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Auditory brainstem volume-conducted responses: origins in the laboratory mouse.

Henry Kr

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Abstract

Volume-conducted, short-latency auditory-evoked potentials were examined in the laboratory mouse with lesions and local recording used to localize their sources. PI corresponds in time with N1 recorded from the round window, while isolation of the eighth cranial nerve from the brainstem results in the loss of all post-PI components. PII latency agrees with that of evoked potentials recorded from the cochlear nucleus. PIII latency corresponds with that of evoked potentials from the vicinity of the contralateral superior olivary nucleus, and lesions of this and closely related contralateral structures abolish PIII from the vertex recordings. PIV is reduced in amplitude by unilateral brainstem lesions between the superior olive and the inferior colliculus. Evoked potentials and lesions localized PV to the vicinity of the lateral regions of the contralateral inferior colliculus. PVI disappeared when areas anterior to the inferior colliculi were lesioned. Although minor species differences may exist, it was concluded that the sources for PI to V in the mouse closely resemble those in the cat, and they agree well with the limited data from the human. This technique may now be applied to studies of the numerous auditory mutants of the laboratory mouse.

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What this paper is about

Volume-conducted, short-latency auditory-evoked potentials were examined in the laboratory mouse with lesions and local recording used to localize their sources. PI corresponds in time with N1 recorded from the round window, while isolation of the eighth cranial nerve from the brainstem results in the loss of all post-PI components. PII latency agrees with that of evoked potentials recorded from the cochlear nucleus. PIII latency corresponds with that of evoked potentials from the vicinity of the contralateral superior olivary nucleus, and lesions of this and closely related contralateral structures abolish PIII from the vertex recordings. PIV is reduced in amplitude by unilateral brainstem lesions between the superior olive and the inferior colliculus. Evoked potentials and lesions localized PV to the vicinity of the lateral regions of the contralateral inferior colliculus. PVI disappeared when areas anterior to the inferior colliculi were lesioned. Although minor species differences may exist, it was concluded that the sources for PI to V in the mouse closely resemble those in the cat, and they agree well with the limited data from the human. This technique may now be applied to studies of the numerous auditory mutants of the laboratory mouse.

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Available abstract

Volume-conducted, short-latency auditory-evoked potentials were examined in the laboratory mouse with lesions and local recording used to localize their sources. PI corresponds in time with N1 recorded from the round window, while isolation of the eighth cranial nerve from the brainstem results in the loss of all post-PI components. PII latency agrees with that of evoked potentials recorded from the cochlear nucleus. PIII latency corresponds with that of evoked potentials from the vicinity of the contralateral superior olivary nucleus, and lesions of this and closely related contralateral structures abolish PIII from the vertex recordings. PIV is reduced in amplitude by unilateral brainstem lesions between the superior olive and the inferior colliculus. Evoked potentials and lesions localized PV to the vicinity of the lateral regions of the contralateral inferior colliculus. PVI disappeared when areas anterior to the inferior colliculi were lesioned. Although minor species differences may exist, it was concluded that the sources for PI to V in the mouse closely resemble those in the cat, and they agree well with the limited data from the human. This technique may now be applied to studies of the numerous auditory mutants of the laboratory mouse.

Key concepts: Inferior colliculus, Brainstem, Superior olivary complex, Inferior Colliculi, Anatomy, Cochlear nucleus, Neuroscience, Midbrain

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