Differential effects of LSD serotonin and l-tryptophan on visually evoked responses

Strahlendorf, J. R.; Goldstein, Frederick J.; Rossi, G; Malseed, Roger T.

doi:10.1016/0091-3057(82)90012-0

Cited by 10 publications

(2 citation statements)

References 18 publications

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“…Almost the same findings with 5-HTnergic drugs were reported by some investigators. For instance, Strahlendorf et al (9) reported that three components of the VEP in cats were significantly depressed by intraraphe injection of 5-HT. Fleming et al (8) also found that the amplitudes of the P 1 -N 1 and P 3 -N 3 components were significantly reduced by amphetamine.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Selective Serotonin-Reuptake Inhibitor on Visual Evoked Potential in Rats

2004

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Abstract. The present study was undertaken to clarify the effects of selective serotoninreuptake inhibitors (SSRIs) on visual evoked potential (VEP) in rats. To elucidate the mechanism of action of SSRIs, some serotonin (5-HT) agonists were used. SSRIs, fluvoxamine and paroxetine, caused a reduction in the amplitudes of P 1 -N 1 , P 3 -N 3 , and N 3 -P 4 components of VEP. The amplitude of the P 1 -N 1 component was also reduced by the 5-HT 1A agonist 8-OH-DPAT and 5-HT 1B agonist anpirtoline. On the other hand, amplitudes of P 3 -N 3 and N 3 -P 4 components were reduced by anpirtoline and the 5-HT 2 agonist DOI. These results indicate that the reduction in the amplitude of the P 1 -N 1 component of VEP induced by SSRIs may participate in 5-HT 1A and 5-HT 1B receptors, and those of P 3 -N 3 and N 3 -P 4 components induced by SSRIs may be closely related with 5-HT 1B and 5-HT 2 receptors.

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Section: Discussionmentioning

confidence: 99%

The Effects of Selective Serotonin-Reuptake Inhibitor on Visual Evoked Potential in Rats

2004

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“…The effects of LSD-25 have been directly attributed to alterations in the functioning of central monoamine neurotransmitters, especially serotonin (White & Appel, 1982). Serotonergic cell bodies have been detected in the midbrain dorsal raphe nucleus, axons of which inner vate forebrain and temporal lobe areas (Strahlendorf, Goldstein, Rossi, & Malseed, 1982). Reduction of raphe-mediated forebrain and temporal lobe inhibition, via LSD-induced depression of raphe activity, could result in the disinhibition of raphe target neurons in the temporal lobes, resulting in an OBE or other related psychical phenomena that have been electrocortically mapped in the same area.…”

Section: It Is Well Established That the Hippocampus Amygdala And Relatedmentioning

confidence: 99%

Near-death experiences: A neurophysiological explanatory model.

1989

JNDS

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Prior hypotheses as to the etiology of near-death experiences (NDEs) have been limited to psychiatric explanations or brief discussions of endorphins as causative agents. We present a neurophysiological explanation for NDEs based on their similarities with lysergic acid-, ketamine-, and hypercapnia-induced hallucinations. We believe the core NDE is genetically imprinted and triggered by serotonergic mechanisms.Near-death experiences (NDEs) are profound transcendental events experienced on the threshold of death. They have been reported by people who have been seriously injured or ill but recovered (Greyson & Stevenson, 1980), and by people who have had anticipated imminent death in a potentially fatal situation but escaped unharmed (Comer, Madow, & Dixon, 1967). They have been documented as occurring primarily in survivors of cardiac arrests and profound comas, as op posed to seriously ill patients who are treated with mechanical ventila tion, narcotics, and anesthetic agents, but who are not critically ill and at risk of dying (

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