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. 1951 Nov;14(6):461-77.
doi: 10.1152/jn.1951.14.6.461.

Ascending conduction in reticular activating system, with special reference to the diencephalon

T E STARZL, C W TAYLOR, H W MAGOUN

Ascending conduction in reticular activating system, with special reference to the diencephalon

T E STARZL et al. J Neurophysiol. 1951 Nov.
No abstract available

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Figures

Fig. 1
Fig. 1
Transverse sections through hemisphere, showing regions exhibiting desynchronization of electrical activity during high frequency stimulation of bulbar or midbrain reticular formation (light shading), and evoked potentials on single shock reticular stimulation (dark shading). Note similarity of distribution. Abbreviations for Figs. 1, 4, 7 and 8 are as follows: A—amygdala, AC—anterior commissure, AM—anteromedial nuc., AV—anteroventral nuc., BIC—brachium of the inferior colliculus, BP—basis pedunculi, C—caudate nuc., CE—nuc. centralis medialis, CL—claustrum, CL—nuc. centralis lateralis, CM—centre median, F—fornix, GP—globus pallidus, H—habenular nuclei, HVM—hypothalamic ventromedial nuc., LA—nuc. lateralis anterior, LG—lateral geniculate nuc., LP—nuc. lateralis posterior, M—medial nuc., MB—mammillary body, MG—medial geniculate nuc., ML—medial lemniscus, NR—red nuc., OC—optic chiasma, OT—optic tract, P—posterior nuc., PC—posterior commissure, PL—pulvinar, PRE—pretectal region, PT—putamen, RE—nuc. reuniens, S—septum, SC—superior colliculus, SG—suprageniculate nuc., SN—substantia nigra, SU—subthalamic nuc., RT—reticular nuc., VA—nuc. ventralis anterior, VL—nuc. ventralis lateralis, VM—ventromedial nuc., VP—nuc. ventralis posterior, VPL—ventroposterolateral nuc., VPM—ventroposteromedial nuc., ZI—zona incerta.
Fig. 2
Fig. 2
Records of electrical activity of cephalic brain stem structures during single shock (left) and repetitive (right) stimulation of reticular activating system at bulbar (A, C—G) and midbrain (B) levels. Single shock stimuli (arrows) had intensities of 2–5 V., repetitive stimuli (heavy line) had intensities of 2 V. and frequencies of 250/sec. Records were obtained from internal capsule (A), ventromedial thalamic nucleus (B), the same point in subthalamus (C and D) before (C) and after (D) removal of cerebellum, centre median (E), and midbrain tegmentum (F). In (G), records from subthalamus show, from left to right, effect of single shock, 20/sec., 50/sec., and 75/sec. stimuli (5 V.) to bulbar reticular formation. Upper channel, in each strip, is record from homolateral anterior cortex (HA).
Fig. 3
Fig. 3
Records of activity between tips of electrodes placed 3 mm. apart and oriented mediolaterally in deep structures, showing subcortical activation and after-discharge of large fast waves induced by 2 V., 250/sec. stimulation of bulbar reticular formation marked by heavy line). In each case electrodes are at 1, 4, and 7 mm. from midline. Areas include: (A) rostral portion of thalamus, with electrodes from medial to lateral in nuc. reuniens, reticular nuc., and internal capsule; (B) mid-thalamus, with electrodes in ventromedial nuc., ventrolateral nuc., and ventroposterolateral nuc.; (C) rostral midbrain, with electrodes in central gray, midbrain tegmentum and substantia nigra; and (D) caudal midbrain, with electrodes in red nucleus, midbrain tegmentum, and substantia nigra. In designating channels, R 1–4 indicates recording to be between tips of electrodes placed at 1 and 4 mm. from midline; R 4–7 between electrodes at 4 and 7 mm. from midline; and R 1–7 between electrodes at 1 and 7 mm. from midline.
Fig. 4
Fig. 4
Transverse sections through hemisphere with shading indicating regions whose direct stimulation yields generalized cortical activation. More darkly shaded areas are those from which effect was most reliable and had lowest threshold. Note similar distribution to that seen in Fig. 1.
