ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2010
Ventral striatal noradrenergic mechanisms contribute to sensorimotor gating deficits induced by amphetamine.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 33 citations in OpenAlex.
- Noradrenergic Signaling Disengages Feedforward Transmission in the Nucleus Accumbens Shell.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Schizophrenia-like reduced sensorimotor gating in intact inbred and outbred rats is associated with decreased medial prefrontal cortex activity and volume.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019Article
- Addressing the Complexity of Tourette's Syndrome through the Use of Animal Models.Frontiers in neuroscience · 2016Review
- The Involvement of Norepinephrine in Behaviors Related to Psychostimulant Addiction.Current neuropharmacology · 2015Review
- Adrenaline rush: the role of adrenergic receptors in stimulant-induced behaviors.Molecular pharmacology · 2014Review
- Antipsychotic-like actions of the satiety peptide, amylin, in ventral striatal regions marked by overlapping calcitonin receptor and RAMP-1 gene expression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Noradrenaline-induced release of newly-synthesized accumbal dopamine: differential role of alpha- and beta-adrenoceptors.Frontiers in cellular neuroscience · 2014Article
- Moderate-level prenatal alcohol exposure enhances acoustic startle magnitude and disrupts prepulse inhibition in adult rhesus monkeys.Alcoholism, clinical and experimental research · 2013Article
- Article
- α-1 Adrenergic receptors are localized on presynaptic elements in the nucleus accumbens and regulate mesolimbic dopamine transmission.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2012Article
- Mutual independence of 5-HT(2) and α1 noradrenergic receptors in mediating deficits in sensorimotor gating.Psychopharmacology · 2012Article
- The role of estrogen and testosterone in female rats in behavioral models of relevance to schizophrenia.Psychopharmacology · 2012Article
- Pharmacological stimulation of locus coeruleus reveals a new antipsychotic-responsive pathway for deficient sensorimotor gating.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2011Article
- Lesions of the dorsomedial striatum disrupt prepulse inhibition.Neuroscience · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The psychotomimetic drug D-amphetamine (AMPH), disrupts prepulse inhibition (PPI) of the startle response, an operational measure of sensorimotor gating that is deficient in schizophrenia patients. Historically, this effect has been attributed to dopaminergic substrates; however, AMPH also increases norepinephrine (NE) levels, and enhancement of central NE transmission has been shown recently to disrupt PPI. This study examined the extent to which NE might participate in AMPH-induced disruptions of PPI and increases in locomotor activity, another classic behavioral effect of AMPH, by determining whether antagonism of postsynaptic NE receptors blocked these effects. Separate groups of male Sprague-Dawley rats received either the α1 receptor antagonist, prazosin (0, 0.3, 1 mg/kg), or the β receptor antagonist timolol (0, 3, 10 mg/kg) before administration of AMPH (0 or 1 mg/kg) before testing for PPI or locomotor activity. As an initial exploration of the anatomical substrates underlying possible α1 receptor-mediated effects on AMPH-induced PPI deficits, the α1 receptor antagonist terazosin (0 or 40 μg/0.5 μl) was microinfused into the nucleus accumbens shell (NAccSh) in conjunction with systemic AMPH administration before startle testing in a separate experiment. Prazosin, but not timolol, blocked AMPH-induced hyperactivity; both drugs reversed AMPH-induced PPI deficits without altering baseline startle responses. Interestingly, AMPH-induced PPI deficits also were partially blocked by terazosin in NAccSh. Thus, behavioral sequelae of AMPH (PPI disruption and hyperactivity) may be mediated in part by NE receptors, with α1 receptors in NAccSh possibly having an important role in the sensorimotor gating deficits induced by this psychotomimetic drug.
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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.