After unilateral lesion of the medial forebrain bundle (MFB) by 6-OHDA rats exhibit lateralized deficits in spontaneous behavior or apomorphine-induced rotations. We investigated whether such lateralization is attenuated by either deep brain stimulation (DBS) or glutamatergic neurotransmission in the inferior colliculus (IC) of Wistar rats. Intracollicular DBS did not affect spontaneous lateralization but attenuated apomorphine-induced rotations. Spontaneous lateralization disappeared after both glutamatergic antagonist MK-801 or the agonist NMDA microinjected in the IC. Apomorphine-induced rotations were potentiated by MK-801 but were not affected by NMDA intracollicular microinjection. After injecting a bidirectional neural tract tracer into the IC, cell bodies and/or axonal fibers were found in the periaqueductal gray, superior colliculus, substantia nigra, cuneiform nucleus and pedunculo-pontine tegmental nucleus, suggesting the involvement of these structures in the motor improvement after IC manipulation. Importantly, the side of the IC microinjection regarding the lesion (ipsi- or contralateral) is particularly important and this effect may not involve the neostriatum directly.Significance StatementThe inferior colliculus, usually viewed as an auditory structure, when properly manipulated may counteract motor deficits in Parkinsonian rats. Indeed, the present study showed that 30 Hz deep brain stimulation or glutamatergic neural network in the inferior colliculus reduced body asymmetry induced by medial forebrain bundle unilateral 6-OHDA lesion in rats, an animal model of Parkinsonism. Understanding how glutamatergic mechanisms in the inferior colliculus influence motor control, classically attributed to the basal nuclei circuitry, could be useful in the development of new therapeutics to treat Parkinson's disease and other motor disorders.
Keywords: 6-OHDA lesion; Parkinson’s disease; deep brain stimulation; glutamate; inferior colliculus; medial forebrain bundle.
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