ISSN:
1573-8221
Source:
Springer Online Journal Archives 1860-2000
Topics:
Biology
,
Medicine
Notes:
Summary Acute and chronic experiments on cats and rabbits demonstrate that nicotine administration causes phasic changes in the bioelectric activity of the brain. In isolated brain and in rostral sections, in which a part of the reticular formation of mesencephalon remains connected to the overlying portions, the administration of nicotine provokes EEG activation as in animals with an intact brain. With the section passing from the dorsal side in front of the superior colliculi of corpora quadrigemina, and from the ventril side — directly behind the corpora mammilaria (premesencephalic section), nicotine administration provokes no change in the slow high-amplitude activity characteristic of the section. The data obtained suggest that the activating effect produced by nicotine on the EEG is connected with the excitation of reticular formation of mesencephalon. The impossibility of preventing nicotine activation by preliminary aminazine administration shows that the excitation of adrenoreactive structures does not participate in the mechanism of this activation. On the basis of studying the interaction of nicotine-provoked activation with substances blocking the central m- and n-cholinoreactive systems (benactisin, bensatsin, metamisyl, atropine, tropacine, trasentin, chlorpromasine) it is suggested that the biochemical structures excited in the reticular formation are n-cholinoreactive.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00785867
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