(Q24815748)

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Prenatal lead exposure and schizophrenia: a plausible neurobiologic connection

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Prenatal lead exposure and schizophrenia: a plausible neurobiologic connection (English)

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Tomás R Guilarte

1

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language of work or name

English

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publication date

September 2004

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published in

Environmental Health Perspectives

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volume

112

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issue

13

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page(s)

A724

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cites work

Prenatal lead exposure, delta-aminolevulinic acid, and schizophrenia

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PubMed Central

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7 April 2017

The NMDA receptor glycine modulatory site: a therapeutic target for improving cognition and reducing negative symptoms in schizophrenia

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28 September 2017

NMDA receptor function, neuroplasticity, and the pathophysiology of schizophrenia

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28 September 2017

Converging Evidence of NMDA Receptor Hypofunction in the Pathophysiology of Schizophrenia

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28 September 2017

Molecular aspects of glutamate dysregulation: implications for schizophrenia and its treatment

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28 September 2017

Glutamatergic mechanisms in schizophrenia

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28 September 2017

Molecular changes in glutamatergic synapses induced by Pb2+: association with deficits of LTP and spatial learning

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28 September 2017

Schizophrenia: genes and environment

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PubMed Central

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28 September 2017

Divalent cations modulate N-methyl-D-aspartate receptor function at the glycine site.

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retrieved

31 May 2018

Identifiers

DOI

10.1289/EHP.112-A724A

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PMC publication ID

1247541

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PubMed publication ID

15345353

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ResearchGate publication ID

8368558

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(Q24815748)

Prenatal lead exposure and schizophrenia: a plausible neurobiologic connection

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