Amygdala stimulation promotes recovery of behavioral performance in a spatial memory task and increases GAP-43 and MAP-2 in the hippocampus and prefrontal cortex of male rats

Mercerón‐Martínez, Daymara; Almaguer‐Melian, William; Alberti‐Amador, Esteban; Bergado, Jorge A.

doi:10.1016/j.brainresbull.2018.06.008

Cited by 8 publications

(13 citation statements)

References 54 publications

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“…The present results were largely supported by the findings of other groups, which demonstrated that exercise accelerated CBF (Pianta et al, 2019), decreased infarct volume (Tian et al, 2013;Pan et al, 2020) and improved functional outcomes (Pianta et al, 2019). In contrast, a few studies have reported no neuroprotective effects of exercise on the neurological deficit and infarct volume after stroke within 3 days (Matsuda et al, 2011;Cui et al, 2020). Future studies are necessary to fully elucidate the effect of post-stroke exercise on brain injury.…”

Section: Discussionsupporting

confidence: 88%

“…PSD-95 is constituent of the postsynaptic membrane that plays a key role in the plasticity and structure of the excitatory chemical synapse (Wu et al, 2017), and multiple studies have associated physical exercise with its induction (Jung and Kim, 2017;Pan et al, 2017). A series of studies have shed light on the relationship between these factors by demonstrating that BDNF/NGF participate in promoting neuroplasticity for motor rehabilitation after focal cerebral infarction (Matsuda et al, 2011;Mang et al, 2013); BDNF was reported to be induced by exercise, and may regulate the expression of synaptic proteins including GAP-43 (Liu W. et al, 2018), SYN (Ferreira et al, 2011), PSD-95 and Tau (Kerling et al, 2017). This research indicates that synaptic plasticity after stroke is determined, at least in part, by the induction and upregulation of axonal or synaptic proteins that, in our study, were found to be increased in both exercise cohorts.…”

Section: Discussionmentioning

confidence: 99%

“…BDNF is an abundant growth factor that is involved in activity-induced neuroplasticity and is upregulated in the animal brain by exercise. The regulation of neuroplasticity depends on a complex set of interactions between a variety of neural proteins, including postsynaptic density 95 (PSD-95; Wang et al, 2019 ), synapsin I (SYN; Pan et al, 2017 ), growth-associated protein 43 (GAP-43), and microtubule-associated protein (also known as Tau; Biundo et al, 2018 ; Mercerón-Martínez et al, 2018 ; Pu et al, 2019 ). Changes in these neuroplastic factors are related to exercise-induced activation of BDNF (Kim and Leem, 2016 ; Belviranli and Okudan, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

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In Search of a Dose: The Functional and Molecular Effects of Exercise on Post-stroke Rehabilitation in Rats

Huber

et al. 2020

Front. Cell. Neurosci.

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Although physical exercise has been demonstrated to augment recovery of the post-stroke brain, the question of what level of exercise intensity optimizes neurological outcomes of post-stroke rehabilitation remains unsettled. In this study, we aim to clarify the mechanisms underlying the intensity-dependent effect of exercise on neurologic function, and thereby to help direct the clinical application of exercisebased neurorehabilitation. To do this, we used a well-established rat model of ischemic stroke consisting of cerebral ischemia induction through middle cerebral artery occlusion (MCAO). Ischemic rats were subsequently assigned either to a control group entailing post-stroke rest or to one of two exercise groups distinguished by the intensity of their accompanying treadmill regimens. After 24 h of reperfusion, exercise was initiated. Infarct volume, apoptotic cell death, and neurological defects were quantified in all groups at 3 days, and motor and cognitive functions were tracked up to day-28. Additionally, Western blotting was used to assess the influence of our interventions on several proteins related to synaptogenesis and neuroplasticity (growth-associated protein 43, a microtubule-associated protein, postsynaptic density-95, synapsin I, hypoxia-inducible factor-1α, brain-derived neurotrophic factor, nerve growth factor, tyrosine kinase B, and cAMP response element-binding protein). Our results were in equal parts encouraging and surprising. Both mild and intense exercise significantly decreased infarct volume, cell death, and neurological deficits. Motor and cognitive function, as determined using an array of tests such as beam balance, forelimb placing, and the Morris water maze, were also significantly improved by both exercise protocols. Interestingly, while an obvious enhancement of neuroplasticity proteins was shown in both exercise groups, mild exercise rats demonstrated a stronger effect on the expressions of Tau (p < 0.01), brain-derived neurotrophic factor (p < 0.01), and tyrosine kinase B (p < 0.05). These findings contribute to the growing body of literature regarding the positive effects of both mild and intense long-term treadmill exercise on brain injury, functional outcome, and

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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In Search of a Dose: The Functional and Molecular Effects of Exercise on Post-stroke Rehabilitation in Rats

Huber

et al. 2020

Front. Cell. Neurosci.

