This issue covers our current understanding of the pathophysiological roles of the ion channels and exchangers involved in non-glutamate mechanisms in cerebral ischemia and stroke, as well as their potential for therapeutic intervention. These non-glutamate mechanisms include TRP channels, KATP channels, chloride channels, acid-sensing ion channels, hemichannels, volume-regulated anion channels, adenosine receptors, nitrogen species, neural precursor cells, retinal ischemia, and neuron glial cells. The articles highlight novel therapeutic strategies for targeting non-glutamate mechanisms to prevent neuronal damage in stroke and to promote neuronal survival, regeneration and functional recovery after stroke, thus providing long-term economic, social, and healthcare benefits worldwide.
