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Adolescent maturation of cortical dopamine
1Department of Anatomy & Neurobiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA. podon002@umaryland.edu
Neurotoxicity Research
|February 13, 2010
Summary
Schizophrenia may stem from disrupted dopamine signaling during adolescent brain development. This study reveals abnormal maturation in dopamine control of brain cells, potentially impairing cognitive functions.
Area of Science:
- Neuroscience
- Developmental Neuroscience
- Psychiatry
Background:
- Dopamine critically regulates prefrontal cortex function, with dysregulation implicated in schizophrenia.
- Schizophrenia hypotheses emphasize developmental and genetic factors, yet symptoms emerge during adolescence.
- Key prefrontal cortex circuits and dopamine modulation mature postnatally, extending into adolescence.
Purpose of the Study:
- To review the postnatal development of dopamine's control over GABA interneurons.
- To investigate the role of these interneurons in schizophrenia pathophysiology.
- To examine how dopamine modulation of interneurons changes during adolescence.
Main Methods:
- Review of studies on the postnatal trajectory of dopamine control of GABA interneurons.
- Analysis of dopamine modulation changes in fast-spiking interneurons during adolescence in rats.
- In vivo recordings in adult rats, including a neonatal ventral hippocampal lesion (NVHL) model of schizophrenia.
Main Results:
- Dopamine modulation of fast-spiking interneurons undergoes significant adolescent maturation.
- D2 agonists shift from inhibitory to excitatory effects on interneurons during this period.
- In the NVHL schizophrenia model, this critical maturation of D2 modulation fails, leading to prefrontal cortex disinhibition.
Conclusions:
- Abnormal maturation of dopamine's control over GABA interneurons during adolescence may be a key factor in schizophrenia.
- This developmental disruption results in a disinhibited prefrontal cortex.
- Impaired interneuron maturation could underlie cognitive deficits observed in schizophrenia models and patients.
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