ReviewPsychopharmacology2005
Rate-dependent behavioral effects of stimulation of central motoric alpha(1)-adrenoceptors: hypothesized relation to depolarization blockade.
Review in Psychopharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- The role of the central noradrenergic system in behavioral inhibition.Brain research reviews · 2011Review
- alpha1-noradrenergic receptor antagonism blocks dependence-induced increases in responding for ethanol.Alcohol (Fayetteville, N.Y.) · 2008Article
- Alpha(1)-adrenergic and alpha(2)-adrenergic balance in the dorsal pons and gross behavioral activity of mice in a novel environment.Psychopharmacology · 2005Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
aimThe purpose of this review is to clarify how central alpha(1)-adrenoceptors control behavioral activity under varying conditions of activity and stress.
methodThe literature is reviewed regarding the behavioral actions of alpha(1)-agonists and antagonists, and alpha(2)-agonists and antagonists under conditions of high and low baseline activity and stress.
resultsIt was found that alpha(1)-receptor stimulation of active behavior has a number of similarities to rate dependency including: (1) a dependence on low-active, low-stress conditions or on the prior depletion of endogenous brain catecholamines; (2) a nonmonotonic dose-response relationship with high doses producing a fall-off or actual depression of activity; (3) a failure to be blocked at high agonist doses by alpha(1)-antagonists; and (4) a facilitation by alpha(2)-adrenoceptor agonists which produce an opposing hyperpolarization. DISCUSSION: To explain these findings, it is proposed that high levels of stimulation of central alpha(1)-receptors produce, in host neurons, a depolarization block that impedes nerve impulse generation and inhibits active behavior. This effect is assumed to be precluded or mitigated by low-active, low-stress conditions, depletion of brain catecholamines, and by hyperpolarizing alpha(2)-agonists, and to be reversed at high agonist doses by alpha(1)-antagonists.
conclusionBecause brain alpha(1)-receptors are not only involved in motor activity but also in the mechanism of action of antidepressant and stimulant drugs, arousal, anxiety, stress and psychosis, a depolarization block from intense stimulation of these receptors could have broad psychopharmacological consequences and underlie rate dependency to a variety of stimulant drugs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.