scholarly journals Effect of the aerobic exercise and the environmental enrichment on the reduction of the anxiety levels in the aging

Author(s):  
Patricia Sampedro

The environmental enrichment (EE) and the aerobic exercise (EX) are interventions capable of reducing anxiety levels in the aging, but few is known about how they modulating the projections to the hypothalamic-pituitary axis (HPA). We studied the effect of an EE and EX programs carried out during two months in 18 month-old Wistar rats assigned to 3 groups: (CO, N=6), EE (N=8) y EX (N=8). The EX program was carried out during 15min/day and the EE group was housed in a big cage with different objects frequently changed. Through the cytochrome c oxidase histochemistry (COx), we analysed the metabolic activity of several brain regions involved in the anxiety response. The EE reduced the brain activity of regions involved in the activation of the HPA axis (infralimbic cortex, basolateral amygdala and the hypothalamic paraventricular nucleus (p<0.05). On the other hand, the EX program increased the activity of brain regions involved in the inhibition of the HPA axis (cingulate cortex, bed nucleus of the stria terminalis and the dorsal hippocampus (p<0.05). In conclusion, it seemed that the EE and the EX modulate in different way the activity of brain regions that project to the HPA axis and they could constitute successful interventions to reduce the anxiety levels in the aging.

Author(s):  
Patricia Sampedro

The environmental enrichment (EE) and the aerobic exercise (EX) are interventions capable of reducing anxiety levels in the aging, but few is known about how they modulating the projections to the hypothalamic-pituitary axis (HPA). We studied the effect of an EE and EX programs carried out during two months in 18 month-old Wistar rats assigned to 3 groups: (CO, N=6), EE (N=8) y EX (N=8). The EX program was carried out during 15min/day and the EE group was housed in a big cage with different objects frequently changed. Through the cytochrome c oxidase histochemistry (COx), we analysed the metabolic activity of several brain regions involved in the anxiety response. The EE reduced the brain activity of regions involved in the activation of the HPA axis (infralimbic cortex, basolateral amygdala and the hypothalamic paraventricular nucleus (p<0.05). On the other hand, the EX program increased the activity of brain regions involved in the inhibition of the HPA axis (cingulate cortex, bed nucleus of the stria terminalis and the dorsal hippocampus (p<0.05). In conclusion, it seemed that the EE and the EX modulate in different way the activity of brain regions that project to the HPA axis and they could constitute successful interventions to reduce the anxiety levels in the aging.


2021 ◽  
Vol 22 (7) ◽  
pp. 3695
Author(s):  
Johannes Kornhuber ◽  
Iulia Zoicas

Neuropeptide Y (NPY) has anxiolytic-like effects and facilitates the extinction of cued and contextual fear in rodents. We have previously shown that the intracerebroventricular administration of NPY reduces the expression of social fear in a mouse model of social fear conditioning (SFC). In the present study, we aimed to identify the brain regions that mediate these effects of NPY. We show that NPY (0.1 nmol/0.2 µL/side) reduces the expression of SFC-induced social fear in a brain-region-dependent manner. In more detail, NPY reduced the expression of social fear when administered into the dorsolateral septum (DLS) and central amygdala (CeA), but not when administered into the dorsal hippocampus (DH), medial amygdala (MeA) and basolateral amygdala (BLA). We also investigated whether the reduced expression of social fear might partly be due to a reduced anxiety-like behavior, and showed that NPY exerted anxiolytic-like effects when administered into the DH, DLS, CeA and BLA, but not when administered into the MeA. This study identifies the DLS and the CeA as brain regions mediating the effects of NPY on the expression of social fear and suggests that partly distinct neural circuitries mediate the effects of NPY on the expression of social fear and on anxiety-like behavior.


2019 ◽  
Author(s):  
Hugo Cruces-Solis ◽  
Olga Babaev ◽  
Heba Ali ◽  
Carolina Piletti Chatain ◽  
Vasyl Mykytiuk ◽  
...  

