Several studies have proposed that high levels of KYNA

Several studies have proposed that high levels of KYNA in the salbutamol sulfate contribute to cognitive dysfunctions presented by patients who suffer from schizophrenia [30], [31], [32], [33]. Considering that: (i) KYNA is a known GPR35 agonist [2], (ii) cognitive impairments in patients with schizophrenia and in preclinical rodent models of the disease appear to be linked to decreased interneuron function [34], [35], and (iii) GPR35 activation, as shown here, leads to a reduction of SRI firing, it is tempting to hypothesize that KYNA-induced activation of GPR35 in SRIs may be one of the molecular mechanisms underlying the pathophysiology of this catastrophic disorder. If this hypothesis holds true, then centrally acting GPR35 antagonists would emerge as promising therapeutic measures to mitigate signs and symptoms resulting from KYNA-induced disruption of the functionality of hippocampal networks in schizophrenia.
Author contributions Participated in research design: Alkondon, Pereira, Randall, Albuquerque. Conducted experiments: Alkondon (electrophysiology), Todd, Randall, Lane, Albuquerque (histochemistry). Performed data analysis: Alkondon, Pereira, Albuquerque (electrophysiology), Todd, Randall, Lane (histochemistry). Wrote or contributed to the writing of the manuscript: Alkondon, Pereira, Albuquerque.
Acknowledgements The authors are second law of thermodynamics (entropy) indebted to Mabel Zelle and Bhagavathy Alkondon for technical assistance. The work was supported by the National Institutes of Health National Institute of Neurological Disorders and Stroke (Grant NS25296, EXA).