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Dopamine receptor supersensitivity

R M Kostrzewa1

  • 1Department of Pharmacology, Quillen College of Medicine, East Tennessee State University, Johnson City 37614, USA.

Neuroscience and Biobehavioral Reviews
|January 1, 1995
PubMed
Summary
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Neonatal dopamine neuron damage in rats leads to receptor supersensitivity, particularly for D1 and D2 dopamine receptors. This enhanced response can be influenced by serotonin systems and involves receptor proliferation for D2 but not D1.

Area of Science:

  • Neuroscience
  • Neuropharmacology
  • Developmental Neuroscience

Background:

  • Dopamine (DA) receptor supersensitivity is an amplified response to DA agonists.
  • Ontogenetic aspects of DA receptor supersensitivity are crucial for understanding neurodevelopmental adaptations.
  • Serotonin (5-HT) systems interact with DA pathways, potentially modulating receptor sensitivity.

Purpose of the Study:

  • To review and synthesize literature on the ontogenetic aspects of dopamine receptor supersensitivity.
  • To investigate the mechanisms underlying D1 and D2 dopamine receptor supersensitivity in developing rats.
  • To explore the influence of serotonin systems on dopamine receptor sensitization.

Main Methods:

  • Neonatal 6-hydroxydopamine (6-OHDA) lesioning of rat brain dopamine neurons.

Related Experiment Videos

  • Administration of dopamine agonists (D1 and D2) to assess behavioral responses (oral activity, stereotypy, locomotion).
  • Treatment with serotonin neurotoxins (5,7-dihydroxytryptamine) and antagonists (mianserin) to evaluate 5-HT system influence.
  • Analysis of dopamine receptor density (D1 and D2) and receptor-mediated processes (c-fos expression).

    • Main Results:

    • Neonatal 6-OHDA lesions induced overt sensitization to D1 agonists and some D2 agonist effects, plus latent D1 sensitization.
    • Latent D1 sensitization was unmasked by homologous (D1) or heterologous (D2) agonist priming.
    • Serotonin neurotoxins and 5-HT2C antagonism attenuated some D1 agonist-induced behaviors.
    • D2 receptor proliferation accompanied D2 sensitization, contrasting with unchanged D1 receptor numbers.
    • Repeated D2 agonist (quinpirole) treatment in intact rats induced D2 receptor supersensitization, including vertical jumping, antinociception, and yawning (putative D3 sensitization).

    Conclusions:

    • Dopamine receptor supersensitivity in developing rats involves distinct mechanisms for D1 and D2 receptors.
    • Serotonergic systems modulate D1 receptor sensitization, highlighting neurochemical interactions.
    • Adaptive mechanisms in 'in series' neurons with different neurotransmitters likely underlie receptor supersensitivity.