The serotonin (5-HT) hy
pothesis of schizo
phrenia arose from early studies on interactions between the hallucinogenic drug LSD (d-lysergic acid diethylamide) and 5-HT in
peri
pheral systems. More recent studies have shown that the two major classes of
psychedelic hallucinogens, the indoleamines (e.g., LSD) and
phenethylamines (e.g., mescaline),
produce their central effects through a common action u
pon 5-HT
2 rece
ptors. This review focuses on two brain regions, the locus coeruleus and the cerebral cortex, where the actions of indoleamine and the
phenethylamine hallucinogens have been shown to be mediated by 5-HT
2A rece
ptors; in each case, the hallucinogens (via 5-HT
2A rece
ptors) have been found to enhance glutamatergic transmission. In the
prefrontal cortex, 5-HT
2A-rece
ptors stimulation increases the release of glutamate, as indicated by a marked increase in the frequency of excitatory
postsyna
ptic
potentials/currents (EPSPs/EPSCs) in the a
pical dendritic region of layer V
pyramidal cells; this effect is blocked by inhibitory grou
p II/III metabotro
pic glutamate agonists acting
presyna
ptically and by an AMPA/kainate glutamate antagonist, acting
postsyna
ptically at non-NMDA glutamate rece
ptors. A major alternative drug model of schizo
phrenia,
previously believed to be entirely distinct from that of the
psychedelic hallucinogens, is based on the
psychotomimetic
pro
perties of antagonists of the NMDA subty
pe of glutamate rece
ptor (e.g.,
phencylidine and ketamine). However, recently it has been found that many of the effects of the NMDA antagonists may also (1) involve 5-HT
2A rece
ptors and (2) be mediated through excess activity at non-NMDA (i.e., AMPA/kainate) glutamate rece
ptors. Moreover,
pharmacological mani
pulations of glutamate transmission (e.g., by inhibitory metabotro
pic glutamate agonists)
provide unex
pected
parallels between the actions of these two classes of drugs. Given an emerging recognition of the im
portance of alterations in glutamatergic transmission in the actions of both
psychedelic hallucinogens an NMDA antagonists, this review concludes with of im
plications for the
patho
physiology and thera
py of schizo
phrenia.
p""> Publisher: | p""> Elsevier Science |
p""> Language of Publication: | p""> English |
p""> Item Identifier: | p""> S0165-0173(99)00046-6 |
p""> Publication Type: | p""> Article |
p""> ISSN: | p""> 0165-0173 |
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| Footnotes: - <p>Part of this review was presented at the Seventh International Congress of Biological Psychiatry in Berlin, Germany, 1-7 July 2001.
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