Vol 54, No 2 (2023)

Abstract—A mechanism for the interdependent functioning of the olfactory and hippocampal neural networks has been proposed. In this functioning, a significant role belongs to the long-term changes in the efficacy of connections between neurons from these networks, as well as from the ventral part of the basal ganglia, the frontal neocortical areas, the reuniens and mediodorsal thalamic nuclei. Odors are involved in spatial mapping and navigation since these two kinds of information are processed simultaneously and interdependently. The proposed mechanism for the formation of representations of “odor–object–place” associations in the activity of neurons from different hippocampal fields may underlie the participation of odors in the definition of “place fields”. The CA2 hippocampal field makes an important contribution to this process, facilitating the memorization and retrieval of information related to odors and their location. Due to hippocampal projections to olfactory structures, a spatial mapping of the environment is also formed in the activity of neurons in the piriform cortex. According to the proposed mechanism, damage to various parts of the analyzed chains, as well as weakening of neurogenesis in the dentate gyrus and olfactory bulb, should impair odor perception and memory for odors. This consequence is consistent with olfactory deficits in various neurodegenerative and viral diseases, as well as in aging.

Abstract—Inflammatory Bowel Disease (IBD) including Ulcerative colitis (UC) and Crohn’s disease (CD) is a group of chronic immune-mediated diseases of the gastrointestinal tract (GIT) with complex pathophysiology and pathogenesis. Although the exact pathophysiological mechanisms are poorly understood, in recent years, studies have described the activation and alteration of nociceptor functions and their signaling pathways in the inflammation development in IBD and associated hyperalgesia, in particular, the key role of the transient receptor potential vanilloid channel 1 (TRPV1) has been demonstrated. The highest expression level of TRPV1 is specific for sensory neurons, however, it can also be expressed by other cell types, including epithelial cells of the intestine and bladder, immunoreactive cells such as lymphocytes, mast and dendritic cells, vascular endothelial cells, etc. An increasing number of studies in various experimental models, including humans, demonstrate that activation of the TRP superfamily channels, which includes TRPV1, can significantly enhance visceral hypersensitivity, mediate the development of inflammation and pain. In this review, we highlight the present knowledge on the structure, functions and potential role of TRPV1 in the pathogenesis of IBD. Much attention is paid to the discussion of the signaling pathways underlying TRPV1 modulation. We propose that further research in this area will contribute to a better understanding of the general mechanisms of inflammatory and pain response formation and may facilitate the development of new therapeutic targets for the treatment of IBD.