem cell , immunolabeling , chemistry , central nervous system , microbiology and biotechnology , endocrinology , receptor , myelin , stem cell , immunohistochemistry , immunology , biochemistry
Oligodendrocyte progenitor cells (OPCs) are responsible for generating oligodendrocytes, the myelinating cells of the CNS. Life‐long myelination is promoted by neuronal activity and is essential for neural network plasticity and learning. OPCs are known to contact synapses and it is proposed that neuronal synaptic activity in turn regulates their behavior. To examine this in the adult, we performed unilateral injection of the synaptic blocker botulinum neurotoxin A (BoNT/A) into the hippocampus of adult mice. We confirm BoNT/A cleaves SNAP‐25 in the CA1 are of the hippocampus, which has been proven to block neurotransmission. Notably, BoNT/A significantly decreased OPC density and caused their shrinkage, as determined by immunolabeling for the OPC marker NG2. Furthermore, BoNT/A resulted in an overall decrease in the number of OPC processes, as well as a decrease in their lengths and branching frequency. These data indicate that synaptic activity is important for maintaining adult OPC numbers and cellular integrity, which is relevant to pathophysiological scenarios characterized by dysregulation of synaptic activity, such as age‐related cognitive decline, Multiple Sclerosis and Alzheimer's disease.