Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 102, Issue 37, Pages 13301-13306Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0506034102
Keywords
amygdala; hippocampus; long-term potentiation; GABA; picrotoxin
Categories
Funding
- NIMH NIH HHS [MH62822] Funding Source: Medline
- NINDS NIH HHS [NS045625, R01 NS044185, R01 NS045625, NS44185] Funding Source: Medline
Ask authors/readers for more resources
The pathology of schizophrenia is characterized by increased hippocampal activity at baseline and during auditory hallucinations. Animal-model studies in which the flow of activity to the hippocampus is increased through decreased amygdalar GABAergic inhibition have shown alterations of hippocampal circuitry similar to schizophrenia, but the functional importance of this phenomenon remains unclear. We provide evidence of decreased hippocampal feed-forward and tonic GABA-mediated inhibition in this animal model, complementing increased hippocampal activity seen in neuroimaging and postmortem studies. We demonstrate that GABA dysfunction increases long-term potentiation through activation of the cholinergic system, offering a new mechanism for pharmacological strategies of this disorder.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available