GABA(A) and mu-opioid receptor binding in the globus pallidus and endopeduncular nucleus of animals symptomatic for and recovered from experimental Parkinsonism.

The expression of parkinsonian motor symptoms may be partly attributed to an increase in GABAergic neurotransmission from hyperactive GABA/enkephalinergic striatopallidal efferents. The present study measured pallidal GABA(A) and mu-opioid receptor binding in normal cats and cats symptomatic for and recovered from MPTP-induced parkinsonism. GABA(A) receptor binding was significantly decreased in the globus pallidus (GP) in symptomatic cats and returned to normal levels in spontaneously recovered cats. Mu-opioid receptor binding in the GP was significantly decreased in symptomatic cats and remained significantly decreased in recovered cats. These results suggest that GABA(A) but not mu-opioid receptor binding may correlate with the expression of parkinsonian motor deficits and may reflect increased pallidal GABA and ENK release in parkinsonian animals. Upon recovery from experimental parkinsonism, however, pallidal GABA(A) receptor binding returns to normal levels while mu-opioid receptor binding reflecting enkephalin release remains elevated.