M
Mark E. Molliver
Researcher at Johns Hopkins University School of Medicine
Publications - 72
Citations - 11783
Mark E. Molliver is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Cerebral cortex & Neocortex. The author has an hindex of 49, co-authored 72 publications receiving 11567 citations. Previous affiliations of Mark E. Molliver include Johns Hopkins University & National Institute on Drug Abuse.
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D-serine, an endogenous synaptic modulator: localization to astrocytes and glutamate-stimulated release.
TL;DR: D-Serine appears to be the endogenous ligand for the glycine site of NMDA receptors, suggesting a mechanism by which astrocyte-derived D-serine could modulate neurotransmission.
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Methylenedioxyamphetamine (MDA) and methylenedioxymethamphetamine (MDMA) cause selective ablation of serotonergic axon terminals in forebrain: immunocytochemical evidence for neurotoxicity
TL;DR: The results establish that MDA and MDMA produce structural damage to 5-HT axon terminals followed by lasting denervation of the forebrain, and the selective degeneration of 5- HT axons indicates that these drugs may serve as experimental tools to analyze the organization and function of5-HT projections.
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In situ injection of kainic acid: A new method for selectively lesioning neuronal cell bodies while sparing axons of passage
TL;DR: These morphologic studies provide (direct) evidence that in situ injection of kainic acid in brain causes a selective degeneration of neurons with cell bodies in the area of the injection but spares axons that arise from perikarya outside the region but pass through or terminate in the injected area.
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An immunohistochemical study of serotonin neuron development in the rat: Ascending pathways and terminal fields
Hart G.W. Lidov,Mark E. Molliver +1 more
TL;DR: The delay in serotonin innervation of the suprachiasmatic nucleus, striatum, and middle cortical layers long after the axons have reached these structures suggests that the formation of serotonin axon terminals is dependent on maturation of other elements in local neuronal circuitry.
Journal Article
3,4-Methylenedioxymethamphetamine and 3,4-methylenedioxyamphetamine destroy serotonin terminals in rat brain: quantification of neurodegeneration by measurement of [3H]paroxetine-labeled serotonin uptake sites.
TL;DR: It is demonstrated that MDMA and MDA cause long-lasting neurotoxic effects with respect to both the functional and structural integrity of serotonergic neurons in brain and measurement of reductions in the density of 5-HT uptake sites provides a means for quantification of the neurodegenerative effects of MDMA andMDA on presynaptic 5- HT terminals.