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Striatal glutamatergic function: modifications following specific lesions.

P J Roberts, G J McBean, N A Sharif

    Brain Research
    |March 4, 1982
    PubMed
    Summary
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    Investigating striatal lesions revealed glutamate receptor changes. Lesions affecting glutamatergic fibers caused increased glutamate binding, suggesting receptor supersensitivity.

    Area of Science:

    • Neuroscience
    • Neurochemistry
    • Neuropharmacology

    Background:

    • The striatum plays a crucial role in motor control and reward processing.
    • Glutamatergic and dopaminergic pathways are key neurotransmitter systems within the striatum.
    • Understanding the interplay between these systems is vital for comprehending striatal function and dysfunction.

    Purpose of the Study:

    • To investigate the impact of specific striatal lesions on glutamate binding.
    • To elucidate the role of glutamatergic and dopaminergic terminals in glutamate receptor regulation.
    • To examine the concept of presynaptic glutamate receptors on dopamine terminals.

    Main Methods:

    • Induction of specific lesions: hemidecortication, striatal ibotenate injection, and substantia nigra 6-hydroxydopamine (6-OHDA) injection.

    Related Experiment Videos

  • Measurement of specific [3H]glutamate binding to striatal membranes.
  • Assessment of calcium-dependent glutamate release from striatal slices.

    • Main Results:

    • Hemidecortication led to reduced glutamate release and a ~30% increase in striatal glutamate binding, attributed to receptor density.
    • Ibotenate lesions decreased striatal glutamate binding.
    • 6-OHDA lesions also reduced glutamate binding, supporting presynaptic glutamate receptors on dopamine terminals.
    • 6-OHDA lesions induced dopamine receptor supersensitivity on cortico-striatal terminals, enhancing dopamine's inhibition of glutamate release.

    Conclusions:

    • Striatal lesions significantly alter glutamate binding and release dynamics.
    • Evidence supports the existence of presynaptic glutamate receptors on striatal dopamine terminals.
    • Dopamine receptor supersensitivity occurs following 6-OHDA lesions, affecting glutamate release regulation.