Enhanced cholinergic-tone during the stress induce a depressive-like state in mice

Fernandes, Sara; Koth, André Peres; Parfitt, Gustavo M.; Cordeiro, Marcos Freitas; Peixoto, Carolina; Soubhia, Andréa; Moreira, Fernanda Pedrotti; Wiener, Carolina David; Oses, Jean Pierre; Kaszubowski, Erikson; Barros, Daniela M.

doi:10.1016/j.bbr.2018.02.044

Cited by 24 publications

(18 citation statements)

References 52 publications

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“…Our in vivo data show that transient restraint stress induces ACh release in vHPC ( Figure 2); this is consistent with previous studies showing that stress increases ACh level in the hippocampus (Mark et al, 1996;Dong et al, 2004). Furthermore, pharmacological and molecular genetic decreases in hippocampal AChE activity increased anxiety-like behaviors (Mineur et al, 2013;Fernandes et al, 2018). Our study indicated that the ACh modulates mouse emotion behavior via mAChRs.…”

Section: Discussionsupporting

confidence: 91%

Acetylcholine Muscarinic Receptors in Ventral Hippocampus Modulate Stress-Induced Anxiety-Like Behaviors in Mice

Mei

Zhou

Sun

et al. 2020

Front. Mol. Neurosci.

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Chronic stress exposure increases the risk of developing various neuropsychiatric illnesses. The ventral hippocampus (vHPC) is central to affective and cognitive processing and displays a high density of acetylcholine (ACh) muscarinic receptors (mAChRs). However, the precise role of vHPC mAChRs in anxiety remains to be fully investigated. In this study, we found that chronic restraint stress (CRS) induced social avoidance and anxiety-like behaviors in mice and increased mAChR expression in the vHPC. CRS increased the vHPC ACh release in behaving mice. Moreover, CRS altered the synaptic activities and enhanced neuronal activity of the vHPC neurons. Using pharmacological and viral approaches, we showed that infusing the antagonist of mAChRs or decreasing their expression in the vHPC attenuated the anxiety-like behavior and rescued the social avoidance behaviors in mice probably due to suppression of vHPC neuronal activity and its excitatory synaptic transmission. Our results suggest that the changes of neuronal activity and synaptic transmission in the vHPC mediated by mAChRs may play an important role in stress-induced anxiety-like behavior, providing new insights into the pathological mechanism and potential pharmacological target for anxiety disorders.

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Section: Discussionsupporting

confidence: 91%

Acetylcholine Muscarinic Receptors in Ventral Hippocampus Modulate Stress-Induced Anxiety-Like Behaviors in Mice

Mei

Zhou

Sun

et al. 2020

Front. Mol. Neurosci.

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“…Both stress and centrally (i.c.v.) administered CRF stimulate acetylcholine release in the hippocampus via activation of CRF-R1 receptors on cholinergic basal forebrain diagonal band projection neurons (Day et al, 1998a,b;Sauvage and Steckler, 2001;Fernandes et al, 2018). Moreover, this enhanced cholinergic transmission and nicotinic receptor activation in the hippocampus can lead to an increase in anxiety-and depression-like behavior (Mineur et al, 2013;Fernandes et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Striatal Cholinergic Interneurons Are a Novel Target of Corticotropin Releasing Factor

2019

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Cholinergic interneurons (CINs) are critical regulators of striatal network activity and output. Changes in CIN activity are thought to encode salient changes in the environment and stimulus-response-outcome associations. Here we report that the stress-associated neuropeptide corticotropin releasing factor (CRF) produces a profound and reliable increase in the spontaneous firing of CINs in both dorsal striatum and nucleus accumbens (NAc) through activation of CRF type 1 receptors, production of cAMP and reduction in spike accommodation in male mice. The increase of CIN firing by CRF results in the activation muscarinic acetylcholine receptors type 5, which mediate potentiation of dopamine transmission in the striatum. This study provides critical mechanistic insight into how CRF modulates striatal activity and dopamine transmission in the NAc to likely account for CRF facilitation of appetitive behaviors.Although the presence of CRF receptors in the dorsal and ventral striatum has been acknowledged, the cellular identity and the functional consequences of receptor activation is unknown. Here we report that striatal cholinergic interneurons express CRF-R1 receptors and are acutely activated by the neuropeptide CRF that is released in response to salient environmental stimuli. Cholinergic interneurons make Ͻ1% of the cells in the striatum but are critical regulators of the striatal circuitry and its output. CRF's fast and potent activation of cholinergic interneurons could have far reaching behavioral implications across motivated behaviors controlled by the striatum.

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“…Кроме того, КРГ оказывает прямое иммуносупрессивное действие, наиболее уязвимой мишенью которого являются Т-цитотоксические лимфоциты. Это быстрый эффект: после инфузии КРГ снижение активности цитотоксических лимфоцитов селезенки на 50% отмечается в течение 20 мин, естественных киллеров кровив течение 1 ч. Введение антител к КРГ животным полностью предотвращает эти эффекты [19,20].…”

Section: механизмы развития адаптивного ответа на эустрессunclassified

“…Недостаточный выброс катехоламинов и/или недостаточное снижение тонуса парасимпатической нервной системы, затянувшийся сдвиг баланса в сторону симпатической импульсации в ЦНС и на периферии могут привести к развитию депрессии [19]. Эксперименты на мышиных моделях с применением ингибиторов холинэстеразы показали, что повышенный базальный уровень холинергических медиаторов в гиппокампе и отсутствие его снижения после воздействия стрессового фактора уменьшают способность справиться со стрессом [19]. Достоверно подтвержден гипотонус парасимпатической нервной системы у больных РА и лиц, предрасположенных к заболеванию [50].…”

Section: общие патогенетические механизмы развития дистресса и ревматunclassified

Psychological stress and rheumatoid arthritis – interference of pathogenetic mechanisms

Tuaeva

Nosyrev

Ренадино

et al. 2019

Naučno-praktičeskaâ revmatologiâ

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Molecular mechanisms of development of normal and pathological neuroendocrine and immune adaptive response to psychological (mental) stress are analyzed considering its possible provoking role in the development of rheumatoid arthritis (RA). A detailed analysis reveals the synergism of mechanisms that provoke the development of pathological anti-stress adaptive response and RA. It is possible that in persons at risk of developing RA minimal and unobtrusive for the individual stressful situations, periodically provoking prolonged production of pro-inflammatory cytokines, can, finally, lead to the development of rheumatic disease.

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Enhanced cholinergic-tone during the stress induce a depressive-like state in mice

Cited by 24 publications

References 52 publications

Acetylcholine Muscarinic Receptors in Ventral Hippocampus Modulate Stress-Induced Anxiety-Like Behaviors in Mice

Acetylcholine Muscarinic Receptors in Ventral Hippocampus Modulate Stress-Induced Anxiety-Like Behaviors in Mice

Striatal Cholinergic Interneurons Are a Novel Target of Corticotropin Releasing Factor

Psychological stress and rheumatoid arthritis – interference of pathogenetic mechanisms

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