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Published on: December 14, 2014
Maternal caffeine exposure alters neuromotor development and hippocampus acetylcholinesterase activity in rat
Ana Claudia Souza1, Andressa Souza2, Liciane Fernandes Medeiros2
1Medical Sciences-Medicine School, Universidade Federal do Rio Grande do Sul, Porto Alegre 90035-003, RS, Brazil; Pharmacology of Pain and Neuromodulation Laboratory, Animals Models, Department of Pharmacology, Universidade Federal do Rio Grande do Sul, ICBS, Porto Alegre 90050-170, RS, Brazil; Animal Experimentation Unit and Graduate Research Group, Hospital de Clínicas de Porto Alegre, Porto Alegre 90035-003, RS, Brazil.
Insights
Maternal caffeine intake during pregnancy and lactation negatively impacts rat pup neuromotor development. This study found altered reflexes, reduced activity, and changes in brain chemistry, suggesting interference with cholinergic neurotransmission.
Area of Science:
- Neuroscience
- Developmental Biology
- Pharmacology
Background:
- Maternal caffeine consumption is widespread globally.
- The impact of prenatal and early postnatal caffeine exposure on offspring neurodevelopment requires further investigation.
- Cholinergic system plays a critical role in brain development and function.
Purpose of the Study:
- To investigate the effects of maternal caffeine intake on the neuromotor development of rat offspring.
- To examine the impact of maternal caffeine on acetylcholine degradation and acetylcholinesterase (AChE) expression in the hippocampus.
- To assess behavioral changes including locomotor activity, exploratory behavior, and anxiety-like behaviors in offspring exposed to caffeine.
Main Methods:
- Rat dams were administered caffeine (0.3g/L) throughout gestation and lactation.
- Offspring were divided into control, caffeine, and washout groups (caffeine withdrawn at postnatal day 7).
- Neuromotor reflexes (righting reflex, negative geotaxis), open-field test behaviors, and hippocampal AChE activity were assessed.
Main Results:
- Caffeine exposure prolonged righting reflex and negative geotaxis latencies.
- Offspring exhibited reduced locomotion and exploratory behaviors in the open-field test.
- Decreased AChE activity was observed in the caffeine-exposed group, without changes in AChE transcriptional regulation.
Conclusions:
- Chronic maternal caffeine exposure adversely affects neuromotor development in rat offspring.
- Maternal caffeine intake can interfere with cholinergic neurotransmission during critical periods of brain development.
- These findings underscore the potential neurodevelopmental risks associated with maternal caffeine consumption.
Abstract:
The objective of this study was to evaluate the effects of maternal caffeine intake on the neuromotor development of rat offspring and on acetylcholine degradation and acetylcholinesterase (AChE) expression in the hippocampus of 14-day-old infant rats. Rat dams were treated with caffeine (0.3g/L) throughout gestation and lactation until the pups were 14 days old. The pups were divided into three groups: (1) control, (2) caffeine, and (3) washout caffeine. The washout group received a caffeine solution until the seventh postnatal day (P7). Righting reflex (RR) and negative geotaxis (NG) were assessed to evaluate postural parameters as an index of neuromotor reflexes. An open-field (OF) test was conducted to assess locomotor and exploratory activities as well as anxiety-like behaviors. Caffeine treatment increased both RR and NG latency times. In the OF test, the caffeine group had fewer outer crossings and reduced locomotion compared to control, while the washout group showed increased inner crossings in relation to the other groups and fewer rearings only in comparison to the control group. We found decreased AChE activity in the caffeine group compared to the other groups, with no alteration in AChE transcriptional regulation. Chronic maternal exposure to caffeine promotes important alterations in neuromotor development. These results highlight the ability of maternal caffeine intake to interfere with cholinergic neurotransmission during brain development.
