Changes in γ-aminobutyric acid, μ-opioid and neurotensin receptors in the accumbens-pallidal projection after discrete quinolinic acid lesions in the nucleus accumbens

Abstract

Discrete quinolinic acid lesions in the nucleus accumbens altered [ 3H]muscimol binding to γ-aminobutyric acid receptors, [ 125I]neurotensin binding to neurotensin receptors, [ 125I]Tyr- d-Ala-Gly-NMePhe-Gly-OH binding to μ-opioid receptors, and [ 3H]quinuclidinyl benzilate binding to muscarinic receptors. Within lesions of the lateral accumbens core, [ 3H]muscimol binding increased and [ 125I]Tyr- d-Ala-Gly-NMePhe-Gly-OH, [ 125I]eurotensin and [ 3H]quinuclidinyl benzilate binding decreased. Lesions of the medial nucleus accumbens resulted in decreased [ 125I]Tyr- d-Ala-Gly-NMePhe-Gly-OH and [ 3H]quinuclidinyl benzilate binding while no alterations were observed for [ 3H]muscimol or [ 125I]neurotensin binding. These data support anatomical distinctions between medial and lateral nucleus accumbens. Destruction of intrinsic neurons in the dorsomedial nucleus accumbens core increased [ 3H]muscimol binding in the dorsal rim of the ventral pallidum and the rostral globus pallidus without altering [ 125I]Tyr- d-Ala-Gly-NMePhe-Gly-OH binding. Destruction of neurons in the lateral nucleus accumbens core or medial shell did not alter [ 3H]muscimol binding in the ventral pallidum. The lack of upregulation in γ-aminobutyric acid receptors suggests that the γ-aminobutyric acid-containing projection from the dorsomedial core to the dorsal rim of the ventral pallidum differs from the projection from the lateral accumbens core and medial shell to the more ventral regions of the pallidum. Fluoro-gold retrogade tracer histochemistry confirmed the specific projection from the dorsomedial core to the dorsal ventral pallidum; and from the shell of the nucleus accumbens to more ventral regions of the ventral pallidum.