Abstract:These findings suggest that the chronic co-administration of caffeine and ethanol and the acute withdrawal from these drugs lead to anxiogenic effects and increased seizure vulnerability.
“…In juvenile rats, caffeine combined with ethanol increased the vulnerability to seizures triggered with PTZ, whereas caffeine alone had a protective effect [49].…”
Purpose of review: Caffeine is the most widely consumed central nervous stimulant. For people with epilepsy, it is often unclear whether drinking coffee carries a risk of triggering seizures. Recent findings: The relationship between caffeine, seizures, epilepsy and anti-seizure drugs is not fully understood. Clinical studies are scarce. In animal models, caffeine can increase seizure susceptibility but can also protect from seizures. Effects seem dose-dependent and, influenced but the duration of intake and the developmental stage at which caffeine exposure started. Caffeine lowers the efficacy of several anti-seizure medication, especially topiramate. Summary: It is unclear how these findings, mainly from animal studies can be translated to the clinical condition. At present, there is no evidence to advice people with epilepsy against the use or overuse of caffeine. Until clinical studies suggest otherwise, caffeine intake should be considered as a factor in achieving and maintaining seizure control in epilepsy.
“…In juvenile rats, caffeine combined with ethanol increased the vulnerability to seizures triggered with PTZ, whereas caffeine alone had a protective effect [49].…”
Purpose of review: Caffeine is the most widely consumed central nervous stimulant. For people with epilepsy, it is often unclear whether drinking coffee carries a risk of triggering seizures. Recent findings: The relationship between caffeine, seizures, epilepsy and anti-seizure drugs is not fully understood. Clinical studies are scarce. In animal models, caffeine can increase seizure susceptibility but can also protect from seizures. Effects seem dose-dependent and, influenced but the duration of intake and the developmental stage at which caffeine exposure started. Caffeine lowers the efficacy of several anti-seizure medication, especially topiramate. Summary: It is unclear how these findings, mainly from animal studies can be translated to the clinical condition. At present, there is no evidence to advice people with epilepsy against the use or overuse of caffeine. Until clinical studies suggest otherwise, caffeine intake should be considered as a factor in achieving and maintaining seizure control in epilepsy.
“…In accordance with this possibility, chronic caffeine was shown to increase anxiogenic-like effects associated with nicotine and alcohol withdrawal in rodents. 14,80 Here, we failed to identify alterations in the expression of hippocampal 5-HT 1A , which suggests that this receptor, in the hippocampus, does not play a critical role in the anxiety-like behavior evoked by lifetime caffeine. Arnold and colleagues 71 showed that caffeine exposure during adolescence does not affect mRNA expression of htr1a, the serotonin 1a receptor gene, however, it downregulates mRNA expression of other proteins involved in serotonergic transmission in the dorsal raphe nucleus of rats.…”
Caffeine consumption occurs throughout life, while nicotine use typically begins during adolescence, the period when caffeine-nicotine epidemiological association begins in earnest. Despite that, few studies in animal models parallel the pattern of coexposure that occurs in humans. Therefore, the neurobehavioral consequences of the association between these drugs remain unclear. Here, we exposed Swiss mice to lifetime caffeine. Caffeine solutions of 0.1 g/L (CAF0.1), 0.3 g/L (CAF0.3), or water (CTRL) were used as the sole liquid source, being offered to progenitors until weaning and, after that, directly to the offspring until the last day of adolescent behavioral evaluation. The open field test was used to evaluate acute effects of nicotine, of lifetime caffeine and of their interaction on locomotion and anxiety-like behavior, while the conditioned place preference test was used to assess the impact of caffeine on nicotine (0.5 mg/Kg, i.p.) reward. Frontal cerebral cortex dopamine content, dopamine turnover, and norepinephrine levels, as well as hippocampal serotonin 1A receptor expression were assessed. CAF0.3 mice exhibited an increase in anxiety-like behavior when compared to CAF0.1 and CTRL ones, but nicotine coexposure mitigated the anxiogenic-like caffeine-induced effect. Distinctively, caffeine had no effect on locomotion and failed to interfere with both nicotine-induced hyperactivity and place preference. There were no significant effects on dopaminergic and serotonergic markers. In conclusion, although caffeine did not affect nicotine reward, considering the strong association between anxiety disorders and tobacco consumption, caffeine-induced anxiety-like behavior advises limiting its consumption during development, including adolescence, as caffeine could be a risk factor to nicotine use.
“…Initially, the Elevated Plus-Maze (EPM) was used to assess anxiety in rats (Matovu D et al, 2018). EPM is made up of two open arms (50 10 cm) with a 5cm-high edge and two closed arms (50 10 cm) with 40-cm-high walls that extend from a shared center platform (5 5 cm).…”
Autism spectrum disorder (ASD) is characterized by complex behavioral and memory impairments resulting from abnormal brain development. The research objective is to identify the lack of understanding of the etiology of autism. The Ayurvedic system of medicine recognizes Bacopa monnieri for their potential nootropic activity to maximize brain and neuronal processes such as learning and memory. Brahmi, Bacopa monnieri has been demonstrated in Ayurvedic preparation as memory booster medicine. The neuroprotective properties of hydroalcoholic extract of Bacopa monnieri against propionic acid-induced neuroprotective effect in autistic rat models were investigated in the present study. The animal species used in the study are adult Sprague Dawley rats of both sexes were divided into four groups and administered the vehicle/extract for 28 days. Between the 22nd and 28th days of the trial, autism was caused by an intracerebroventricular infusion of propionic acid. Rats were treated to the fundamental methods such as different in vivo behavior and memory evaluation procedures during this infusion period, including the actophotometer test and the Morris water maze test. Animals were euthanized on the 29th day of the investigation to obtain brain material. Extracted brain tissues were used to calculate levels of neuroinflammatory markers (TNF-) and histological examination.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.