ArticleBritish journal of pharmacology2000
Hippocampal noradrenergic neurotransmission in concurrent EEG desynchronization and inhibition of penile erection induced by cocaine in the rat.
Article in British journal of pharmacology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 10 citations in OpenAlex.
- Review
- Differential contributions of nitric oxide synthase isoforms at hippocampal formation to negative feedback regulation of penile erection in the rat.British journal of pharmacology · 2002Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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. Unilateral microinjection of cocaine (100 nmoles) into the hippocampal CA1 or CA3 subfield or dentate gyrus elicited significant 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. Co-administration of equimolar doses (250 pmoles) of prazosin, naftopidil, yohimbine or rauwolscine significantly reversed those effects elicited by cocaine on cEEG, hEEG and ICP. 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. We conclude that cocaine may activate cEEG and hEEG and decrease ICP via noradrenergic neurotransmission, possibly engaging at least alpha(1A/D)-, alpha(2B)- and alpha(2C)-adrenoceptors at the hippocampal formation.
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