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Strahlendorf JCR. 
“Mechanism of Lysergic Acid Diethylamide Influence Upon Optically Evoked Potentials”. 
Dissertation Abstr.Intern.B. 1980;40(12, Part 1):5631.
The effects of LSD and 5-HT in the ventrolateral geniculate nucleus (LGN) and the dorsal raphe nucleus on visual evoked potentials (VEP). Amplitude changes in averaged cortical(CVEP) and thalamic VEP (TVEP) were employed to monitor neurophyeiological events modified by systemic andmicroinjected LSD in immobilized, artificially respired cats. Preliminary studies revealed that i.v. LSD elicited an increase in the amplitude of primary components of the VEP recorded from the occipital cortex. LSD augmentation may be representative of synaptic facilitation, suggesting increased reactivity of the visual pathway to afferent stimuli. Intrageniculate carbachol and ACh depressed all components of the CVEP, whereas dopamine in low doses enhanced and in higher doses depressed the CVEP. Intrageniculate serotonin, a putative inhibitory transmitter in LGN, decreased each component of the CVEP and TVEP, suggesting both a net decrease inthalamocortical transmission and attenuation of Intrageniculate responses to light stimuli. Intrageniculate LSD decreased both cortical and local LGN evoked responses in low doses, whereas higher doses enhanced both potentials. LSD-induced attenuations of CVEP and aubcortical VEP suggest this agent may act as an agonist at low doses on an inhibitory serotonergic system. Intrageniculate cinanserin reduced the inhibitory influence of Intrageniculate 5-HT and LSD on CVEP, suggesting that LGN contains receptors responsive to both 5-HT and LSD. Cinanserin antagonism of 5-HT was surmountable in that higher doses of 5-HT reinstated the initial depressant response. However, higher doses of LSD were incapable of reversing cinanserin blockade, suggesting LSD also be a partial agonist. Intraraphe LSD increased CVEP, whereas intraraphe serotonin attenuated the responses. A depressant effect of LSD on the raphe nucleus, an area which tonically inhibits forebrain structures via 5-HT release, would effect disinhibition reaulting in increased LGN to cortex transmission, evidenced by increased CVEP. Aninhibitory influence on raphe neurons could explain the hallucinogenic properties of LSD, namely, perceptual disturbances resulting from depression of activity in a system normally inhibiting VEP and other sensory impute. In contrast, intraraphe serotonin may increase the tonic inhibitory influence of raphe on LGN, thus decreasing LGN neuronal reaponsiveneasto visual afferent inputs. The finding that intraraphe serotonin inhibited visual cortical potentials aligned with findings that systemic tryptophan, a serotonin precursor, also depressed the cortical reaponse. Intraraphe cinanserin diminished or slightly reversed the effects of microinjected serotonin, did not aignificanbly affect the responses to i.v. tryptophan, and completely reversed LSD elicited enhancements. The findings suggest that the dorsal raphe nucleus is an important site of action of LSD.
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