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Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice

Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice

Published on: March 11, 2020

Dysbindin-1 Mutation Alters Prefrontal Cortex Extracellular Glutamate and Dopamine In Vivo.

Karen K Szumlinski^1,2, Michael C Datko¹, Kevin D Lominac¹

¹Department of Psychological and Brain Sciences, University of California Santa Barbara, Santa Barbara, CA 93106, USA.

International Journal of Molecular Sciences

|December 17, 2024

Summary

Schizophrenia risk is linked to the DTNBP1 gene. This study shows DTNBP1 mutations impair glutamate and dopamine release in the prefrontal cortex, potentially explaining cognitive deficits.

Keywords:

NMDA receptors dysbindin-1 extracellular dopamine extracellular glutamate in vivo microdialysis prefrontal cortex

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Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins

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Published on: August 15, 2017

Area of Science:

Neuroscience
Genetics
Psychiatry

Background:

Schizophrenia is linked to DTNBP1 gene variations, potentially causing cognitive impairments.
Cognitive symptoms involve prefrontal cortex (PFC) glutamate and dopamine signaling anomalies.
DTNBP1 mutations in mice cause memory deficits linked to glutamate release and NMDA receptor dysfunction.

Purpose of the Study:

Investigate the impact of DTNBP1 mutations on in vivo glutamate and dopamine release in the PFC.
Examine NMDA receptor-evoked neurotransmitter release in DTNBP1 mutant mice.
Assess basal extracellular neurotransmitter levels in the PFC of mutant mice.

Main Methods:

In vivo microdialysis in the prefrontal cortex of wild-type, heterozygous, and mutant mice.
Stimulation with high K+ and NMDA to evoke neurotransmitter release.
No net-flux microdialysis to measure basal extracellular neurotransmitter content.

Main Results:

High K+ and NMDA failed to evoke dopamine and glutamate release in DTNBP1 mutants.
Heterozygous mice showed blunted K+-evoked dopamine release.
Elevated basal extracellular glutamate and dopamine levels were observed in mutant and heterozygous mice.

Conclusions:

DTNBP1 mutations disrupt evoked dopamine and glutamate release in the PFC.
Provides in vivo evidence for impaired NMDA receptor function in the PFC.
Abnormally elevated basal neurotransmitter levels may contribute to cognitive deficits in schizophrenia.