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Plant-Derived Compounds as New Therapeutics for Substance Use Disorders
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
Kevin S. Murnane, Mary Frances Vest
Administration of LSD directly into the hippocampus promotes learning (Romano et al., 2010). Administration of the novel psychedelic TCB-2 enhances the consolidation of object memory (Zhang et al., 2013). Ayahuasca enhances learned responses, as does the administration of TCB-2 into the basolateral amygdala (Clinard et al., 2015; Favaro et al., 2015). Viral-mediated induced re-expression of 5-HT2A receptors in mice genetically devoid of 5-HT2A receptors rescues learning and synaptic plasticity deficits (Barre et al., 2016). Microdosing of LSD has been reported to improve cognition in humans, and psilocybin microdosing improves attention in low-performing rats (Higgins et al., 2021; Hutten et al., 2020). As with cannabinoids, the fact that plant-based psychedelics may directly affect the dopamine reward system may improve cognition and behavioral flexibility and may have potential disease-modifying anti-inflammatory and antioxidant effects suggest that psychedelics may provide compelling medications for SUDs.
Preclinical insights into therapeutic targeting of KCC2 for disorders of neuronal hyperexcitability
Published in Expert Opinion on Therapeutic Targets, 2020
Phan Q. Duy, Miao He, Zhigang He, Kristopher T. Kahle
Other neurotransmitters acting on G protein-coupled receptors (GPCRs) may also enhance KCC2 function. A series of two studies demonstrated that administration of TCB-2, an activator of the 5-hydroxytryptamine (5-HT, serotonin) type 2A receptor, increases cell membrane expression of KCC2, restores GABAergic inhibition, and improves functional outcomes in a rat spinal cord injury model [98,99]. Another recent study showed that TCB-2 augments KCC2 activity by promoting phosphorylation of KCC2 at the S940 site and rescues GABAergic disinhibition in the ventral tegmental area following exposure to acute stress [100]. These studies provide proof-of-principle for yet another strategy to modulate KCC2 function for therapeutic benefit in hyperexcitable states by targeting the brain’s serotonergic system.