Labyrinthine Input to Reticular Neurons

Labyrinthine Input to Reticular Neurons

642 COMMENTS Labyrinthine Input to Reticular Neurons B. W. PETERSON The Rockefeller University, New York, N . Y., U.S.A. We have recently been inve...

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COMMENTS

Labyrinthine Input to Reticular Neurons B. W. PETERSON The Rockefeller University, New York, N . Y., U.S.A.

We have recently been investigating labyrinthine input to neurons of the medial pontobulbar reticular formation. Experiments have been performed on cerebellectomized cats under chloralose-urethane anesthesia. We activate the labyrinth and VllI nerve by applying shocks to a pair of electrodes implanted in the scala vestibuli. Shock intensity is adjusted to produce large field potentials in the vestibular nuclei but no input to facial or cochlear nuclei. As illustrated in Fig. 1 such stimulation can produce excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs) with latencies as short

EPSP 'I

MSEC

I PSP

MSEC

Fig. 1. Synaptic potentials evoked in reticular neurons by stimulation of labyrinth. Pairs of oscilloscope traces at left are examples of the short latency EPSPs and IPSPs recorded intracellularly in reticular neurons following labyrinthine stimulus. Upper trace in each pair contains several superimposed intracellular responses, lower trace shows extracellular potential recorded nearby. Histograms at right show number of EPSPs and IPSPs recorded at various latencies following stimulation of ipsilateral labyrinth.

COMMENTS

643

as 1 .O msec. Since vestibular neurons fire as early as 0.7 msec alter labyrinthine stimulation, the early reticular responses are probably disynaptic. Short latency (1.0 to 2.5 msec, see Fig. 1) EPSPs have been observed in 45 % of the reticular neurons studied, short latency (1.3-2.5 msec) IPSPs in 12%. Another 21 ”/, exhibited EPSPs or IPSPs of longer latency and 22% did not respond. In experiments in which we identified reticulospinal neurons by stimulating the spinal cord we have observed short latency EPSPs and IPSPs in neurons projecting to both cervico-thoracic and lumbo-sacral levels. With extracellular recording only 8 % of these cells fired at latencies ranging from 1.8 to 3.0 msec while another 27 % fired at longer latencies. By contrast we have found that 90 % of reticulospinal neurons fire i n response to stimulation of cerebral cortex, 72% in response to stimulation of optic tectum and 48 % in response to cutaneous stimulation. Thus, although reticulospinal neurons receive both short and long latency labyrinthine input, this input is less likely to evoke firing than are inputs from other sources.

Vestibular Influences on the Lateral Geniculate Nucleus 0 .POMPEIANO

Institute of Physiology II, University of Pisa, Pisa, Italy

The demonstration that vestibular and visual impulses converge on the cat’s visual cortex is well established. The possibility, however, that some integration of vestibular and visual impulses occurs at the level of the lateral geniculate nucleus (LGN) should also be considered. The demonstration that vestibular volleys impinge upon the LGN has been given in unrestrained, unanaesthetized cats during the rapid eye movements (REM) phase of desynchronized sleep (Pompeiano and Morrison, 1966; Morrison and Pompeiano 1966; cf. also Ghelarducci and Pompeiano, 1971). In these experiments the integrated activity of the all-or-none events in the LGN has been recorded during desynchronized sleep, before and after bilateral electrolytic lesion of the medial and descending vestibular nuclei. Two kinds of geniculate activity have been differentiated with this technique (Fig. 4 in Pompeiano, 1972). The first type of activity is represented by short-lasting rhythmic enhancements, referred to as type-I LGN waves, which may be related only with single ocular jerks. The second type of geniculate activity is characterized by phasic increases, 1.5 to 2.0 times larger in amplitude and 2 to 6 times longer in duration than those described above. Only these waves, designated as type-I1 LGN waves, are strictly related in time with the Iarge bursts of REM. Following a bilateral lesion of the vestibular nuclei the type I1 lateral geniculate waves disappear and the related bursts of REM are abolished. However, the rhythmic References pp. 644-645