Chronic Variable Stress Alters Inflammatory and Cholinergic Parameters in Hippocampus of Rats

Tagliari, Bárbara; Tagliari, Ana Paula; Schmitz, Felipe; Cunha, Aline Andrea da; Dalmaz, Carla; Wyse, Ângela T. S.

doi:10.1007/s11064-010-0367-0

Cited by 37 publications

(27 citation statements)

References 66 publications

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“…Considering that acetylcholine (ACh) is well known to inhibit tumor necrosis factor-α, interleukin-1β, and macrophage migration (29), the increased AChE activity may indicate a modulation in ACh levels and in its ability in regulating inflammatory processes (30). In the present study, AChE activity was increased in the CWI group.…”

Section: Discussionmentioning

confidence: 99%

Cryotherapy: biochemical alterations involved in reduction of damage induced by exhaustive exercise

Furtado

Hartmann

Martins

et al. 2018

Braz J Med Biol Res

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When exercises are done in intense or exhaustive modes, several acute biochemical mechanisms are triggered. The use of cryotherapy as cold-water immersion is largely used to accelerate the process of muscular recovery based on its anti-inflammatory and analgesic properties. The present study aimed to study the biochemical effects of cold-water immersion treatment in mice submitted to exercise-induced exhaustion. Swiss albino mice were divided into 4 treatment groups: control, cold-water immersion (CWI), swimming exhaustive protocol (SEP), and SEP+CWI. Treatment groups were subdivided into times of analysis: 0, 1, 3, and 5 days. Exhaustion groups were submitted to one SEP session, and the CWI groups submitted to one immersion session (12 min at 12°C) every 24 h. Reactive species production, inflammatory, cell viability, and antioxidant status were assessed. The SEP+CWI group showed a decrease in inflammatory damage biomarkers, and reactive species production, and presented increased cell viability compared to the SEP group. Furthermore, CWI increased acetylcholinesterase activity in the first two sessions. The present study showed that CWI was an effective treatment after exercise-induced muscle damage. It enhanced anti-inflammatory response, decreased reactive species production, increased cell viability, and promoted redox balance, which could decrease the time for the recovery process.

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Section: Discussionmentioning

confidence: 99%

Cryotherapy: biochemical alterations involved in reduction of damage induced by exhaustive exercise

Furtado

Hartmann

Martins

et al. 2018

Braz J Med Biol Res

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“…Ascending from the NTS, the vagus reaches the parabrachial nucleus, thalamus, paraventricular nucleus, amygdala, hippocampus, insula, anterior cingulate cortex, and the PFC [173]. Chronic systemic/neuroinflammation may cause synaptic transmission perturbation and attenuate multitude of efferent signaling pathways from the dysfunctional NTS [170,[174][175][176][177][178][179]. A dysfunctional NTS would be deleterious to a multitude of CNS foci and body systems that have reciprocal projection to this nucleus.…”

Section: Nucleus Of the Solitary Tract (Nts)mentioning

confidence: 99%

Dysfunctional Nucleus Tractus Solitarius: Its Crucial Role in Promoting Neuropathogentic Cascade of Alzheimer’s Dementia—A Novel Hypothesis

