Chronic methamphetamine interacts with BDNF Val66Met to remodel psychosis pathways in the mesocorticolimbic proteome

@article{Greening2019ChronicMI,
  title={Chronic methamphetamine interacts with BDNF Val66Met to remodel psychosis pathways in the mesocorticolimbic proteome},
  author={David W. Greening and Michael J. Notaras and Maoshan Chen and Rong Xu and Joel D. Smith and Lesley Cheng and Richard J. Simpson and Andrew F. Hill and Maarten van den Buuse},
  journal={Molecular Psychiatry},
  year={2019},
  volume={26},
  pages={4431-4447},
  url={https://api.semanticscholar.org/CorpusID:209169489}
}
It is revealed that long-term Meth-induced brain changes are strongly dependent upon BDNF genetic variation, illustrating how drug-induced psychosis may be modulated at the molecular level by a single genetic locus.

Analysis of Acute and Chronic Methamphetamine Treatment in Mice on Gdnf System Expression Reveals a Potential Mechanism of Schizophrenia Susceptibility

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Interaction of Brain-Derived Neurotrophic Factor with the Effects of Chronic Methamphetamine on Prepulse Inhibition in Mice Is Independent of Dopamine D3 Receptors

Results show a significant involvement of BDNF in the long-term effects of METH on PPI, particularly in male mice, but these effects appear independent of D3 receptors, and the role of this receptor in psychosis endophenotypes remains unclear.

Medial prefrontal cortex Notch1 signalling mediates methamphetamine-induced psychosis via Hes1-dependent suppression of GABAB1 receptor expression

A previously unrecognised Notch1-Hes1-GABAB1 receptor-dependent mechanism involved in regulating mPFC neuronal activity and behavioural phenotypes in MIP is uncovered and provides mechanistic insight into the aetiology and pathophysiology of MIP.

Association Between Brain-Derived Neurotrophic Factor Val66Met Polymorphism and Methamphetamine Use Disorder: A Meta-Analysis

The results showed a significant correlation between BDNF Val66Met polymorphism and METH dependence in overall population under different genetic models, however, subgroup analysis indicated that the association only existed in Han Chinese but not in other Asian populations.

BDNF-Deficient Mice Show Reduced Psychosis-Related Behaviors Following Chronic Methamphetamine

Chronic methamphetamine exposure induces contrasting profiles of behavioral changes in wild-type and brain-derived neurotrophic factor heterozygous mice, with attenuation of behaviors relevant to psychosis in methamphetamine-treated brain- derived neurotrophicFactor heterozygotes mice, suggesting that brain- derive neurotrophicfactor signalling changes may contribute to development of psychosis inamphetamine users.

BDNF (Val66Met) genetic polymorphism is associated with vulnerability for methamphetamine dependence.

The present findings indicate that rs6265 is associated with METH dependence in the Thai population, with the GG genotype greater in METH-dependent subjects but reducing the emergence of Meth-dependent psychosis.

A sex- and region-specific role of Akt1 in the modulation of methamphetamine-induced hyperlocomotion and striatal neuronal activity: implications in schizophrenia and methamphetamine-induced psychosis.

A sex- and region-specific effect of Akt1 is highlighted in the regulation of dopamine-dependent behaviors and implies the importance of AKT1 in the modulation of sex differences in Meth sensitivity and schizophrenia.

Variant Brain-Derived Neurotrophic Factor Val66Met Polymorphism Alters Vulnerability to Stress and Response to Antidepressants

It is found that heterozygous BDNF+/Met mice displayed hypothalamic-pituitary-adrenal axis hyperreactivity, increased depressive-like and anxiety-like behaviors, and impaired working memory compared with WT mice after 7 d restraint stress, suggesting selective behavioral, molecular, and structural deficits resulting from the interaction between stress and the human genetic BDNFMet polymorphism.

Positive association of AKT1 haplotype to Japanese methamphetamine use disorder.

The results indicate that AKT1 may play a possible role in the development of Meth-use disorder and further investigation of these associations, together with evidence from previous animal studies, may open the way to elucidation of the pathophysiology of this condition.

Val66Met Polymorphism of BDNF Alters Prodomain Structure to Induce Neuronal Growth Cone Retraction

It is shown that the isolated BDNF prodomain is detected in the hippocampus and that it can be secreted from neurons in an activity-dependent manner, and identified the Met66 prodomain as a new active ligand, which modulates neuronal morphology.
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