Cortical nitric oxide required for presynaptic long-term potentiation in the insular cortex.
Kiyofumi YamamotoQi-Yu ChenZhaoxiang ZhouMasayuki KobayashiMin ZhuoPublished in: Philosophical transactions of the Royal Society of London. Series B, Biological sciences (2024)
Nitric oxide (NO) is a key diffusible messenger in the mammalian brain. It has been proposed that NO may diffuse retrogradely into presynaptic terminals, contributing to the induction of hippocampal long-term potentiation (LTP). Here, we present novel evidence that NO is required for kainate receptor (KAR)-dependent presynaptic form of LTP (pre-LTP) in the adult insular cortex (IC). In the IC, we found that inhibition of NO synthase erased the maintenance of pre-LTP, while the induction of pre-LTP required the activation of KAR. Furthermore, NO is essential for pre-LTP induced between two pyramidal cells in the IC using the double patch-clamp recording. These results suggest that NO is required for homosynaptic pre-LTP in the IC. Our results present strong evidence for the critical roles of NO in pre-LTP in the IC. This article is part of a discussion meeting issue 'Long-term potentiation: 50 years on'.
Keyphrases
- nitric oxide
- induced apoptosis
- functional connectivity
- hydrogen peroxide
- resting state
- white matter
- signaling pathway
- multiple sclerosis
- low grade
- high grade
- brain injury
- endoplasmic reticulum stress
- blood brain barrier
- cell death
- subarachnoid hemorrhage
- binding protein
- stress induced
- cerebral ischemia
- endothelial cells