====== Calcium/calmodulin-dependent protein kinase II ======
Calcium/calmodulin-dependent protein kinases (CaMKs) are key regulators of calcium signaling in health and disease. CaMKII is the most abundant isoform in the heart; although classically described as a regulator of excitation–contraction coupling, recent studies show that it can also mediate inflammation in cardiovascular diseases (CVDs). Among CVDs, cardiorenal syndrome (CRS) represents a pressing issue to be addressed, considering the growing incidence of kidney diseases worldwide.

Choy et al. developed an optogenetic kindling model through repeated [[stimulation]] of ventral hippocampal [[CaMKII]] [[neuron]]s in [[adult]] [[rat]]s. They then combined [[fMRI]] with [[electrophysiology]] to track brain-wide circuit dynamics resulting from non-afterdischarge (AD)-generating stimulations and individual convulsive [[seizure]]s. [[Kindling]] induced widespread increases in non-AD-generating stimulation response and ipsilateral [[functional connectivity]] and elevated [[anxiety]]. Individual seizures in kindled animals showed more significant increases in brain-wide activity and bilateral functional [[connectivity]]. Onset time quantification provided evidence for kindled seizure propagation from the ipsilateral to the contralateral [[hemisphere]]. Furthermore, a core of slow-migrating hippocampal activity was identified in both non-kindled and kindled seizures, revealing a novel mechanism of seizure sustainment and propagation
((Choy M, Dadgar-Kiani E, Cron GO, Duffy BA, Schmid F, Edelman BJ, Asaad M, Chan RW, Vahdat S, Lee JH. Repeated [[hippocampal seizure]]s lead to brain-wide reorganization of circuits and [[seizure]] propagation pathways. Neuron. 2021 Oct 23:S0896-6273(21)00778-9. doi: 10.1016/j.neuron.2021.10.010. Epub ahead of print. PMID: 34706219.)).