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Dopamine D1 autoreceptor function: possible expression in developing rat prefrontal cortex and striatum.

M H Teicher1, A L Gallitano, H A Gelbard

  • 1Department of Psychiatry, Harvard Medical School, McLean Hospital, Belmont, MA 02178.

Brain Research. Developmental Brain Research
|November 19, 1991
PubMed
Summary
This summary is machine-generated.

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Dopamine (DA) synthesis regulation by D1-like receptors emerges in developing rat brains but is lost by adulthood, with D2-like receptors taking over in the striatum. This highlights transient developmental roles for DA autoreceptors.

Area of Science:

  • Neuroscience
  • Neuropharmacology
  • Developmental Biology

Background:

  • Dopamine (DA) autoreceptors modulate DA synthesis and release.
  • Understanding the developmental trajectory of these autoreceptor functions is crucial for comprehending brain maturation.

Purpose of the Study:

  • To investigate the in vivo function of dopamine autoreceptors in modulating DA synthesis during postnatal development.
  • To determine the specific roles of D1-like and D2-like receptors in regulating DA synthesis in developing and adult rats.

Main Methods:

  • Used gamma-butyrolactone (GBL) to block axonal propagation and measured DA synthesis via L-DOPA accumulation.
  • Administered selective D1 (SKF-38393, CY-208-243) and D2/D3 (quinpirole) receptor agonists/antagonists (SCH-23390) in developing and adult rats.

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Main Results:

  • GBL increased L-DOPA accumulation in striatum and prefrontal cortex of developing rats.
  • D1-like receptor agonists inhibited GBL-induced DA synthesis in developing rats but not adults.
  • D2/D3 receptor agonists attenuated DA synthesis in adult striatum but not developing prefrontal cortex.

Conclusions:

  • D1-like autoreceptor function modulating DA synthesis is transiently present in the developing mammalian forebrain.
  • In adults, D2-like receptors appear to mediate these functions in the striatum.
  • DA synthesis modulation via autoreceptors is largely lost in the adult prefrontal cortex.