ArticleBritish journal of pharmacology2014
The behavioural response of mice lacking NK₁ receptors to guanfacine resembles its clinical profile in treatment of ADHD.
Article in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Adrenoceptors: A Focus on Psychiatric Disorders and Their Treatments.Handbook of experimental pharmacology · 2024Review
- Dissection of neuronal circuits underlying sustained attention with the five-choice serial reaction time task.Neuroscience and biobehavioral reviews · 2023Review
- Control of sustained attention and impulsivity by GTranslational psychiatry · 2023Article
- Animal Models of ADHD?Current topics in behavioral neurosciences · 2022Article
- Sex differences in noradrenergic modulation of attention and impulsivity in rats.Psychopharmacology · 2021Article
- Control of impulsivity by GCommunications biology · 2021Article
- Guanfacine treatment improves ADHD phenotypes of impulsivity and hyperactivity in a neurofibromatosis type 1 mouse model.Journal of neurodevelopmental disorders · 2020Article
- The use of reaction time distributions to study attention in male rats: the effects of atomoxetine and guanfacine.Psychopharmacology · 2019Article
- Effect of ADHD medication in male C57BL/6J mice performing the rodent Continuous Performance Test.Psychopharmacology · 2019Article
- Operant Assessment of DMTP Spatial Working Memory in Mice.Frontiers in behavioral neuroscience · 2019Article
- The NK1R-/- mouse phenotype suggests that small body size, with a sex- and diet-dependent excess in body mass and fat, are physical biomarkers for a human endophenotype with vulnerability to attention deficit hyperactivity disorder.Journal of psychopharmacology (Oxford, England) · 2016Article
- Perseveration by NK1R-/- ('knockout') mice is blunted by doses of methylphenidate that affect neither other aspects of their cognitive performance nor the behaviour of wild-type mice in the 5-Choice Continuous Performance Test.Journal of psychopharmacology (Oxford, England) · 2016Article
- Differences in the performance of NK1R-/- ('knockout') and wildtype mice in the 5‑Choice Continuous Performance Test.Behavioural brain research · 2016Article
- The angiotensin converting enzyme inhibitor, captopril, prevents the hyperactivity and impulsivity of neurokinin-1 receptor gene 'knockout' mice: sex differences and implications for the treatment of attention deficit hyperactivity disorder.European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology · 2015Article
- Atomoxetine reduces hyperactive/impulsive behaviours in neurokinin-1 receptor 'knockout' mice.Pharmacology, biochemistry, and behavior · 2014Article
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6 authors at 2 institutions in 1 country.
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Abstract
background and purposeMice with functional ablation of substance P-preferring neurokinin-1 receptors (NK1R-/- mice) display behavioural abnormalities resembling those in attention deficit hyperactivity disorder (ADHD). Here, we investigated whether the ADHD treatment, guanfacine, alleviated the hyperactivity and impulsivity/inattention displayed by NK1R-/- mice in the light/dark exploration box (LDEB) and 5-choice serial reaction-time task (5-CSRTT), respectively. Following reports of co-morbid anxiety in ADHD, we also investigated effects of guanfacine on anxiety-like behaviour displayed by NK1R-/- and wild-type (WT) mice in the elevated plus maze (EPM). EXPERIMENTAL APPROACH: Mice were treated with guanfacine (0.1, 0.3 or 1.0 mg·kg(-1), i.p.), vehicle or no injection and tested in the 5-CSRTT or the LDEB. Only the lowest dose of guanfacine was used in the EPM assays. KEY
resultsIn the 5-CSRTT, a low dose of guanfacine (0.1 mg·kg(-1)) increased attention in NK1R-/- mice, but not in WT mice. This dose did not affect the total number of trials completed, latencies to respond or locomotor activity in the LDEB. Impulsivity was decreased by the high dose (1.0 mg·kg(-1)) of guanfacine, but this was evident in both genotypes and is likely to be secondary to a generalized blunting of behaviour. Although the NK1R-/- mice displayed marked anxiety-like behaviour, guanfacine did not affect the behaviour of either genotype in the EPM. CONCLUSIONS AND IMPLICATIONS: This evidence that guanfacine improves attention at a dose that did not affect arousal or emotionality supports our proposal that NK1R-/- mice express an attention deficit resembling that of ADHD patients.
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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.