Abstract

Immobile Parkinsonian patients [1] may be able to make quick movements, such as catching a ball or running, when excited by external stimuli. There are several reports of this phenomenon called paradoxical kinesia which refers to a sudden transient ability of akinetic Parkinsonian patients to perform motor tasks they are otherwise unable to perform [2]. The mechanisms underlying this phenomenon are unknown due to a paucity of valid animal models that faithfully reproduce paradoxical kinesia. However, in a previous study [3] we proposed a new animal model to investigate paradoxical kinesia in akinetic rats using species-relevant signals, namely rat ultrasonic vocalizations (USV) which are typical for social situations with positive valence like juvenile play or sexual encounters [4]. Our aim in the present study was to uncover underlying brain mechanisms. We focused on the inferior colliculus (IC) since it not only serves as an acoustic relay station, but can also modulate haloperidol-induced catalepsy [5]. To test the role of the IC in paradoxical kinesia induced by 50-kHz USV, male rats received intracollicular administration of NMDA (30 nmol) or diazepam (10 µg or 20 µg) or its respective controls (i.e. physiological saline or vehicle) 10 min before haloperidol (0.5 mg/kg; ip). Approximately 50 min later, they were exposed to playback of 50-kHz USV, time- and amplitude-matched white noise, background noise or silence, 10 min each with 5 min intervals. The catalepsy test was measured during the bar test, which consists of placing the rat with its forepaws on a horizontal bar. The time until it stepped down with both forepaws was measured (maximum 600s). In animals which had received saline microinjections into the IC, playback of 50-kHz USV significantly reduced haloperidol-induced catalepsy (main effect stimulus: F3,20 = 3.14, P = 0.048), and no such effects were observed in the case of other stimuli. However, the intracollicular administration of NMDA prevented this effect of 50-kHz playback presentation on haloperidol–induced catalepsy (main effect drug treatment: F1,12 = 32.78, P

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