Evidence map›Paper›PMID 25378161›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

Parvalbumin and GAD65 interneuron inhibition in the ventral hippocampus induces distinct behavioral deficits relevant to schizophrenia.

Robin Nguyen, Mark D Morrissey, Vivek Mahadevan, Janine D Cajanding, Melanie A Woodin, John S Yeomans, Kaori Takehara-Nishiuchi, Jun Chul Kim

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.3field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

55 citing papers in PubMed, 97 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Terminal nucleotidyltransferaseRNA (New York, N.Y.) · 2025
    Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Robin NguyenDepartment of Psychology and.
Mark D MorrisseyDepartment of Psychology and.
Vivek MahadevanDepartment of Cell & Systems Biology, University of Toronto, Toronto, Ontario M5S 3G5, Canada.ORCID http://orcid.org/0000-0002-0805-827X
Janine D CajandingDepartment of Cell & Systems Biology, University of Toronto, Toronto, Ontario M5S 3G5, Canada.
Melanie A WoodinDepartment of Cell & Systems Biology, University of Toronto, Toronto, Ontario M5S 3G5, Canada.ORCID http://orcid.org/0000-0003-2984-8630
John S YeomansDepartment of Psychology and Department of Cell & Systems Biology, University of Toronto, Toronto, Ontario M5S 3G5, Canada.
Kaori Takehara-NishiuchiDepartment of Psychology and Department of Cell & Systems Biology, University of Toronto, Toronto, Ontario M5S 3G5, Canada.
Jun Chul KimDepartment of Psychology and Department of Cell & Systems Biology, University of Toronto, Toronto, Ontario M5S 3G5, Canada kim@psych.utoronto.ca.
University of Toronto · CA

Funding

Canadian Institutes of Health Research MOP 496401
6 · The paper itself

Abstract

Hyperactivity within the ventral hippocampus (vHPC) has been linked to both psychosis in humans and behavioral deficits in animal models of schizophrenia. A local decrease in GABA-mediated inhibition, particularly involving parvalbumin (PV)-expressing GABA neurons, has been proposed as a key mechanism underlying this hyperactive state. However, direct evidence is lacking for a causal role of vHPC GABA neurons in behaviors associated with schizophrenia. Here, we probed the behavioral function of two different but overlapping populations of vHPC GABA neurons that express either PV or GAD65 by selectively inhibiting these neurons with the pharmacogenetic neuromodulator hM4D. We show that acute inhibition of vHPC GABA neurons in adult mice results in behavioral changes relevant to schizophrenia. Inhibiting either PV or GAD65 neurons produced distinct behavioral deficits. Inhibition of PV neurons, affecting ∼80% of the PV neuron population, robustly impaired prepulse inhibition of the acoustic startle reflex (PPI), startle reactivity, and spontaneous alternation, but did not affect locomotor activity. In contrast, inhibiting a heterogeneous population of GAD65 neurons, affecting ∼40% of PV neurons and 65% of cholecystokinin neurons, increased spontaneous and amphetamine-induced locomotor activity and reduced spontaneous alternation, but did not alter PPI. Inhibition of PV or GAD65 neurons also produced distinct changes in network oscillatory activity in the vHPC in vivo. Together, these findings establish a causal role for vHPC GABA neurons in controlling behaviors relevant to schizophrenia and suggest a functional dissociation between the GABAergic mechanisms involved in hippocampal modulation of sensorimotor processes.

Indexed as

Maze LearningNeural InhibitionReflex, StartleAction PotentialsAnimalsClozapineGABAergic NeuronsGlutamate DecarboxylaseHippocampusInterneuronsLocomotionMiceParvalbuminsReceptor, Muscarinic M4SchizophreniaSynaptic PotentialsClozapineclozapine N-oxideGlutamate Decarboxylaseglutamate decarboxylase 2ParvalbuminsReceptor, Muscarinic M4DREADDGABAparvalbuminschizophreniaventral hippocampus

Identifiers

PMID25378161
PMCPMC4220027
OpenAlexW2123250120

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.