<p>The inferior colliculus (IC) represents a pivotal midbrain area involved in processing sensory/emotional facets of auditory stimuli, potentially influencing motor responses. Our prior investigations showed that electric or chemical stimulation of the IC ameliorates haloperidol-induced catalepsy, a manifestation of Parkinsonism in animals. We hypothesized that this amelioration stems from a sensory-motor gating mechanism via IC activation of the mesencephalic locomotor region (MLR). Aiming to investigate this hypothesis, we performed IC optogenetic stimulation and electrophysiological recordings of MLR neuronal activity in anesthetized rats. Additionally, we examined whether optogenetic manipulation of IC could improve motor deficits and affect emotional states in awake rats. Electrophysiological data revealed an excitatory response in MLR neurons following IC optogenetic stimulation, with a longer onset latency in MLR neurons suggesting synaptic modulation from IC to MLR. Behavioral results showed that IC optogenetic stimulation improved haloperidol-induced motor deficits without affecting emotional state or basal locomotor activity.</p>

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Optogenetic stimulation of inferior colliculus neurons elicits mesencephalic locomotor region activity and reverses haloperidol-induced catalepsy in rats

  • José A. Pochapski,
  • Jan Franke,
  • Wolfgang Kruse,
  • Ralf Jacob,
  • Stefan Herlitze,
  • Claudio Da Cunha,
  • Rainer K. W. Schwarting,
  • Liana Melo-Thomas

摘要

The inferior colliculus (IC) represents a pivotal midbrain area involved in processing sensory/emotional facets of auditory stimuli, potentially influencing motor responses. Our prior investigations showed that electric or chemical stimulation of the IC ameliorates haloperidol-induced catalepsy, a manifestation of Parkinsonism in animals. We hypothesized that this amelioration stems from a sensory-motor gating mechanism via IC activation of the mesencephalic locomotor region (MLR). Aiming to investigate this hypothesis, we performed IC optogenetic stimulation and electrophysiological recordings of MLR neuronal activity in anesthetized rats. Additionally, we examined whether optogenetic manipulation of IC could improve motor deficits and affect emotional states in awake rats. Electrophysiological data revealed an excitatory response in MLR neurons following IC optogenetic stimulation, with a longer onset latency in MLR neurons suggesting synaptic modulation from IC to MLR. Behavioral results showed that IC optogenetic stimulation improved haloperidol-induced motor deficits without affecting emotional state or basal locomotor activity.