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Updated: Mar 24, 2026
Assessment of Memory Function in Pilocarpine-induced Epileptic Mice
Published on: June 4, 2020
Piracetam prevents memory deficit induced by postnatal propofol exposure in mice
Yuan-Lin Wang1, Feng Li2, Xin Chen1
1Department of Anesthesiology, Huai'an First People's Hospital, Nanjing Medical University, Huai'an 223300, China.
Insights
Piracetam effectively reversed propofol-induced memory and synaptic plasticity impairments in rats. This neuroprotective effect appears linked to increased Brain-Derived Neurotrophic Factor (BDNF) signaling.
Area of Science:
- Neuroscience
- Pharmacology
- Developmental Biology
Background:
- Postnatal exposure to anesthetics like propofol can negatively impact brain development.
- Impaired hippocampal synaptic function and memory deficits are known consequences of propofol exposure.
- The specific therapeutic agents to counteract these propofol-induced neurodevelopmental deficits remain largely unverified.
Purpose of the Study:
- To investigate the efficacy of piracetam in mitigating propofol-induced impairments in hippocampal synaptic plasticity and memory.
- To elucidate the underlying molecular mechanisms, particularly the role of Brain-Derived Neurotrophic Factor (BDNF) and mTOR signaling.
Main Methods:
- Rats were exposed to propofol for seven days during the postnatal period.
- Two months post-exposure, cognitive function and hippocampal long-term potentiation (LTP) were assessed.
- Piracetam was administered intraperitoneally at doses of 50mg/kg and 100mg/kg after the propofol regime.
- Levels of BDNF, phosphorylated mTOR, and synaptic plasticity-related proteins were analyzed.
Main Results:
- Propofol exposure led to significant decreases in hippocampal LTP and long-term memory.
- Piracetam administration (50mg/kg and 100mg/kg) successfully reversed these memory and LTP deficits.
- Piracetam treatment normalized the reduced levels of BDNF and phosphorylated mTOR caused by propofol.
- Direct supplementation of BDNF also ameliorated propofol-induced synaptic abnormalities and memory impairments.
Conclusions:
- Piracetam demonstrates significant neuroprotective effects against postnatal propofol-induced neurodevelopmental toxicity.
- The mechanism of piracetam's action involves the upregulation of BDNF synthesis and signaling pathways.
- Targeting BDNF pathways represents a promising therapeutic strategy for managing anesthetic-induced neurodevelopmental impairments.
Abstract:
Postnatal propofol exposure impairs hippocampal synaptic development and memory. However, the effective agent to alleviate the impairments was not verified. In this study, piracetam, a positive allosteric modulator of AMPA receptor was administered following a seven-day propofol regime. Two months after propofol administration, hippocampal long-term potentiation (LTP) and long-term memory decreased, while intraperitoneal injection of piracetam at doses of 100mg/kg and 50mg/kg following last propofol exposure reversed the impairments of memory and LTP. Mechanically, piracetam reversed propofol exposure-induced decrease of BDNF and phosphorylation of mTor. Similar as piracetam, BDNF supplementary also ameliorated propofol-induced abnormalities of synaptic plasticity-related protein expressions, hippocampal LTP and long-term memory. These results suggest that piracetam prevents detrimental effects of propofol, likely via activating BDNF synthesis.
