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CORTICAL AND RETICULAR EFFECTS UPON EVOKED ACTIVITY OF THALAMIC SOMATOSENSORY RELAY NUCLEUS
Author(s) -
Iwama Kitsuya,
Yamamoto Chosaburo
Publication year - 1963
Publication title -
psychiatry and clinical neurosciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.609
H-Index - 74
eISSN - 1440-1819
pISSN - 1323-1316
DOI - 10.1111/j.1440-1819.1963.tb00682.x
Subject(s) - reticular formation , stimulation , reticular connective tissue , neuroscience , somatosensory system , thalamus , reticular activating system , midbrain reticular formation , thalamic stimulator , thalamic reticular nucleus , somatosensory evoked potential , cortex (anatomy) , chemistry , anatomy , medicine , biology , deep brain stimulation , disease , parkinson's disease
Summary Using cats and dogs, effects of cortical and reticular formation stimulation were examined upon the thalamic evoked potential produced by single shock stimulation of the posterior funiculus. Cortical stimulation was done with a single shock applied to the sensorimotor cortex of one side ipsilateral to the thalamic somatosensory relay nucleus which is to be activated by posterior fimiculus stimulation. The reticular formation was stimulated at the mesencephalic level repetitively with shocks of varying frequencies for about 0.1 second. 1. Cortical stimulation, when made 100–200 msec prior to posterior funiculus stimulation, was followed by an augmentation of the delayed component of the thalamic evoked potential and a suppression of the initial one. 2. The thalamic evoked potential suffered suppression by repetitive stimulation of the reticular formation. Among the initial and delayed components of the thalamic evoked potential, the former was more resistant to the reticular suppression than the latter. The suppression was most marked immediately after the end of reticular stimulation. 3. A small dose of barbiturate, injected intravenously, abolished the suppressing effect of reticular origin with the cortical effect well preserved. 4. An extensive lesion of the reticular core at the intercollicular level facilitated the delayed component of the thalamic evoked potential. Even under this condition the cortical facilitatory action could be elicited.