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Cortical modulation of striatal function.

B Scatton, P Worms, K G Lloyd

    Brain Research
    |January 28, 1982
    PubMed
    Summary
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    Bilateral lesions of corticostriatal pathways or frontal cortex in rats prevent haloperidol-induced catalepsy and alter apomorphine stereotypy. This suggests the frontal cortex influences extrapyramidal function antagonistically to dopamine, potentially via glutamatergic and GABAergic pathways.

    Area of Science:

    • Neuroscience
    • Behavioral Neuroscience
    • Neuropharmacology

    Background:

    • The frontal cortex plays a role in motor control and behavior.
    • Striatal function is modulated by dopaminergic and glutamatergic pathways.
    • Understanding corticostriatal interactions is crucial for deciphering extrapyramidal system regulation.

    Purpose of the Study:

    • To investigate the impact of corticostriatal and frontal cortex lesions on behavioral and biochemical aspects of striatal function in rats.
    • To elucidate the role of the frontal cortex in modulating dopamine-mediated behaviors and neurotransmitter levels within the striatum.

    Main Methods:

    • Bilateral section of corticostriatal projections or selective bilateral ablation of the frontal cortex in rats.
    • Assessment of haloperidol-induced catalepsy and apomorphine-induced stereotyped behavior.

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  • Biochemical analysis of neurotransmitter levels (dopamine, acetylcholine, substance P) and uptake (glutamate) in the striatum and substantia nigra.

    • Main Results:

    • Lesions prevented haloperidol-induced catalepsy and reduced striatal glutamate uptake.
    • Lesions enhanced apomorphine-induced stereotyped behavior.
    • Striatal dopamine, acetylcholine, and substance P levels, along with related enzyme activities, remained largely unaffected by the lesions.

    Conclusions:

    • The frontal cortex influences extrapyramidal function through a mechanism antagonistic to dopamine-mediated events.
    • This mechanism does not appear to involve direct changes in striatal dopaminergic or cholinergic neuron activity.
    • Corticostriatal glutamatergic and nigral GABAergic pathways are implicated in this frontal cortex-mediated regulation.