Nicotine effects on rat seizures susceptibility and hippocampal neuronal degeneration
Language English Country Sweden Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
21196917
PII: NEL310610A08
Knihovny.cz E-resources
- MeSH
- Nerve Degeneration drug therapy pathology MeSH
- Electrophysiology MeSH
- Evoked Potentials * MeSH
- Hippocampus drug effects pathology MeSH
- Electrodes, Implanted MeSH
- Injections, Intraperitoneal MeSH
- Rats MeSH
- Disease Models, Animal MeSH
- Motor Cortex pathology MeSH
- Cerebral Cortex drug effects pathology physiopathology MeSH
- Disease Susceptibility MeSH
- Random Allocation MeSH
- Neurons pathology MeSH
- Nicotine administration & dosage adverse effects MeSH
- Nicotinic Agonists adverse effects MeSH
- Rats, Wistar MeSH
- Dose-Response Relationship, Drug MeSH
- Seizures drug therapy pathology physiopathology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Nicotine MeSH
- Nicotinic Agonists MeSH
OBJECTIVES: Nicotine is a widely used drug of abuse exerting number of effects on the central nervous system. The study was aimed at the effects of nicotine in various doses on the excitability of cerebral cortex and - by using the methods of histochemistry - to identify possible signs of neuronal degeneration after nicotine administration. METHODS: Cortical afterdischarges were elicited by repeated stimulation of the right sensorimotor cortex. The duration of evoked ADs was monitored in animals treated with nicotine (0.75 or 1.0mg/kg) and in animals treated with saline. Methods of histochemistry (Fluoro-Jade B and bis-benzimide) were used to detect possible neuronal degeneration in hippocampus or in cerebral cortex. RESULTS: No Fluoro-Jade B positive cells were found in hippocampi of control animals, or animals treated with nicotine. ADs length was significantly influenced by administration of nicotine. CONCLUSION: Nicotine in 0.75 or 1.0 mg/kg dose leads to the decrease in ADs duration, influences the seizure susceptibility, and doesn't cause any detectable neuronal damage.
