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Titolo:
DOI-induced activation of the cortex: Dependence on 5-HT2A heteroceptors on thalamocortical glutamatergic neurons
Autore:
Scruggs, JL; Patel, S; Bubser, M; Deutch, AY;
Indirizzi:
Vanderbilt Univ, Sch Med, Ctr Mol Neurosci, Nashville, TN 37212 USA Vanderbilt Univ Nashville TN USA 37212 Neurosci, Nashville, TN 37212 USA Vanderbilt Univ, Sch Med, Dept Psychiat, Nashville, TN 37212 USA Vanderbilt Univ Nashville TN USA 37212 Psychiat, Nashville, TN 37212 USA Vanderbilt Univ, Sch Med, Dept Pharmacol, Nashville, TN 37212 USA Vanderbilt Univ Nashville TN USA 37212 Pharmacol, Nashville, TN 37212 USA
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 23, volume: 20, anno: 2000,
pagine: 8846 - 8852
SICI:
0270-6474(200012)20:23<8846:DAOTCD>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
V PYRAMIDAL CELLS; DISCRIMINATIVE STIMULUS PROPERTIES; EXCITATORY POSTSYNAPTIC CURRENTS; ATYPICAL ANTIPSYCHOTIC-DRUGS; CENTRAL-NERVOUS-SYSTEM; BARREL FIELD CORTEX; C-FOS EXPRESSION; HALLUCINOGENIC DRUGS; PREFRONTAL CORTEX; SEROTONIN 5-HT2A;
Keywords:
AMPA receptor; DOI; Fos; glutamate; hallucinogen; pyramidal cell; serotonin; somatosensory cortex; thalamus; 5-HT2A receptor;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
75
Recensione:
Indirizzi per estratti:
Indirizzo: Scruggs, JL Vanderbilt, Hosp Psychiat, Suite 313,1601 23rd Ave S, Nashville, TN 37212 USA Vanderbilt Suite 313,1601 23rd Ave S Nashville TN USA 37212SA
Citazione:
J.L. Scruggs et al., "DOI-induced activation of the cortex: Dependence on 5-HT2A heteroceptors on thalamocortical glutamatergic neurons", J NEUROSC, 20(23), 2000, pp. 8846-8852

Abstract

Administration of the hallucinogenic 5-HT2A/2C agonist 1-[2,5-dimethoxy- 4-iodophenyl]-2-aminopropane (DOI) induces expression of Fos protein in the cerebral cortex. To understand the mechanisms subserving this action of DOI, we examined the consequences of pharmacological and surgical manipulations on DOI-elicited Fos expression in the somatosensory cortex of the rat. DOI dose-dependently increased cortical Fos expression. Pretreatment with theselective 5-HT2A antagonist MDL 100,907 completely blocked DOI-elicited Fos expression, but pretreatment with the 5-HT2C antagonist SB 206,553 did not modify DOI-elicited Fos expression. These data suggest that DOI acts through 5-HT2A receptors to increase cortical Fos expression. However, we foundthat DOI did not induce Fos in cortical 5-HT2A immunoreactive neurons but did increase expression in a band of neurons spanning superficial layer V to deep III, within the apical dendritic fields of layer V 5-HT2A-immunoreactive cells. This band of Fos immunoreactive neurons was in register with anterogradely labeled axons from the ventrobasal thalamus, which have previously been shown to be glutamatergic and express the 5-HT2A transcript. The effects of DOI were markedly reduced in animals pretreated with the AMPA/KA antagonist GYKI 52466, and lesions of the ventrobasal thalamus attenuated DOI-elicited Fos expression in the cortex. These data suggest that DOI activates 5-HT2A receptors on thalamocortical neurons and thereby increases glutamate release, which in turn drives Fos expression in cortical neurons through an AMPA receptor-dependent mechanism. These data cast new light on the mechanisms of action of hallucinogens.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 07/07/20 alle ore 06:23:31