(Q35784627)

English

GAD67 deficiency in parvalbumin interneurons produces deficits in inhibitory transmission and network disinhibition in mouse prefrontal cortex

scientific article published on 24 November 2013

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scholarly article

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Europe PubMed Central

PubMed publication ID

10 August 2017

GAD67 deficiency in parvalbumin interneurons produces deficits in inhibitory transmission and network disinhibition in mouse prefrontal cortex (English)

1 reference

Europe PubMed Central

PubMed publication ID

10 August 2017

1 reference

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author name string

Matthew S Lazarus

1

1 reference

Europe PubMed Central

PubMed publication ID

10 August 2017

Keerthi Krishnan

2

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Europe PubMed Central

PubMed publication ID

10 August 2017

Z Josh Huang

3

1 reference

Europe PubMed Central

PubMed publication ID

10 August 2017

publication date

24 November 2013

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Europe PubMed Central

PubMed publication ID

10 August 2017

Cerebral Cortex

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Europe PubMed Central

PubMed publication ID

10 August 2017

25

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Europe PubMed Central

PubMed publication ID

10 August 2017

5

1 reference

Europe PubMed Central

PubMed publication ID

10 August 2017

1290-1296

1 reference

Europe PubMed Central

PubMed publication ID

10 August 2017

describes a project that uses

1 reference

Europe PubMed Central

11 June 2022

https://www.ebi.ac.uk/europepmc/webservices/rest/PMC4481616/fullTextXML

based on heuristic

inferred from PubMed Central ID database lookup

Activity-dependent regulation of inhibition via GAD67

1 reference

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Homeostatic strengthening of inhibitory synapses is mediated by the accumulation of GABA(A) receptors

1 reference

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1 reference

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Neuregulin 1 regulates pyramidal neuron activity via ErbB4 in parvalbumin-positive interneurons.

1 reference

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Postnatal NMDA receptor ablation in corticolimbic interneurons confers schizophrenia-like phenotypes

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GAD67-mediated GABA synthesis and signaling regulate inhibitory synaptic innervation in the visual cortex

1 reference

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Molecular and cellular mechanisms of altered GAD1/GAD67 expression in schizophrenia and related disorders

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Glutamic acid decarboxylase (GAD)67, but not GAD65, is constitutively expressed during development and transiently overexpressed by activity in the granule cells of the rat.

1 reference

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Gene expression deficits in a subclass of GABA neurons in the prefrontal cortex of subjects with schizophrenia.

1 reference

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Activity deprivation reduces miniature IPSC amplitude by decreasing the number of postsynaptic GABA(A) receptors clustered at neocortical synapses.

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Decrease in reelin and glutamic acid decarboxylase67 (GAD67) expression in schizophrenia and bipolar disorder: a postmortem brain study

1 reference

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Uniqueness and redundancy in GABA production.

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Identification and characterization of the vesicular GABA transporter

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Activity-dependent ubiquitination of GABA(A) receptors regulates their accumulation at synaptic sites.

1 reference

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No association between the glutamate decarboxylase 67 gene (GAD1) and schizophrenia in the Japanese population.

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Activity-dependent regulation of inhibitory synaptic transmission in hippocampal neurons.

1 reference

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Mutational screening and association study of glutamate decarboxylase 1 as a candidate susceptibility gene for bipolar affective disorder and schizophrenia

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1 reference

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GAD1 (2q31.1), which encodes glutamic acid decarboxylase (GAD67), is associated with childhood-onset schizophrenia and cortical gray matter volume loss

1 reference

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Glutamic acid decarboxylase 65 and 67 kDa proteins are reduced in autistic parietal and cerebellar cortices

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1 reference

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Postnatal development of a GABA deficit and disturbance of neural functions in mice lacking GAD65.

1 reference

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1 reference

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1 reference

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1 reference

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1 reference

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1 reference

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1 reference

https://pubmed.ncbi.nlm.nih.gov/24275833

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Altering the concentration of GABA in the synaptic cleft potentiates miniature IPSCs in rat occipital cortex

1 reference

https://pubmed.ncbi.nlm.nih.gov/24275833

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based on heuristic

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1 reference

https://pubmed.ncbi.nlm.nih.gov/24275833

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1 reference

https://pubmed.ncbi.nlm.nih.gov/24275833

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based on heuristic

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Identifiers

10.1093/CERCOR/BHT322

1 reference

Europe PubMed Central

PubMed publication ID

10 August 2017

PMC publication ID

1 reference

Europe PubMed Central

PubMed publication ID

10 August 2017

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

10 August 2017

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