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Published on: June 23, 2023
Involvement of microglia in the ethanol-induced neuropathic pain-like state in the rat
Minoru Narita1, Kan Miyoshi, Michiko Narita
1Department of Toxicology, Hoshi University School of Pharmacy and Pharmaceutical Sciences, 2-4-41 Ebara, Shinagawa-ku, Tokyo 142-8501, Japan. narita@hoshi.ac.jp
Abstract:
Central mechanisms of neuropathy induced by chronic ethanol treatment are almost unknown. In this study, rats were treated with ethanol-diet for 72 days. Mechanical hyperalgesia was observed during ethanol consumption, even after ethanol withdrawal. Under these conditions, a microglial marker ionized calcium-binding adaptor molecule 1-, but not a neuron marker microtuble associated protein-2-, like immunoreactivies were increased in the rat spinal cord. Furthermore, hypertrophy of microglia was clearly observed following chronic ethanol consumption. These findings support the idea that the activation and hypertrophy of microglia in the spinal cord may be, at least in part, associated with in the induction of ethanol-dependent neuropathic pain-like state.
Insights
Chronic ethanol consumption in rats induced neuropathic pain, linked to spinal cord microglial activation and hypertrophy. These changes persisted even after ethanol withdrawal, suggesting a role in persistent pain.
Area of Science:
- Neuroscience
- Toxicology
- Pain Research
Background:
- Chronic ethanol consumption is a known cause of neuropathy, but its central mechanisms remain poorly understood.
- Ethanol-induced neuropathic pain can manifest as mechanical hyperalgesia.
- The role of glial cells in the spinal cord during ethanol-induced neuropathic pain is an area requiring further investigation.
Purpose of the Study:
- To investigate the central mechanisms of neuropathy induced by chronic ethanol treatment in a rat model.
- To examine the involvement of spinal cord microglia in the development of ethanol-dependent neuropathic pain.
Main Methods:
- Rats were administered an ethanol-containing diet for 72 days.
- Mechanical hyperalgesia was assessed during ethanol consumption and withdrawal.
- Immunoreactivity for microglial marker ionized calcium-binding adaptor molecule 1 (Iba1) and neuronal marker microtubule-associated protein-2 (MAP2) was evaluated in the spinal cord.
Main Results:
- Chronic ethanol treatment induced mechanical hyperalgesia, which persisted after ethanol withdrawal.
- Increased Iba1 immunoreactivity, a marker for microglia, was observed in the spinal cord.
- No significant changes were noted in MAP2 immunoreactivity, indicating specific microglial involvement.
- Hypertrophy of microglia was evident in rats subjected to chronic ethanol consumption.
Conclusions:
- Activation and hypertrophy of microglia in the spinal cord are associated with the induction of ethanol-dependent neuropathic pain.
- These findings suggest that neuroinflammation, mediated by microglia, plays a significant role in ethanol-induced neuropathic pain.