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“…In previous papers, we have provided consistent data that FF-lesion provokes an almost complete hippocampal cholinergic denervation (Almaguer-Melian et al, 2003;Almaguer-Melian et al, 2005;Almaguer-Melian et al, 2006;Almaguer-Melian et al, 2015;Jas, Almaguer, Frey, & Bergado, 2000;Merceron-Martinez et al, 2013;Merceron-Martinez et al, 2016;Mercerón-Martínez et al, 2018), which is evidenced by the loss of AChE staining. Additionally, lesioned animals display a severe impairment in spatial memory in the MWM, (Almaguer-Melian et al, 2003;Almaguer-Melian et al, 2005;Almaguer-Melian et al, 2015;de Bruin, Moita, de Brabander, & Joosten, 2001;Cassel et al, 1998;Merceron-Martinez et al, 2013;Merceron-Martinez et al, 2016;Mercerón-Martínez et al, 2018). Interestingly, FF-lesion also affects Long-Term Potentiation (LTP), which is considered a cellular model for memory (Bergado, Moreno, & Nuñez, 1996;Bergado, Moreno, Soto, Castellano, & Castillo, 1997;Buzsáki and Gage, 1989).…”

Section: F I G U R Esupporting

confidence: 78%

Amygdala stimulation ameliorates memory impairments and promotes c‐Fos activity in fimbria‐fornix‐lesioned rats

Mercerón‐Martínez

Almaguer‐Melian

Alberti‐Amador

et al. 2020

Synapse

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In a series of studies, we have identified the basolateral amygdala (BLA) as a key player mediating affective modulation of LTP. The electrical stimulation of the BLA during a time window around the induction of LTP prolongs an Early-LTP into a Late-LTP (Frey et al., 2001) while the transient or permanent inactivation of the BLA abolishes the effect of behavioral reinforcers (Almaguer-Melian, Martinez-Marti, Frey, &

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“…Evidence-Based Complementary and Alternative Medicine downregulation of MMP-2/9, VEGF, and HIF-1α. Further to this, previous evidence has shown that the upregulation of Map-2 and GAP-43 promoted dendrite branching and synaptogenesis [67]. Similarly, this study has suggested that LSZ possesses neural restoration effects.…”

supporting

confidence: 74%

Longshengzhi Capsules Improve Ischemic Stroke Outcomes and Reperfusion Injury via the Promotion of Anti‐Inflammatory and Neuroprotective Effects in MCAO/R Rats

Yang

Zhang

Chen

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Stroke is the leading cause of death in the elderly. Traditional Chinese medicine provides an exciting strategy for treating stroke. Previous reports indicated that Longshengzhi capsules (LSZ), a modified Chinese formula, reduced formed thrombi and oxidative stress and were promising in the clinical treatment of ischemic stroke. However, the specific therapeutic effect and mechanism of LSZ are still ambiguous. This study aimed to define the effects of LSZ on proinflammatory mediators and neuroprotective effects on middle cerebral artery occlusion and refusion (MCAO/R) rats. Rats were treated with different doses of LSZ (0.54, 1.62, and 4.32 g/(kg·d)) in a week after model building. LSZ could improve the survival rate, ischemic stroke outcome, and infarct volume. In addition, significant decrease was observed in reactive oxygen species (ROS) levels and inflammatory factor levels in LSZ-treated groups, concomitant with increase in activities of superoxide dismutase (SOD), neurosynaptic remodeling, and decrease in brain edema. It is proposed that LSZ has anti-inflammatory and neuroprotective effects resulting in downregulating matrix metalloproteinase 2/9 (MMP-2/9) and vascular endothelial growth factor (VEGF) and nuclear factor kappa-B (NF-κB) and upregulating microtubule-associated protein-2 (Map-2) and growth-associated protein-43 (GAP-43) via p38 MAPK and HIF-1α signaling pathways in MCAO/R rats. This study provides potential evidences that p38 MAPK and HIF-1α/VEGF signaling pathways play significant roles in the anti-inflammatory and neuroprotective effects of LSZ.

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Amygdala stimulation promotes recovery of behavioral performance in a spatial memory task and increases GAP-43 and MAP-2 in the hippocampus and prefrontal cortex of male rats

Cited by 8 publications

References 54 publications

In Search of a Dose: The Functional and Molecular Effects of Exercise on Post-stroke Rehabilitation in Rats

In Search of a Dose: The Functional and Molecular Effects of Exercise on Post-stroke Rehabilitation in Rats

Amygdala stimulation ameliorates memory impairments and promotes c‐Fos activity in fimbria‐fornix‐lesioned rats

Longshengzhi Capsules Improve Ischemic Stroke Outcomes and Reperfusion Injury via the Promotion of Anti‐Inflammatory and Neuroprotective Effects in MCAO/R Rats

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