AbstractInhibitory synaptic transmission plays a key role in the circuits underlying anxiety behaviors, but the network mechanisms by which disruptions in synaptic inhibition contribute to pathological anxiety processing remain largely unknown. Here we addressed this question in mice lacking the inhibitory synapse-specific adhesion protein Neuroligin-2 (Nlgn2), which display widespread reduction in inhibitory synaptic transmission as well as a pronounced anxiety phenotype. To investigate how the lack of synaptic inhibition alters the communication between key brain regions in anxiety processing, we recorded local field potentials (LFPs) simultaneously from a network of brain regions involved in anxiety processing, including the basolateral amygdala (BLA), centromedial amygdala, bed nucleus of the stria terminalis, prefrontal cortex and ventral hippocampus (vHPC). We found that LFP power in the vHPC was profoundly increased while vHPC-directed theta frequency synchrony was disrupted in Nlgn2 KO mice under anxiogenic conditions. Instead, deletion of Nlgn2 increased beta frequency synchrony across the anxiety network, and the theta / beta synchrony ratio strongly predicted anxiety behaviors in an open field paradigm. Local deletion of Nlgn2 in the vHPC and BLA revealed that they encode distinct aspects of the anxiety phenotype of the Nlgn2 KO mice, with vHPC linked to anxiety induced freezing and BLA linked to reduction in exploratory activity. Together, our data demonstrate that alterations in long-range functional connectivity link synaptic inhibition to abnormal anxiety behaviors, and that Nlgn2 KO mice represent an interesting model to study the role of inhibitory synaptic transmission in the circuits underlying anxiety disorders.


2021 ◽  
Vol 46 (4) ◽  
pp. E459-E471
Author(s):  
Alessandra Matzeu ◽  
Rémi Martin-Fardon

Background: Orexin-A (OrxA) administration in the posterior paraventricular nucleus of the thalamus (pPVT) reinstates extinguished cocaine-seeking behaviour following extended access to the drug (a model of dependence). The pPVT receives and integrates information associated with emotionally salient events and sends excitatory inputs to brain regions involved in the expression of emotional states, such as those driving cocaine-seeking behaviour (i.e., the nucleus accumbens, the central nucleus of the amygdala [CeA], the basolateral amygdala, the bed nucleus of the stria terminalis [BNST] and the prefrontal cortex). Methods: We monitored the activation pattern of these regions (measured by Fos) during cocaine-seeking induced by OrxA administered to the pPVT. The BNST and CeA emerged as being selectively activated. To test whether the functionality of these regions was pivotal during OrxA-induced cocaine-seeking behaviour, we transiently inactivated these regions concomitantly with OrxA administration to the pPVT. We then tested the participation of corticotropin-releasing factor receptors (CRF1) in the CeA during OrxA-induced cocaine-seeking using the CRF1 antagonist CP154526. Results: We observed selective activation of the CeA and BNST during cocaine-seeking induced by OrxA administered to the pPVT, but only transient inactivation of the CeA prevented cocaine-seeking behaviour. Administration of CP154526 to the CeA prevented OrxAinduced cocaine-seeking behaviour. Limitations: The use of only male rats could have been a limitation. Other limitations could have been the use of an indirect approach to test the hypothesis that administration of OrxA to the pPVT drives cocaine-seeking via CRF1 signalling in the CeA, and a lack of analysis of the participation of CeA subregions. Conclusion: Cocaine-seeking behaviour induced by OrxA administered to the pPVT is driven by activation of the CeA via CRF1 signalling.


2022 ◽  
Author(s):  
Ana Rocio Conde-Moro ◽  
Florbela Rocha-Almeida ◽  
Elias Gebara ◽  
Jose Maria Delgado-Garcia ◽  
Carmen Sandi ◽  
...  

Social behaviors such as cooperation are crucial for mammals. A deeper knowledge of the neuronal mechanisms underlying cooperation can be beneficial for people suffering from pathologies with impaired social behavior. Our aim was to study the brain activity when two animals synchronize their behavior to obtain a mutual reinforcement. In a previous work, we showed that the activity of the prelimbic cortex (PrL) was enhanced during cooperation in rats, especially in the ones leading most cooperative trials (leader rats). In this study, we investigated the specific cell type/s in the PrL contributing to cooperative behaviors. To this end, we collected rats' brains at key moments of the learning process to analyze the levels of c-FOS expression in the main cellular groups of the PrL (glutamatergic cells containing D1 and D2 receptors and interneurons). Leader rats showed increased c-FOS activity in cells expressing D1 receptors during cooperation. In addition, we analyzed the levels of anxiety, dominance, and locomotor behavior, finding that leader rats are in general less anxious and less dominant than followers. We also recorded local field potentials (LFPs) from the PrL, the nucleus accumbens septi (NAc), and the basolateral amygdala (BLA). Spectral analysis showed that delta activity in PrL and NAc increased when rats cooperated, while BLA activity in delta and theta bands decreased considerably during cooperation. The PrL and NAc also increased their connectivity in the high theta band during cooperation. Thus, the present work identifies the specific PrL cell types engaged in this behavior, as well as its connectivity with subcortical brain regions (BLA, NAc) during cooperation.


