Literature DB >> 14741749

Drugs of abuse that cause developing neurons to commit suicide.

Nuri B Farber1, John W Olney.   

Abstract

When neuronal activity is abnormally suppressed during the developmental period of synaptogenesis, the timing and sequence of synaptic connections is disrupted, and this causes nerve cells to receive an internal signal to commit suicide, a form of cell death known as "apoptosis". By altering glutamate and GABA transmission alcohol suppresses neuronal activity, causing millions of nerve cells to commit suicide in the developing brain. This proapoptotic effect of alcohol provides a likely explanation for the diminished brain size and lifelong neurobehavioral disturbances associated with the human fetal alcohol syndrome. These findings have public health significance, not only in relation to fetal alcohol syndrome, but also in relation to several other drugs of abuse and various drugs used in obstetric and pediatric medicine, because these additional drugs (e.g. phencyclidine, ketamine, benzodiazepines, barbiturates) also suppress neuronal activity and drive developing neurons to commit suicide.

Entities:  

Mesh:

Substances:

Year:  2003        PMID: 14741749     DOI: 10.1016/j.devbrainres.2003.09.009

Source DB:  PubMed          Journal:  Brain Res Dev Brain Res        ISSN: 0165-3806


  14 in total

1.  Propylene glycol produces excessive apoptosis in the developing mouse brain, alone and in combination with phenobarbital.

Authors:  Karen Lau; Brant S Swiney; Nick Reeves; Kevin K Noguchi; Nuri B Farber
Journal:  Pediatr Res       Date:  2012-01       Impact factor: 3.756

2.  Differences between adolescents and adults in the acute effects of PCP and ketamine and in sensitization following intermittent administration.

Authors:  Angelica Rocha; Nigel Hart; Keith A Trujillo
Journal:  Pharmacol Biochem Behav       Date:  2017-04-22       Impact factor: 3.533

Review 3.  Acute and chronic effects of ethanol on learning-related synaptic plasticity.

Authors:  Charles F Zorumski; Steven Mennerick; Yukitoshi Izumi
Journal:  Alcohol       Date:  2013-12-16       Impact factor: 2.405

4.  Long-lasting effects of repeated ketamine administration in adult and adolescent rats.

Authors:  M L Shawn Bates; Keith A Trujillo
Journal:  Behav Brain Res       Date:  2019-04-26       Impact factor: 3.332

Review 5.  Alcoholic cardiomyopathy: pathophysiologic insights.

Authors:  Mariann R Piano; Shane A Phillips
Journal:  Cardiovasc Toxicol       Date:  2014-12       Impact factor: 3.231

Review 6.  Reviewing the ketamine model for schizophrenia.

Authors:  Joel Frohlich; John D Van Horn
Journal:  J Psychopharmacol       Date:  2013-11-20       Impact factor: 4.153

7.  Latent inhibition-related dopaminergic responses in the nucleus accumbens are disrupted following neonatal transient inactivation of the ventral subiculum.

Authors:  Francisca F Meyer; Alain Louilot
Journal:  Neuropsychopharmacology       Date:  2011-03-23       Impact factor: 7.853

8.  Ketamine exposure in adult mice leads to increased cell death in C3H, DBA2 and FVB inbred mouse strains.

Authors:  Chalon R Majewski-Tiedeken; Cara R Rabin; Steven J Siegel
Journal:  Drug Alcohol Depend       Date:  2007-10-24       Impact factor: 4.492

9.  Purkinje cells loss in off spring due to maternal morphine sulfate exposure: a morphometric study.

Authors:  Mohammad Jafar Golalipour; Soraya Ghafari
Journal:  Anat Cell Biol       Date:  2012-06-30

10.  Dual regulation by ethanol of the inhibitory effects of ketamine on spinal NMDA-induced pressor responses in rats.

Authors:  Nien-Tzu Keng; Hsun-Hsun Lin; Huei-Ru Lin; Wei-Kung Hsieh; Chih-Chia Lai
Journal:  J Biomed Sci       Date:  2012-02-02       Impact factor: 8.410

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.