Locus coeruleus-induced inhibition of dorsal cochlear nucleus neurons in comparison with lateral vestibular nucleus neurons

• Published in: Brain research Vol. 194; no. 1; p. 53
• Main Authors: Chikamori, Y, Sasa, M, Fujimoto, S, Takaori, S, Matsuoka, I
• Format: Journal Article
• Language: English
• Published: Netherlands 21-07-1980
• Subjects: Animals; Cats; Cochlear Nerve - physiology; Evoked Potentials - drug effects; Locus Coeruleus - physiology; Neural Inhibition - drug effects; Neurons - physiology; Norepinephrine - pharmacology; Reserpine - pharmacology; Synapses - physiology; Vestibular Nuclei - physiology; Vestibulocochlear Nerve - physiology
• ISSN: 0006-8993
• DOI: 10.1016/0006-8993(80)91318-9

The effects of conditioning stimulation of the locus coeruleus (LC) on the neuron activity of dorsal cochlear nucleus (DCN), which is rich in noradrenergic nerve terminals, were compared with those on the lateral vestibular nucleus (LVN), devoid of such terminals, to determine whether or not noradrenaline is responsible for the LC-induced inhibition. The conditioning stimuli applied to the LC had no effect on either the field potential or the spike generation of mono- and polysynaptic neurons in the LVN elicited by VIIIth cranial nerve stimulation. In contrast, the spike firing of the DCN neurons with VIIIth cranial nerve stimulation was significantly inhibited by LC conditioning stimulation. The inhibition of spike generation was mainly observed in the DCN neurons which fired spikes with a longer latency. The inhibition of DCN neurons by LC conditioning stimulation did not occur in the cats pretreated with reserpine; however, a rapid recovery of the inhibition was produced by intraventricular application of noradrenaline. These results are in good agreement with the histochemical findings and support our previous conclusion that noradrenaline acts as an inhibitory transmitter or modulator on the nuclei where noradrenergic nerve terminals derived from the LC are located. In addition, the vestibular input in the primary relay nucleus is apparently not regulated by noradrenaline originating in the LC.