Epilepsy is a disorder characterized by an imbalance between excitability and inhibition, leading to uncontrolled hyperexcitability of neurons in the central nervous system. Despite the prevalence of epileptic seizures, the underlying mechanisms driving this hyperexcitability remain poorly understood. This review article aims to enhance our understanding of the mechanisms of epilepsy, with a specific focus on the role of cholecystokinin (CCK) in this debilitating disease. We will begin with an introduction to the topic, followed by an examination of the role of GABAergic neurons and the synaptic plasticity mechanisms associated with seizures. As we delve deeper, we will elucidate how CCK and its receptors contribute to seizure behavior. Finally, we will discuss the CCK-dependent synaptic plasticity mechanisms and highlight their potential implications in seizure activity. Through a comprehensive examination of these aspects, this review provides valuable insights into the involvement of CCK and its receptors in epilepsy. By improving our understanding of the mechanisms underlying this condition, particularly the role of CCK, we aim to contribute to the development of more effective treatment strategies.
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http://dx.doi.org/10.1016/j.neuint.2024.105870 | DOI Listing |
Diabetes Metab J
December 2024
Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences (CAMS) & Comparative Medicine Center, Peking Union Medical College (PUMC), and Beijing Engineering Research Center for Experimental Animal Models of Human Critical Diseases, Beijing, China.
Background: Both sodium-glucose cotransporters (SGLTs) and Na+/H+ exchangers (NHEs) rely on a favorable Na-electrochemical gradient. Gastrin, through the cholecystokinin B receptor (CCKBR), can induce natriuresis and diuresis by inhibiting renal NHEs activity. The present study aims to unveil the role of renal CCKBR in diabetes through SGLT2-mediated glucose reabsorption.
View Article and Find Full Text PDFPancreatic endocrine-exocrine crosstalk plays a key role in normal physiology and disease. For instance, endocrine islet beta (β) cell secretion of insulin or cholecystokinin (CCK) promotes progression of pancreatic adenocarcinoma (PDAC), an exocrine cell-derived tumor. However, the cellular and molecular mechanisms that govern endocrine-exocrine signaling in tumorigenesis remain incompletely understood.
View Article and Find Full Text PDFBiochem Pharmacol
December 2024
Faculty of Health, School of Medicine, Institute for Mental and Physical Health and Clinical Translation (IMPACT), Deakin University, Waurn Ponds, Victoria 3216, Australia.
The relaxin-family peptide 3 receptor (RXFP3) and its native ligand, relaxin-3, are expressed in specific populations of brain neurons, and research on this system has focused on its role in the central nervous system. However, some studies have indicated that relaxin-3 and RXFP3 are also expressed in peripheral organs, including the gut. In this study, we characterised the identity of RXFP3-expressing cells in the gastrointestinal tract, using RXFP3-Cre/tdTomato reporter mice.
View Article and Find Full Text PDFCytokine Growth Factor Rev
December 2024
KU Leuven Department of Microbiology, Immunology and Transplantation, Rega Institute, Division of Virology, Antiviral Drug and Vaccine Research, Laboratory of Molecular Vaccinology and Vaccine Discovery, Leuven, Belgium. Electronic address:
Cholecystokinin (CCK) and gastrin are gastrointestinal hormones traditionally recognised for their roles in digestion. However, it has been recognised that these hormones may also modulate immune function. Here, we examine the immune-modulating effects of CCK and gastrin, and explore the functional significance of this dual role.
View Article and Find Full Text PDFBiomed Pharmacother
December 2024
University of Palermo, Dept. of Biomedicine, Neuroscience and Advanced Diagnostics, via del Vespro 129, Palermo 90127, Italy.
The interaction between the main psychotropic ingredient of Cannabis, Δ⁹- tetrahydrocannabinol (THC), with the endogenous cannabinoid system (ECS) is a critical and underrated issue that deserves utmost attention. The ECS, indeed, contributes to the formation and regulation of excitatory and inhibitory (E/I) neuronal networks that in the hippocampus underly spatial memory. This study explored sex-specific consequences of prenatal exposure to THC in hippocampus-dependent memory and the underlying cellular and molecular contributors of synaptic plasticity and E/I homeostasis.
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