Abstract
Mice pretreated with drugs known to depress the firing rate of dopaminergic neurones (gamma-hydroxybutyrate up to 350 mg kg −1, gamma-butyrolactone 750 mg kg −1 or baclofen 20 mg kg −1) exhibit a hyper-responsiveness to all test doses of apomorphine in terms of climbing behaviour (which depends on stimulation of striatal dopamine receptors), as soon as the acute effects of these drugs have vanished (3–6 hr). This increased response is relatively long-lasting (2–3 days) and is prevented by the inhibition of protein synthesis. This hyper-responsiveness to apomorphine shares many similarities with hypersensitivity induced by other treatments interrupting striatal dopaminergic transmission.
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