A new animal model of paradoxical kinesia induced by 50-kHz ultrasonic vocalizations playback in rats: implications of the inferior colliculus

Motor impairments such as bradykinesia (slowness of movement) or akinesia (loss of movement) are among the most troubling symptoms seen in Parkinson’s disease (PD) patients. PD patients exposed to visual or auditory stimuli might be able to exhibit normal motor responses, experiencing a phenomenon n...

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Bibliographic Details
Main Author: Tonelli, Luan
Contributors: Melo-Thomas, Liana (Dr.) (Thesis advisor)
Format: Dissertation
Language:English
Published: Philipps-Universität Marburg 2018
Psychologie
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Online Access:PDF Full Text
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Summary:Motor impairments such as bradykinesia (slowness of movement) or akinesia (loss of movement) are among the most troubling symptoms seen in Parkinson’s disease (PD) patients. PD patients exposed to visual or auditory stimuli might be able to exhibit normal motor responses, experiencing a phenomenon named paradoxical kinesia. Paradoxical kinesia is a sudden transient ability of akinetic patients to perform normal motor tasks. This phenomenon is known to depend on the patient’s emotional state and external stimuli; however, the neural mechanisms underlying it are unknown. Here, a new animal model was developed (Study I) to investigate paradoxical kinesia by “awakening” cataleptic rats through presenting appetitive 50-kHz ultrasonic vocalizations (USV) which are typical for social situations with positive valence, like juvenile play or sexual encounters (“rat laughter”). Rats received systemic haloperidol to induce catalepsy which was assessed by means of the bar test. During that test, 50-kHz USV, 22-kHz USV or acoustic control stimuli were played back and compared to SILENCE. Only the 50-kHz USV was able to induce paradoxical kinesia in cataleptic rats. In addition, the role of the inferior colliculus (IC) was investigated in paradoxical kinesia induced by 50-kHz USV (Study II), since the IC not only serves as an acoustic relay station, but also modulates haloperidol-induced catalepsy. Glutamatergic and GABAergic neurotransmissions were selected, with rats receiving intracollicular NMDA, a glutamatergic agonist, or diazepam, a GABA/benzodiazepine agonist, 10 min before systemic haloperidol. During the catalepsy test rats were exposed to playback of 50-kHz USV and control stimuli. The results show that playback of 50-kHz USV induced paradoxical kinesia in rats which had systemically received haloperidol and vehicle into the IC. This paradoxical kinesia effect of 50-kHz USV playback on haloperidol-induced catalepsy was prevented by intracollicular NMDA administration. Although diazepam microinjected into the IC potentiated haloperidol-induced catalepsy, it did not affect the response to 50-kHz USV playback. Therefore, the NMDA receptor agonist suppressed the effectiveness of 50-kHz USV playback, whereas diazepam did not. These findings suggest that the IC is a key structure involved in paradoxical kinesia, with relevant processes being glutamatergic rather than GABAergic. This animal model thus appears useful for uncovering neural mechanisms of paradoxical kinesia and it might help to identify novel therapeutic targets for PD.
Physical Description:73 pages.
DOI:https://doi.org/10.17192/z2018.0234