Mirae Jang

Abstract Understanding the neurobiological alterations associated with neuropathic pain is crucial for treatment interventions, but the underlying mechanisms remain unclear. We focused on the medial prefrontal cortex (mPFC), which undergoes various processes of plasticity during the development of neuropathic pain. In particular, in the neuropathic pain state, the pyramidal neuron activity is decreased and metabotropic glutamate receptor 5 (mGluR5) activity is increased in the mPFC.

Abstract Two forms of plasticity, synaptic and intrinsic, are neural substrates for learning and memory. Abnormalities in homeostatic plasticity cause severe neuropsychiatric diseases, such as schizophrenia and autism. This suggests that the balance between synaptic transmission and intrinsic excitability is important for physiological function in the brain.

Animals All experimental protocols were performed in compliance with the Guide for the Care and Use of Laboratory Animals from the Seoul National University, and approved by the Seoul National University Institutional Animal Care and Use Committee. Mice were housed on a 08:00 to 20:00 light cycle (temperature 22 ± 1 °C, humidity 50 ± 10%) with standard mouse chow (38057, Purina Rodent chow) and water provided ad libitum, unless otherwise noted.