Long-term effects of amygdala GABA receptor blockade on specific subpopulations of hippocampal interneurons
Abstract
Growing evidence indicates that the amygdala modulates hippocampal functions. To test the hypothesis that this modulation may involve long-lasting effects on interneuronal networks in the hippocampus, changes in the expression of neurochemical markers specific for different interneuronal subpopulations were assessed in adult rats 96 h following acute infusion of low doses of the GABAA receptor antagonist picrotoxin into the amygdala. The numerical density (Nd) of somata showing immunoreactivity (IR) for parvalbumin (PVB) was decreased in dentate gyrus (DG) and the CA4-2 region, while that of calretinin (CR)-IR was decreased in DG and CA2. The Nd of calbindin D28k (CB)-IR somata was decreased in CA3-2. The densities of axon terminals arising from PVB-IR and cholecystokinin (CCK)-IR basket neurons were also altered, with those of CCK-IR terminals increased across all sectors, while PVB-IR terminals were decreased only in the CA region. Increases in CCK-IR terminals were paralleled by increases of terminals with IR for the 65-kD isoform of glutamate decarboxylase (GAD65). Mixed-effects statistical models, adapted specifically for these analyses, indicated that perturbations of amygdalar inputs to the hippocampus significantly alter the drive that hippocampal PVB-, CR-, and CB-IR neurons within the dentate gyrus/CA4 region exercise on CCK-IR terminals within the same region as well as in CA3-1. These results suggest that amygdalar modulation of specific neuronal subpopulations may induce lasting and far-reaching changes in the hippocampus during normal functioning, as well as in diseases involving a disruption of amygdalar activity. In particular, changes in specific interneuronal markers within selective hippocampal sectors detected in the present results are strikingly similar to those reported in this region in schizophrenia. These similarities suggest that, in this disease, a disruption of GABAergic transmission within the amygdala may play a significant role in the induction of abnormalities in the hippocampus.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In animal models, increased activity from the amygdala results in decreased GABA neurons in sector CA2/3 of the hippocampus, potentially contributing to hippocampal abnormalities in schizophrenia.
“In animal models, increased activity from the amygdala has been shown to result in decreased GABA neurons in sector CA2/3 of the hippocampus, thus potentially contributing to hippocampal abnormalities in this region in SZ (Benes and Berretta, 2000, 2001; Berretta et al., 2004; Heckers and Benes, 2005; Konradi et al., 2011; Wang et al., 2011).”
From Losing the sugar coating: Potential impact of perineuronal net abnormalities on interneurons in schizophrenia (2015) · cites this paper as Berretta et al., 2004
The citation lists haven’t been fetched yet
References 94 · Cited by 61
- Authors
- Berretta, S., Lange, N., Bhattacharyya, S., Sebro, R., Garces, J., & Benes, F. M.
- Affiliations
- Harvard University (US)
- McLean Hospital (US)
- Corresponding author
- Benes, Francine M.
- Venue
- Hippocampus
- Publisher
- Wiley
- Published
- 2004-01
- Volume
- 14
- Issue
- 7
- Pages
- 876-894
- ISSN
- 1050-9631 (ISSN-L)
- 1098-1063
- OpenAlex
- W1993259058
- Cited by
- 61
- References
- 94
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 1 · 2022: 3 · 2020: 2 · 2019: 2 · 2018: 3 · 2017: 1 · 2016: 4 · 2015: 3 · 2014: 1 · 2013: 4 · 2012: 4
- FWCI
- 2.35
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Hippocampus (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Mental Health (P50MH060450, MH-60450, MH-42261, MH00423)
- National Institute of Neurological Disorders and Stroke (NS 37483, R01NS037483)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
- Keywords
- amygdala, GABAA receptor, picrotoxin, hippocampal interneurons, parvalbumin, calretinin, calbindin-D28k, cholecystokinin, GAD65, dentate gyrus, schizophrenia, GABAergic neurotransmission
- MeSH terms
- Algorithms, Amygdala, Animals, Cell Count, Cholecystokinin, Glutamate Decarboxylase, Hippocampus, Immunohistochemistry, Interneurons, Male, Parvalbumins, Phenotype, Picrotoxin, Linear Models, Rats, Sprague-Dawley, Presynaptic Terminals, GABA Antagonists, Dentate Gyrus, Rats, S100 Calcium Binding Protein G, Calbindin 2
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
