Deficits in LTP and recognition memory in the genetically hypertensive rat are associated with decreased expression of neurotrophic factors and their receptors in the dentate gyrus

Hennigan, Amy; Callaghan, Charlotte K.; Kealy, John; Rouine, Jennifer; Kelly, Aine Marie

doi:10.1016/j.bbr.2008.09.037

Cited by 43 publications

(30 citation statements)

References 41 publications

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“…It initiates various cell signaling pathways that are necessary for neuronal development, axonal growth, neurotransmission and synaptogenesis by activating its two types of membrane-bound receptors, TrkA (tropomyosin-related kinase A) and p75 receptors (p75NTR) (Kaplan and Miller, 2000;Patapoutian and Reichardt, 2001). It was suggested that acute stimulation with NGF enhance the glutamate release in rat cortical synaptosome (Knipper et al, 1994), treated NGF effectively reverse the cognitive decline in aged animals (Zou et al, 2002), genetic deletion of NGF or anti-NGF blocking induced the deficits in memory (Chen et al, 1997) and LTP induction (Hennigan et al, 2009). Moreover, decreased level of NGF is correlated with the dementia extent of Alzheimer's disease (AD) (Gelfo et al, 2011) and supplement of NGF reverse the memory deficits in AD patients (Gu et al, 2009).…”

Section: Introductionmentioning

confidence: 98%

NGF promotes long-term memory formation by activating poly(ADP-ribose)polymerase-1

et al. 2012

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Section: Introductionmentioning

confidence: 98%

NGF promotes long-term memory formation by activating poly(ADP-ribose)polymerase-1

et al. 2012

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“…Therefore, the consequences of vascular risk factors for brain remodeling are incompletely understood. In spontaneously hypertensive rats, subtle reductions in brain concentrations of neurotrophic factors and their receptors (namely BDNF, neutrophins-3/4, TrkA, TrkB) have been noted in the dentate gyrus [85]. In focal cerebral ischemia, these alterations did not result in major disturbances of contralesional axonal sprouting in response to neutralizing NogoA antibody treatment, enabling neurological recovery in a way that is very similar to that in non-hypertensive rats [17].…”

Section: Challenges For Neurorestorative Therapiesmentioning

confidence: 99%

Promoting Neurological Recovery in the Post-Acute Stroke Phase: Benefits and Challenges

Hermann

Chopp

2014

Eur Neurol

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Background: Profound cellular and biochemical remodeling processes occur in the brain following an ischemic stroke, raising the possibility that we may be able to promote neurological recovery by harnessing the brain's endogenous recovery processes with pharmacological or cell-based therapies. There is a compelling body of evidence that cerebral plasticity and neurological recovery can be stimulated in the post-acute ischemic brain in this manner. Summary: This overview of neurorestorative therapies highlights the main challenges in their development, and summarizes the implications of these findings to stroke patients. Key Message: Neurorestorative therapies are a highly promising avenue of treatment for the restitution of neuronal networks damaged by stroke. Clinical Implications: The key supporting data have so far been obtained using in vivo models in animals, underscoring the need to validate these findings in humans. For human studies, several potentially confounding variables should be kept in mind, including age, and the presence of risk factors and comorbidities (such as hyperlipidemia and diabetes). Stroke patients vary considerably in age and genetic background, as well as in the etiology, localization and size of brain infarcts. The choice of patient population is a critical factor in the success of clinical trials, as patient heterogeneity could mask any potential therapeutic benefits.

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“…In rodent models, exercise has consistently been shown to enhance learning and persistently upregulate expression of brain-derived neurotrophic factor (BDNF) in the hippocampus [12][13][14][15][16]. The indisputable importance of the hippocampus in learning and memory and the role of BDNF in mediating hippocampal synaptic plasticity are well established [17][18][19][20]; while additional evidence indicates a role for insulin-like growth factor (IGF-1) in mediating the cognitive effects of exercise [21][22][23]. Interestingly, serum BDNF concentration has repeatedly been reported to increase following exercise in humans [9,[24][25][26] (for review see [27]), while IGF-1 responses to exercise are more variable [28][29][30].…”

Section: Accepted M Manuscriptmentioning

confidence: 99%

Aerobic exercise improves hippocampal function and increases BDNF in the serum of young adult males

Griffin

Mullally

Foley

et al. 2011

Physiology & Behavior

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324

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Physical activity has been reported to improve cognitive function in humans and rodents, possibly via a brain-derived neurotrophic factor (BDNF)-regulated mechanism. In this study of human subjects, we have assessed the effects of acute and chronic exercise on performance of a face-name matching task, which recruits the hippocampus and associated structures of the medial temporal lobe, and the Stroop word-colour task, which does not, and have assessed circulating concentrations of BDNF and IGF-1 in parallel. The results show that a short period of high-intensity cycling results in enhancements in performance of the face-name matching, but not the Stroop, task. These changes in cognitive function were paralleled by increased concentration of BDNF, but not IGF-1, in the serum of exercising subjects. 3 weeks of cycling training had no effect on cardiovascular fitness, as assessed by VO 2 scores, cognitive function, or serum BDNF concentration. Increases in fitness, cognitive function and serum BDNF response to acute exercise were observed following 5 weeks of aerobic training. These data indicate that both acute and chronic exercise improve medial temporal lobe function concomitant with increased concentrations of BDNF in the serum, suggesting a possible functional role for this neurotrophic factor in exercise-induced cognitive enhancement in humans.

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Deficits in LTP and recognition memory in the genetically hypertensive rat are associated with decreased expression of neurotrophic factors and their receptors in the dentate gyrus

Cited by 43 publications

References 41 publications

NGF promotes long-term memory formation by activating poly(ADP-ribose)polymerase-1

NGF promotes long-term memory formation by activating poly(ADP-ribose)polymerase-1

Promoting Neurological Recovery in the Post-Acute Stroke Phase: Benefits and Challenges

Aerobic exercise improves hippocampal function and increases BDNF in the serum of young adult males

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