A neuropsychopharmacological comparison of d-amphetamine, l-DOPA cocaine

Wallach, Marshall B.; Gershon, Samuel

doi:10.1016/0028-3908(71)90089-x

Cited by 50 publications

(12 citation statements)

References 20 publications

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“…Gradually, however, its focus is starting to shift towards functional genomics, an area of the post-genomic era that deals with the functional analysis of genes and their products (see the article by Go¡eau in this issue). Techniques of functional genomics include methods for gene expression pro¢ling at the transcript (DNA microarrays [3^5]; see also article by Brazma and Vilo in this issue); di¡erential display [6]; serial analysis of gene expression [7^9], and protein levels (proteomics) ([10^12]; see also article by Andersen and Mann in this issue), as well as transgenics [13], phage display [14], procedures for studying protein^protein interactions ( [15,16]; see also article by Legrain and Selig in this issue) and bioinformatics [17].…”

Section: Introductionmentioning

confidence: 99%

Gene expression profiling: monitoring transcription and translation products using DNA microarrays and proteomics

et al. 2000

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Novel and powerful technologies such as DNA microarrays and proteomics have made possible the analysis of the expression levels of multiple genes simultaneously both in health and disease. In combination, these technologies promise to revolutionize biology, in particular in the area of molecular medicine as they are expected to reveal gene regulation events involved in disease progression as well as to pinpoint potential targets for drug discovery and diagnostics. Here, we review the current status of these technologies and highlight some studies in which they have been applied in concert to the analysis of biopsy specimens. ß

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Section: Introductionmentioning

confidence: 99%

Gene expression profiling: monitoring transcription and translation products using DNA microarrays and proteomics

et al. 2000

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“…It is well‐known from animal and human studies ( Wallach & Gershon, 1971 ; Altshuler et al ., 1976 ; Herning et al ., 1985 ; Yabase et al ., 1990 ) that, as a central nervous stimulant ( Van Dyke & Byck, 1977 ), cocaine induces electroencephalographic (EEG) desynchronization. Acute use of cocaine may also increase sexual behaviour as an aphrodisiac ( Cohen, 1975 ), and has been associated with penile erection ( Cregler & Mark, 1986 ) or priapism ( Fiorelli et al ., 1990 ; Rodriguez‐Blazquez et al ., 1990 ).…”

Section: Introductionmentioning

confidence: 99%

Hippocampal noradrenergic neurotransmission in concurrent EEG desynchronization and inhibition of penile erection induced by cocaine in the rat

Chang

Chan

2000

British J Pharmacology

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1 We previously reported that cocaine may induce activation of cortical (cEEG) and hippocampal (hEEG) electroencephalographic signals, concurrent with inhibition of penile erection, via an action on the hippocampal formation. The present study further evaluates the role of noradrenergic neurotransmission at the hippocampal formation in this process, using adult, male Sprague-Dawley rats anaesthetized and maintained by chloral hydrate. 2 Unilateral microinjection of cocaine (100 nmoles) into the hippocampal CA1 or CA3 sub®eld or dentate gyrus elicited signi®cant activation of both cEEG and hEEG activity. At the same time, the intracavernous pressure (ICP), our experimental index for penile erection, underwent a discernible reduction. 3 Co-administration of equimolar doses (250 pmoles) of prazosin, naftopidil, yohimbine or rauwolscine signi®cantly reversed those e ects elicited by cocaine on cEEG, hEEG and ICP. 4 Microinjection unilaterally of equimolar doses (5 nmoles) of norepinephrine, phenylephrine or BHT 933 into the hippocampal formation, similar to cocaine, also induced appreciable cEEG and hEEG excitation, with a simultaneous decrease in ICP. 5 We conclude that cocaine may activate cEEG and hEEG and decrease ICP via noradrenergic neurotransmission, possibly engaging at least a 1A/D -, a 2B -and a 2C -adrenoceptors at the hippocampal formation.

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“…It is generally assumed that, as a dopamine (DA) reuptake blocker (Izenwasser et al, 1990), the central nervous stimulant, cocaine (Van Dyke and Byck, 1977), produces its effect on electroencephalographic (EEG) activity by accumulation of DA at the terminal field of dopaminergic synapses. The subsequent activation of DA receptors may possibly involve both D-1 and D-2 subtypes, both of which were reported to elicit EEG arousal (Kropf et al, 1989;Wallach and Gershon, 1971). 0 1995 WILEY-LISS, INC Recent microdialysis data from our laboratory (Luoh et al, 1994) also showed that cocaine-induced EEG activation in rats is concomitant upon a parallel peak elevation in extracellular concentration of cocaine and DA at the medial prefrontal cortex (mPFC).…”

Section: Introductionmentioning

confidence: 99%

Power spectral analysis of electroencephalographic desynchronization induced by cocaine in rats: Correlation with evaluation of noradrenergic neurotransmission at the medial prefrontal cortex

Chang¹,

Kuo²,

Tsai

et al. 1995

Synapse

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We applied continuous, on-line and real-time spectral analysis of electroencephalographic (EEG) signals and microdialysis to evaluate the possible participation of noradrenergic neurotransmission at the medial prefrontal cortex (mPFC) in EEG desynchronization induced by cocaine. Male Sprague-Dawley rats that were under chloral hydrate anesthesia were used. Intravenous administration of cocaine (1.5 or 3.0 mg/kg) dose-dependently induced EEG desynchronization, as represented by a decrease in root mean square (RMS) and an increase in mean power frequency (MPF) value of the EEG signals. Power spectral analysis further revealed that whereas both doses of cocaine promoted a reduction in the alpha (8-13 Hz), theta (4-8 Hz), and delta (1-4 Hz) components, the lower dose of cocaine decreased, and the higher dose increased the beta band (13-32 Hz). Microdialysis data indicated an elevation in extracellular concentration of norepinephrine at the mPFC that paralleled temporally and correlated positively with the maximal effect of cocaine on EEG activity. Bilateral microinjection of the selective noradrenergic neurotoxin, DSP4 (50 micrograms), or equimolar concentration (500 pmol) of the alpha 1-adrenoceptor antagonist, prazosin, or alpha 2-adrenoceptor antagonist, yohimbine, into the mPFC significantly blunted the decrease in delta component (prazosin) or both delta and theta components (DSP4 or yohimbine) of EEG activity by the lower dose of cocaine. On the other hand, the same pretreatments appreciably antagonized the increase in beta band by cocaine at 3.0 mg/kg. The potency of the antagonism by yohimbine, however, was higher than prazosin. These results suggest that cocaine may elicit EEG desynchronization via noradrenergic neurotransmission, and that alpha 2-adrenoceptors, and to a lesser extent, alpha 1-adrenoceptors, at the mPFC may be involved in the subtle dose-dependent changes in individual EEG spectral components.

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A neuropsychopharmacological comparison of d-amphetamine, l-DOPA cocaine

Cited by 50 publications

References 20 publications

Gene expression profiling: monitoring transcription and translation products using DNA microarrays and proteomics

Gene expression profiling: monitoring transcription and translation products using DNA microarrays and proteomics

Hippocampal noradrenergic neurotransmission in concurrent EEG desynchronization and inhibition of penile erection induced by cocaine in the rat

Power spectral analysis of electroencephalographic desynchronization induced by cocaine in rats: Correlation with evaluation of noradrenergic neurotransmission at the medial prefrontal cortex

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