Erowid References Database
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Briggs I.
“Excitatory Responses of Neurones in Rat Bulbar Reticular Formation to Bulbar Raphe Stimulation and to Iontophoretically Applied, 5-Hydroxytryptarnine and Their Blockade by LSD 25”.
J.Physiol.. 1977;265(2):327-40.
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Abstract
The effects of electrical stimulation of bulbar raphe nucleus and of iontophoretically applied 5-hydroxytryptamine (5-HT) on the activity of neurones in the bulbar reticular formation were compared. Methods Wistar rats were anesthetized. brains exposed and a stimulating and recording pipette placed in the brain stem. Unit action potentials were recorded extracellularly from neurones in the bulbar reticular formation using 5-barrelled glass micropipettes which permitted recording of iontophoretic administration of LSD tartrate (Sandoz) (0.Z - 1 x 10-3 M). 5-HT (Koch-Light), (0.05-0.1 M), noradrenaline hydrochloride (HA; Sigma), (0.1 M) sodium L-glutamate (Koch-Light) (0.2 M) or acetylcholine chloride (ACh; Sigma) (0.2 M). In 28 rats the stimulating electrodes were in or very near the nucleus raphe magnus, nucleus raphe pallidus or nucleus raphe obscurus and in 26 of these animals long-latency excitatory responses of the neurones in the bulbar reticular formation were seen when stimulation was applied. In 16 other rats the electrodes were outside the raphe nuclei and long-latency excitatory responses were not seen. In rats with the stimulating electrode placed in the raphe nuclei, 48 Of 58 neurones showed similar types of response to stimulation and 5-HT application. In rats with stimulating electrodes outside the raphe nuclei, of 51 41 neurones on which both 5-HT and stimulation effects were studied only 16 showed similar responses to both. The effects of iontophoretically applied LSD were studied on 11 reticular neurones. Raphe stimulation elicited long-latency response from 7. LSD blocked or reduced 5-HT stimulation on all 7 and electrical stimulation in 6. Short-latency excitations to electrical stimulation in 3 neurones were unaffected by LSD but 5-HT excitations were blocked by LSD. The excitatory effects of ACh were unaffected by ASH. Only 1/5 excitations by NA in neurones exhibiting long-latency excitatory responses to raphe stimulation was reduced by LSD. The results provide a physiological basis for the excitatory effects of iontophoretically applied 5-HT in the bulbar reticular formation.
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