ArticleNeuroscience2011
Neurotoxic (+)-methamphetamine treatment in rats increases brain-derived neurotrophic factor and tropomyosin receptor kinase B expression in multiple brain regions.
Article in Neuroscience, 2011. 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, 39 citations in OpenAlex.
- Integrated Assessment of the Cardiotoxic and Neurobehavioral Effects of 3,4-Methylenedioxypyrovalerone (MDPV) in Zebrafish Embryos.International journal of molecular sciences · 2025Article
- Regional Changes in Brain Biomolecular Markers in a Collagen-Induced Arthritis Rat Model.Biology · 2024Article
- A Zebrafish Model of Neurotoxicity by Binge-Like Methamphetamine Exposure.Frontiers in pharmacology · 2021Article
- Neurochemical and behavioral comparisons of contingent and non-contingent methamphetamine exposure following binge or yoked long-access self-administration paradigms.Psychopharmacology · 2020Article
- Effects of lithium on inflammatory and neurotrophic factors after an immune challenge in a lisdexamfetamine animal model of mania.Revista brasileira de psiquiatria (Sao Paulo, Brazil : 1999) · 2019Article
- Methamphetamine augment HIV-1 Tat mediated memory deficits by altering the expression of synaptic proteins and neurotrophic factors.Brain, behavior, and immunity · 2018Article
- Effects of adolescent methamphetamine and nicotine exposure on behavioral performance and MAP-2 immunoreactivity in the nucleus accumbens of adolescent mice.Behavioural brain research · 2017Article
- Time-Dependent Serum Brain-Derived Neurotrophic Factor Decline During Methamphetamine Withdrawal.Medicine · 2016Article
- Psychological intervention with working memory training increases basal ganglia volume: A VBM study of inpatient treatment for methamphetamine use.NeuroImage. Clinical · 2016Article
- The role of astrocyte mitochondria in differential regional susceptibility to environmental neurotoxicants: tools for understanding neurodegeneration.Toxicological sciences : an official journal of the Society of Toxicology · 2015Review
- Methamphetamine self-administration attenuates hippocampal serotonergic deficits: role of brain-derived neurotrophic factor.The international journal of neuropsychopharmacology · 2014Article
- A stress steroid triggers anxiety via increased expression of α4βδ GABAA receptors in methamphetamine dependence.Neuroscience · 2013Article
- MRI of neuronal recovery after low-dose methamphetamine treatment of traumatic brain injury in rats.PloS one · 2013Article
- (±)3,4-methylenedioxymethamphetamine ("ecstasy") treatment modulates expression of neurotrophins and their receptors in multiple regions of adult rat brain.The Journal of comparative neurology · 2012Article
- The effect of 3,4- methylenedioxymethamphetamine on expression of neurotrophic factors in hippocampus of male rats.Medical journal of the Islamic Republic of IranArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Methamphetamine (MA) is an abused stimulant which can result in cognitive deficits and monoamine depletions. Animal models of neurotoxic MA exposure show reductions in dopamine, serotonin, and their associated transporters. MA abuse can result in long-term attention, working memory, and executive function deficits in humans and deficits in route-based egocentric learning, novel object recognition, and novel odor preference in rodents. MA has also been shown to affect brain-derived neurotrophic factor (BDNF) in humans and rodents. This experiment examined the effects of a MA binge dosing regimen (10 mg/kg x 4 at 2 h intervals, s.c.) in Sprague-Dawley rats on BDNF, tropomyosin receptor kinase B (TrkB), and tyrosine hydroxylase (TH) mRNA expression, and plasma corticosterone. Tissues were collected 1, 7, and 24 h following the last MA dose. Expression of BDNF and TrkB mRNA was analyzed using in situ hybridization with cRNA probes. Frontal, parietal, and entorhinal cortical BDNF mRNA expression were increased by MA exposure at all time-points. Increases in BDNF mRNA were also seen in the hippocampal CA1, prefrontal cortex (PFC), piriform cortex, and locus coeruleus but only at specific times. TrkB mRNA expression was modified in several subregions of the hippocampus as well as in PFC and striatum. TH mRNA was increased at the 1 h time-point in the substantia nigra pars compacta with no differences noted at the other times. Corticosterone levels were increased at all three time-points. The findings suggest that BDNF and its receptor may be upregulated as a compensatory mechanism after MA exposure.
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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.