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Elevated synaptophysin I in the prefrontal cortex of human chronic alcoholics
Author(s) -
Henriksson Richard,
Kuzmin Alexander,
Ökvist Anna,
Harper Clive,
Sheedy Donna,
Garrick Therese,
Yakovleva Tatjana,
Bakalkin Georgy
Publication year - 2008
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.20559
Subject(s) - synaptophysin , prefrontal cortex , glutamatergic , glutamate receptor , neuroscience , long term potentiation , synaptic plasticity , synaptic vesicle , neuroplasticity , context (archaeology) , psychology , biology , chemistry , medicine , immunohistochemistry , vesicle , cognition , biochemistry , paleontology , receptor , membrane
Convergent lines of evidence suggest potentiation of glutamatergic synapses after chronic ethanol exposure, and indicate that the presynaptic effect hereof is on modulators of synaptic strength rather than on executors of glutamate release. To address this hypothesis in the context of ethanol dependence in humans, we used semiquantitative immunoblotting to compare the immunoreactivities of synaptophysin I, syntaxin 1A, synaptosome‐associated protein 25, and vesicle‐associated membrane protein in the prefrontal and motor cortices between chronic alcoholics and control subjects. We found a region‐specific elevation in synaptophysin I immunoreactivity in the prefrontal cortex of alcoholics, but detected no significant differences between the groups in the immunoreactivities of the other three proteins. Our findings are consistent with an effect of repeated ethanol exposure on modulators of synaptic strength but not on executors of glutamate release, and suggest a role for synaptophysin I in the enduring neuroplasticity in the prefrontal cortical glutamate circuitry that is associated with ethanol dependence. Synapse 62:829–833, 2008. © 2008 Wiley‐Liss, Inc.