Daulatzai

2012

Neurochem Res

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The pathophysiological mechanism(s) underlying Alzheimer's disease (AD) still remain unclear, and no disease-modifying or prophylactic therapies are currently available. Unraveling the fundamental neuropathogenesis of AD is an important challenge. Several studies on AD have suggested lesions in a number of CNS areas including the basal forebrain, hippocampus, entorhinal cortex, amygdale/insula, and the locus coeruleus. However, plausible unifying studies on the upstream factors that involve these heterogeneous regions and herald the onset of AD pathogenesis are not available. The current article presents a novel nucleus tractus solitarius (NTS) vector hypothesis that underpins several disparate biological mechanisms and neural circuits, and identifies relevant hallmarks of major presumptive causative factor(s) linked to the NTS, in older/aging individuals. Aging, obesity, infection, sleep apnea, smoking, neuropsychological states, and hypothermia-all activate inflammatory cytokines and oxidative stress. The synergistic impact of systemic proinflammatory mediators activates microglia and promotes neuroinflammation. Acutely, the innate immune response is protective defending against pathogens/toxins; however, when chronic, it causes neuroinflammation and neuronal dysfunction, particularly in brainstem and neocortex. The NTS in the brainstem is an essential multiple signaling hub, and an extremely important central integration site of baroreceptor, chemoreceptor, and a multitude of sensory afferents from gustatory, gastrointestinal, cardiac, pulmonary, and upper airway systems. Owing to persistent neuroinflammation, the dysfunctional NTS exerts deleterious impact on nucleus ambiguus, dorsal motor nucleus of vagus, hypoglossal, parabrachial, locus coeruleus and many key nuclei in the brainstem, and the hippocampus, entorhinal cortex, prefrontal cortex, amygdala, insula, and basal forebrain in the neocortex. The neuronal and synaptic dysfunction emanating from the inflamed NTS may affect its interconnected pathways impacting almost the entire CNS--which is already primed by neuroinflammation, thus promoting cognitive and neuropsychiatric symptoms. The upstream factors discussed here may underpin the neuropathopgenesis of AD. AD pathology is multifactorial; the current perspective underscores the value of attenuating disparate upstream factors--in conjunction with anticholinesterase, anti-inflammatory, immunosuppressive, and anti-oxidant pharmacotherapy. Amelioration of the NTS pathology may be of central importance in countering the neuropathological cascade of AD. The NTS, therefore, may be a potential target of novel therapeutic strategies.

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“…64,65 Rodents subjected to stressful stimuli such as chronic mild stress have shown elevated levels of interleukin (IL) 1b, IL-6 and tumor necrosis factor-alpha (TNF-a), indicating changes in the immune system. 62 Moreover, our group found increased TNF-a and IL-b levels in the serum and CSF of maternally deprived rats. By contrast, this same animal model of depression induced reduction of serum IL-10 levels.…”

Section: Animal Models Of Depressionmentioning

confidence: 67%

“…56 The administration of classical antidepressants reverses stress-induced biochemical and behavioral changes. 42,[57][58][59][60][61] The animal models of depression induced by different stressful stimuli (chronic mild stress, maternal deprivation, and restraint stress) reproduce alterations in the immune system, 42,62,63 another pathophysiological aspect found in depressive patients. 64 Classical antidepressants can improve mood and response to treatment in these individuals.…”

Section: Animal Models Of Depressionmentioning

confidence: 99%

Contributions of animal models to the study of mood disorders

Valvassori

Budni

Varela

et al. 2013

Rev. Bras. Psiquiatr.

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Mood disorders are a leading cause of morbidity and mortality, yet their underlying pathophysiology remains unclear. Animal models serve as a powerful tool for investigating the neurobiological mechanisms underlying psychiatric disorders; however, no animal model developed to date can fully mimic the ''corresponding'' human psychiatric disorder. In this scenario, the development of different animal models contributes to our understanding of the neurobiology of these disorders and provides the possibility of preclinical pharmacologic screening. The present review seeks to provide a comprehensive overview of traditional and recent animal models, recapitulating different features and the possible pathologic mechanisms of mood disorders emulated by these models.

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Chronic Variable Stress Alters Inflammatory and Cholinergic Parameters in Hippocampus of Rats

Cited by 37 publications

References 66 publications

Cryotherapy: biochemical alterations involved in reduction of damage induced by exhaustive exercise

Cryotherapy: biochemical alterations involved in reduction of damage induced by exhaustive exercise

Dysfunctional Nucleus Tractus Solitarius: Its Crucial Role in Promoting Neuropathogentic Cascade of Alzheimer’s Dementia—A Novel Hypothesis

Contributions of animal models to the study of mood disorders

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