ArticlePharmacology, biochemistry, and behavior2015
Effects of chronic inhibition of GABA synthesis on attention and impulse control.
Article in Pharmacology, biochemistry, and behavior, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
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- Aberrant glutamatergic systems underlying impulsive behaviors: Insights from clinical and preclinical research.Progress in neuro-psychopharmacology & biological psychiatry · 2024Review
- Biological effects of exposure to 2650 MHz electromagnetic radiation on the behavior, learning, and memory of mice.Brain and behavior · 2023Article
- Electrophysiological resting-state hyperconnectivity and poorer behavioural regulation as predisposing profiles of adolescent binge drinking.Addiction biology · 2022Article
- Translationally relevant mouse model of early life cancer and chemotherapy exposure results in brain and small intestine cytokine responses: A potential link to cognitive deficits.Brain, behavior, and immunity · 2022Article
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- Transcranial Auricular Vagus Nerve Stimulation (taVNS) and Ear-EEG: Potential for Closed-Loop Portable Non-invasive Brain Stimulation.Frontiers in human neuroscience · 2021Article
- Stress, sensitive periods, and substance abuse.Neurobiology of stress · 2019Review
- Impulsive Action and Impulsive Choice Are Differentially Associated With Gene Expression Variations of the GABAFrontiers in behavioral neuroscience · 2019Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundCortical GABA regulates a number of cognitive functions including attention and working memory and is dysregulated in a number of psychiatric conditions. In schizophrenia for example, changes in GABA neurons [reduced expression of glutamic acid decarboxylase (GAD), parvalbumin (PV) and the GABA reuptake transporter (GAT1)] suggest reduced cortical GABA synthesis and release; these changes are hypothesized to cause the cognitive deficits observed in this disorder. The goals of this experiment were to determine whether chronically reducing GAD function within the rat PFC causes attention deficits and alterations in PV and GAT1 expression.
methodsMale Sprague Dawley rats were trained on the 5-choice serial reaction time task (5CSRTT, a task of attention) until they reached criterion performance and then were implanted with a bilateral cannula aimed at the medial PFC. Cannulae were connected to osmotic minipumps that infused the GAD inhibitor l-allylglycine (LAG, 3.2μg/0.5μl/h) for 13days. Following a 5-day recovery from surgery rats were tested on the standard 5CSRTT for 5 consecutive days and then tested on two modifications of the 5CSRTT. Finally, locomotor activity was assessed and the rats sacrificed. Brains were rapidly extracted and flash frozen and analyzed for the expression of GAD67, PV, GAT1 and the obligatory NMDA receptor subunit NR1.
resultsChronic LAG infusions transiently impaired attention, persistently impaired impulse control and increased locomotor activity. Behavioral changes were associated with an upregulation of GAD67, but no change in PV, GAT1 or NR1 expression. SUMMARY: Chronic inhibition of GABA synthesis within the medial PFC, increased impulsive behavior and locomotion, but did not impair attention; results consistent with previous research following acute inhibition of GABA synthesis. Moreover, our data do not support the hypothesis that decreasing GABA synthesis and release is sufficient to cause changes in other GABA-related proteins.
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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.