Morphine versus haloperidol catalepsy in the rat: an electromyographic analysis of postural support mechanisms.

Electromyographic recordings from antagonistic flexor and extensor muscles in the forelegs (biceps and triceps) and hind legs (tibialis and gastrocnemius-soleus) of freely moving rats demonstrated that haloperidol (5 and 10 mg/kg, i.p.) and morphine (20 and 40 mg/kg, i.p.) produced contrasting patterns of rigidity. Haloperidol catalepsy was characterized by increases in frequency, intensity, and duration of simultaneous tonic cocontractions in antagonistic flexor and extensor muscles of the limbs. Such synergistic rigidity suggested the release of an adaptive mechanism involved in static support and the maintenance of stable static equilibrium (the positive supporting reaction of Schoen and Magnus), at the expense of locomotor mechanisms. In contrast, morphine produced antagonistic/reciprocal rigidity, which was insensitive to challenges to static equilibrium, and was compatible with locomotion. Contrary to the haloperidol-induced limb postures, which were enhanced supporting reactions, those induced by morphine were "frozen" phases of the step cycle. Haloperidol-induced synergistic rigidity and morphine-induced antagonistic/reciprocal rigidity are discussed as manifestations of contrasting movement subsystems underlying these functionally opposite immobility states. In addition, we present hypotheses concerning supraspinal and spinal mechanisms underlying cataleptic rigidity states, and their relevance as models of parkinsonian rigidity and akinesia.