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The Role of CBGTC Synaptic Neurotransmission in the Pathophysiology of Tics.

Psychiatr Clin North Am

March 2025

Department of Neurology, Johns Hopkins University School of Medicine, Kennedy Krieger Institute, Baltimore, MD, USA.

The pathophysiology of tic disorders involves an alteration in the transmission of messages through the cortico-basal ganglia-thalamo-cortical circuit. A major requirement for the passage of a message through this circuit is an intact chemically mediated synaptic neurotransmitter system (ie, neurotransmitters and second messengers). This article reviews the scientific evidence supporting the involvement of a variety of neurotransmitters (ie, dopamine, glutamate, gamma-aminobutyric acid, serotonin, acetylcholine, and the opioid system).

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Atherosclerosis is a major cause of morbidity and mortality worldwide; in Israel, ischemic heart disease is the second leading cause of death for both genders aged 45 and above. Atherosclerosis involves stiffening of the arteries due to the accumulation of lipids and oxidized lipids on the blood vessel walls, triggering the development of artery plaque. Coronary artery disease (CAD) is the most common manifestation of atherosclerosis.

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Activation of the brain-penetrant beta3-adrenergic receptor (Adrb3) is implicated in the treatment of depressive disorders. Enhancing GABAergic inputs from interneurons onto pyramidal cells of prefrontal cortex (PFC) represents a strategy for antidepressant therapies. Here, we probed the effects of the activation of Adrb3 on GABAergic transmission onto pyramidal neurons in the PFC using in vitro electrophysiology.

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Neuropathic pain poses a significant clinical challenge, largely due to the incomplete understanding of its molecular mechanisms, particularly the role of mitochondrial dysfunction. Bioinformatics analysis revealed that pyroptosis and inflammatory responses induced by spared nerve injury (SNI) in the spinal dorsal horn play a critical role in the initiation and persistence of neuropathic pain. Among the factors involved, TSPO (translocator protein) emerged as a key regulator.

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Anesthetics are crucial in surgical procedures and therapeutic interventions, but they come with side effects and varying levels of effectiveness, calling for novel anesthetic agents that offer more precise and controllable effects. Targeting Gamma-aminobutyric acid (GABA) receptors, the primary inhibitory receptors in the central nervous system, could enhance their inhibitory action, potentially reducing side effects while improving the potency of anesthetics. In this study, we introduce a proteomic learning of GABA receptor-mediated anesthesia based on 24 GABA receptor subtypes by considering over 4000 proteins in protein-protein interaction (PPI) networks and over 1.

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