A Discussion of Anxiety Over the Last Millennium (1000 to 2000)

Bourin, Michel; Bourin, Monique

doi:10.1007/978-3-030-61721-9_14

Cited by 2 publications

(3 citation statements)

References 9 publications

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“…There is evidence that CCK participates in both associative [ 106 ] and social memories [ 3 ]. Because CCK + -GABA BCs are critical for a correct behavioral function [ 110 ], CCK disturbances may underlie the learning deficits that are associated with anxiety disorders [ 111 ] and schizophrenia [ 44 , 112 ].…”

Section: Physiological Roles Of Cck In Cortico-limbic Areas and Mesolimbic Pathwaysmentioning

confidence: 99%

Cholecystokinin-Mediated Neuromodulation of Anxiety and Schizophrenia: A “Dimmer-Switch” Hypothesis

Ballaz

Bourin

2021

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: Cholecystokin (CCK), the most abundant brain neuropeptide, is involved in relevant behavioral functions like memory, cognition, and reward through its interactions with the opioid and dopaminergic systems in the limbic system. CCK excites neurons by binding two receptors, CCK1 and CCK2, expressed at low and high levels in the brain, respectively. Historically, CCK2 receptors have been related to the induction of panic attacks in humans. Disturbances in brain CCK expression also underlie the physiopathology of schizophrenia, which is attributed to the modulation by CCK1 receptors of the dopamine flux in the basal striatum. Despite this evidence, neither CCK2 receptor antagonists ameliorate human anxiety nor have CCK agonists consistently shown neuroleptic effects in clinical trials. A neglected aspect of the function of brain CCK is its neuromodulatory role in mental disorders. Interestingly, CCK is expressed in pivotal inhibitory interneurons that sculpt cortical dynamics and the flux of nerve impulses across corticolimbic areas and the excitatory projections to mesolimbic pathways. At the basal striatum, CCK modulates the excitability of glutamate, the release of inhibitory GABA, and the discharge of dopamine. Here we focus on how CCK may reduce rather than trigger anxiety by regulating its cognitive component. Adequate levels of CCK release in the basal striatum may control the interplay between cognition and reward circuitry, which is critical in schizophrenia. Hence, it is proposed that disturbances in the excitatory/inhibitory interplay modulated by CCK may contribute to the imbalanced interaction between corticolimbic and mesolimbic neural activity found in anxiety and schizophrenia.

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Section: Physiological Roles Of Cck In Cortico-limbic Areas and Mesolimbic Pathwaysmentioning

confidence: 99%

Cholecystokinin-Mediated Neuromodulation of Anxiety and Schizophrenia: A “Dimmer-Switch” Hypothesis

Ballaz

Bourin

2021

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“…The chemical structures of keratan sulfates are not shown. The chemical structures of the second generation of THIQ-based ATIII activators (9)(10)(11)(12). Pharmacophore approach was exploited to design this generation.…”

Section: Acknowledgmentsmentioning

confidence: 99%

“…At the molecular level, GAGs are known to interact with several proteins and receptors, and thus, modulate a host of biological processes. By interacting with coagulation enzymes and their physiological inhibitors, GAGs have an important role in the coagulation process [11]. It is worth mentioning that the use of GAGs for therapeutic purposes started with the use of heparin as an anticoagulant in 1935 following its discovery in 1916 [12].…”

Section: Introductionmentioning

confidence: 99%

Sulfated Non-Saccharide Glycosaminoglycan Mimetics as Novel Drug Discovery Platform for Various Pathologies

Afosah¹,

Al‐Horani

2020

CMC

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Glycosaminoglycans (GAGs) are very complex, natural anionic polysaccharides. They are polymers of repeating disaccharide units of uronic acid and hexosamine residues. Owing to their template-free, spatiotemporally-controlled, and enzyme-mediated biosyntheses, GAGs possess enormous polydispersity, heterogeneity, and structural diversity which often translate into multiple biological roles. It is well documented that GAGs contribute to physiological and pathological processes by binding to proteins including serine proteases, serpins, chemokines, growth factors, and microbial proteins. Despite advances in the GAG field, the GAG-protein interface remains largely unexploited by drug discovery programs. Thus, Non-Saccharide Glycosaminoglycan Mimetics (NSGMs) have been rationally developed as a novel class of sulfated molecules that modulate GAG-protein interface to promote various biological outcomes of substantial benefit to human health. In this review, we describe the chemical, biochemical, and pharmacological aspects of recently reported NSGMs and highlight their therapeutic potentials as structurally and mechanistically novel anti-coagulants, anti-cancer agents, anti-emphysema agents, and anti-viral agents. We also describe the challenges that complicate their advancement and describe ongoing efforts to overcome these challenges with the aim of advancing the novel platform of NSGMs to clinical use.

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A Discussion of Anxiety Over the Last Millennium (1000 to 2000)

Cited by 2 publications

References 9 publications

Cholecystokinin-Mediated Neuromodulation of Anxiety and Schizophrenia: A “Dimmer-Switch” Hypothesis

Cholecystokinin-Mediated Neuromodulation of Anxiety and Schizophrenia: A “Dimmer-Switch” Hypothesis

Sulfated Non-Saccharide Glycosaminoglycan Mimetics as Novel Drug Discovery Platform for Various Pathologies

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