ReviewJournal of neural transmission (Vienna, Austria : 1996)2008
Pharmacological models of ADHD.
Review in Journal of neural transmission (Vienna, Austria : 1996), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 57 citations in OpenAlex.
- Blood lead concentrations and attention deficit hyperactivity disorder in Korean children: a hospital-based case control study.BMC pediatrics · 2016Article
- Effects of sarizotan in animal models of ADHD: challenging pharmacokinetic-pharmacodynamic relationships.Journal of neural transmission (Vienna, Austria : 1996) · 2015Article
- Attention-deficit/hyperactivity disorder in older adults: prevalence and possible connections to mild cognitive impairment.Current psychiatry reports · 2012Review
- The ADHD-susceptibility gene lphn3.1 modulates dopaminergic neuron formation and locomotor activity during zebrafish development.Molecular psychiatry · 2012Article
- Reinforcement, dopamine and rodent models in drug development for ADHD.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2012Review
- Effect of pre- and postnatal manganese exposure on brain histamine content in a rodent model of Parkinson's disease.Neurotoxicity research · 2012Article
- Animal models to guide clinical drug development in ADHD: lost in translation?British journal of pharmacology · 2011Review
- The effect of reduced dopamine D4 receptor expression in the 5-choice continuous performance task: Separating response inhibition from premature responding.Behavioural brain research · 2011Article
- Annual Research Review: Transgenic mouse models of childhood-onset psychiatric disorders.Journal of child psychology and psychiatry, and allied disciplines · 2011Review
- Neurobehavioral manifestations of developmental impairment of the brain.Interdisciplinary toxicology · 2010Article
- [Neurobiology of attention-deficit hyperactivity disorder].Der Nervenarzt · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
For more than 50 years, heavy metal exposure during pre- or post-natal ontogeny has been known to produce long-lived hyperactivity in rodents. Global brain injury produced by neonatal hypoxia also produced hyperactivity, as did (mainly) hippocampal injury produced by ontogenetic exposure to X-rays, and (mainly) cerebellar injury produced by the ontogenetic treatments with the antimitotic agent methylazoxymethanol or with polychlorinated biphenyls (PCBs). More recently, ontogenetic exposure to nicotine has been implicated in childhood hyperactivity. Because attention deficits most often accompany the hyperactivity, all of the above treatments have been used as models of attention deficit hyperactivity disorder (ADHD). However, the causation of childhood hyperactivity remains unknown. Neonatal 6-OHDA-induced dopaminergic denervation of rodent forebrain also produces hyperactivity - and this model, or variations of it, remain the most widely-used animal model of ADHD. In all models, amphetamine (AMPH) and methylphenidate (MPH), standard treatments of childhood ADHD, typically attenuate the hyperactivity and/or attention deficit. On the basis of genetic models and the noted animal models, monoaminergic phenotypes appear to most-closely attend the behavioral dysfunctions, notably dopaminergic, noradrenergic and serotoninergic systems in forebrain (basal ganglia, nucleus accumbens, prefrontal cortex). This paper describes the various pharmacological models of ADHD and attempts to ascribe a neuronal phenotype with specific brain regions that may be associated with ADHD.
Indexed as
Identifiers
What OpenQuestion holds
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.