Modification of dyskinesias following the intrastriatal injection of prostaglandins in the rodent

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Abstract
1 The abilities of prostaglandin E1 (PGE1), PGE2, PGD2 and PGF2α to antagonize striatal dopamine function were assessed following bilateral and unilateral injections into the striata of the rat and guinea-pig. 2 Three tests were used to assess the effects of the bilateral injections, ability to antagonize dyskinetic biting induced by 2-di-n-propylamino-5, 6-dihydroxytetralin (0.025 mg kg-1 s.c.), ability to antagonize stereotyped behaviour induced by apomorphine (0.5 or 2 mg kg−1 s.c.) and ability to induce catalepsy. Asymmetry/circling behaviour revealed on challenge with apomorphine (0.25 mg kg−1 s.c.) was measured following unilateral injection into the striatum. 3 In the rat, dyskinetic biting induced by 2-di-n-propylamino-5, 6-dihydroxytetralin was antagonized by PGE1 (0.001 − 1 μg) and PGE2 (0.00001 − 1 μg) but not by PGD2 or PGF2α (1 μg). Stereotyped behaviour induced by apomorphine was not antagonized by any of the prostaglandins. A weak catalepsy was induced by PGE1 (1 μg only), PGE2 (0.001 − 1 μg) and PGD2 (0.001 − 1 μg) but not by PGF2α. Asymmetry and circling behaviour was only observed following the unilateral injection into the striatum of PGE1 and PGD2 (0.01 − 1 μg) and challenge with apomorphine. 4 In the guinea-pig the actions of PGE1 and E2 were compared with those of PGF2α. Dyskinetic biting induced by 2-di-n-propylamino-5, 6-dihydroxytetralin was antagonized by bilateral injections into the striatum of PGE2 (0.001 − 1 μg), but not PGE, (0.5 μg) and PGF2α (1 μg) but not PGE, (0.5 μg) and PGF2α (1 μg). Similar injections of PGE1, E2 and F2α all failed to antagonize apomorphine-induced stereotyped behaviour, or to induce catalepsy. PGE1 (0.01-0.5 μg) and PGE2 (0.002 − 1 μg), but not PGF2α, caused asymmetry following unilateral injection into the striatum and peripheral challenge with apomorphine. 5 It is concluded that the major effect in the striatum of the prostaglandins of the E series is to antagonize dyskinetic biting; this action is not shared by other prostaglandins tested, and does not reflect a generalised ability to antagonize striatal dopamine function. It is suggested that the actions of the prostaglandins to modify differentially dopamine-dependent behaviours from the striatum may reflect activity at a site subsequent to the dopamine receptor.

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