2014 ◽  
Vol 28 (3) ◽  
pp. 148-161 ◽  
Author(s):  
David Friedman ◽  
Ray Johnson

A cardinal feature of aging is a decline in episodic memory (EM). Nevertheless, there is evidence that some older adults may be able to “compensate” for failures in recollection-based processing by recruiting brain regions and cognitive processes not normally recruited by the young. We review the evidence suggesting that age-related declines in EM performance and recollection-related brain activity (left-parietal EM effect; LPEM) are due to altered processing at encoding. We describe results from our laboratory on differences in encoding- and retrieval-related activity between young and older adults. We then show that, relative to the young, in older adults brain activity at encoding is reduced over a brain region believed to be crucial for successful semantic elaboration in a 400–1,400-ms interval (left inferior prefrontal cortex, LIPFC; Johnson, Nessler, & Friedman, 2013 ; Nessler, Friedman, Johnson, & Bersick, 2007 ; Nessler, Johnson, Bersick, & Friedman, 2006 ). This reduced brain activity is associated with diminished subsequent recognition-memory performance and the LPEM at retrieval. We provide evidence for this premise by demonstrating that disrupting encoding-related processes during this 400–1,400-ms interval in young adults affords causal support for the hypothesis that the reduction over LIPFC during encoding produces the hallmarks of an age-related EM deficit: normal semantic retrieval at encoding, reduced subsequent episodic recognition accuracy, free recall, and the LPEM. Finally, we show that the reduced LPEM in young adults is associated with “additional” brain activity over similar brain areas as those activated when older adults show deficient retrieval. Hence, rather than supporting the compensation hypothesis, these data are more consistent with the scaffolding hypothesis, in which the recruitment of additional cognitive processes is an adaptive response across the life span in the face of momentary increases in task demand due to poorly-encoded episodic memories.


Author(s):  
A. F. Belyaev ◽  
G. E. Piskunova

Introduction. One of the main tools of an osteopath are soft tissue techniques, which have a number of particular qualities such as minimization of force and duration of indirect techniques with an emphasis on muscle and ligamentous structures; combination of gestures, tendency to maximal relaxation and exclusion of direct action on pathological symptoms such as tension, overtone and pain. Minimization of the force applied during the performance of soft tissue techniques often invites a question whether there are differences between the usual touch and the therapeutic touch of an osteopath.Goal of research - to reveal the changes in the bioelectrical activity of the cerebral cortex arising in the process of osteopathic treatment in order to prove its specifi city in comparison with nonspecifi c tactile stimulation (neutral touch).Materials and methods. 75 people were examined with the use of multiparameter analysis of multichannel EEG in different times. 25 patients were clinically healthy adults, whereas 50 patients had signs of somatic dysfunctions.Results. Computer encephalography permits to perceive the difference between the neutral touch and the therapeutic action. An identifi cation reaction is a response to the neutral touch (changes in brain bioelectrical activity with an increase in statistically signifi cant connections in the temporal lobes), whereas the therapeutic action provokes the state of purposeful brain activity during still point (intensifi cation of frontooccipital interactions).Conclusions. Osteopathic action causes additional tension in the processing of incoming information, which requires participation of different brain regions, including interhemispheric mechanisms associated with analysis, maintenance of attention and regulation of targeted activities.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Leonardo Santana Novaes ◽  
Letícia Morais Bueno-de-Camargo ◽  
Carolina Demarchi Munhoz

AbstractThe persistence of anxiety and the deficit of fear memory extinction are both phenomena related to the symptoms of a trauma-related disorder, such as post-traumatic stress disorder (PTSD). Recently we have shown that single acute restraint stress (2 h) in rats induces a late anxiety-related behavior (observed ten days after stress), whereas, in the present work, we found that the same stress impaired fear extinction in animals conditioned ten days after stress. Fourteen days of environmental enrichment (EE) prevented the deleterious effect of stress on fear memory extinction. Additionally, we observed that EE prevented the stress-induced increase in AMPA receptor GluA1 subunit phosphorylation in the hippocampus, but not in the basolateral amygdala complex and the frontal cortex, indicating a potential mechanism by which it exerts its protective effect against the stress-induced behavioral outcome.


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