Fig. 5
Fig. 5
A–D: Records showing generalized cortical activation induced by high frequency stimulation of activating system at various levels: (A) bulbar reticular formation, (B) midbrain, (C) ventromedial thalamic nucleus, and (D) internal capsule. E–G: Also illustrated are the more specific effects observed upon direct stimulation of sensory pathways: (E) medial geniculate, with predominant effect in auditory cortex; (F) lateral geniculate, with effect limited to visual cortex; and (G) medial lemniscus in midbrain, with generalized activation of cortex but with fast high amplitude waves appearing in sensory area. Period of stimulation (2 V., 250/sec.) is marked by dark lines. Abbreviations of channels indicate: AUD—auditory, AUD ASSOC—auditory to middle suprasylvian association area, LAT ASSOC—lateral association area, MID ASSOC—middle suprasylvian association area, MOT—motor, SEN—sensory, SEN MOT—sensory to motor, VIS ASSOC—visual to lateral association area, VIS—visual.
Fig. 6
Fig. 6
Records showing alterations in cortical electrical activity evoked by 2–5 V. stimulation of activating system in midbrain or bulb (C). Pickups with bipolar concentric electrodes, with point in deeper layers of cortex or subjacent white matter and barrel on surface. Designation of channels indicate: A SIG—anterior sigmoid or motor, LAT ASSOC—lateral association, MID SUP—middle suprasylvian association, PRO—proreus or frontal association, P SIG—posterior sigmoid or sensory, VIS—visual. In (A) are shown the variable responses recorded from visual and lateral association areas initially (1—left) and after 90 sec. of intermittent stimulation (1—right). Potential changes induced by 25/sec. (2) and 250/sec. (3, 4) stimulation are also shown. Evoked potentials are shown in gyrus proreus (B); anterior sigmoid (C, D) with frequency of 7.5 sec. in D; posterior sigmoid (E); lateral association area (F); and middle suprasylvian association area (G) in which gradual increment of response occurred with continued stimulation.
Fig. 7
Fig. 7
Transverse sections through diencephalon (1–4), showing complete functional destruction of thalamus in preparation from which records A–E were obtained. Channels are designated as follows: AUD—auditory cortex, MOT—motor cortex, SEN—sensory cortex, SEN-MOT—sensory to motor cortex, SUB—subthalamus, VIS-MID ASS— visual to lateral association cortex. Records obtained after a lesion show: A: (upper strip), activation of EEG during 250/sec. stimulation of reticular system, with subsequent sporadic high frequency bursts (middle strip), still continuing 25 sec. later (lower strip); B: wave in motor and other cortical areas evoked by single shock stimulation to midbrain’s tegmentum (left) and generalized arousal upon high frequency stimulation (right); C: similar effect induced by bulbar stimulation; D: potential changes in subthalamus induced by single shock bulbar stimuli; E: seizure induced by midbrain’s stimulation (upper left) to succeeding strips showing its course at 15, 25, 35, 50 and 110 sec. after stimulation.
Fig. 8
Fig. 8
Transverse sections through diencephalon (1–4) from animal in which lesions destroyed that part of internal capsule transmitting extrathalamic corticipetal influences of reticular activating system. Records obtained after the lesion show: (A) spontaneous activity of cortex; (B) potentials evoked in cortical areas by click stimuli, although geniculate bodies were inadvertently injured and no primary auditory potentials could be evoked; (C) cortical potentials induced by 3/sec. stimulation of midbrain reticular substance; (D, E) generalized cortical arousal produced by 2–5 V. stimulation at 250/sec. in bulbar or midbrain reticular formation. Channels are as designated: AUD—auditory, MID ASS—middle suprasylvian association, MOT—motor, SEN—sensory, VIS—visual.
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