The induction of LTP increases BDNF and NGF mRNA but decreases NT-3 mRNA in the dentate gyrus

Ċastrén, Eero; Pitkänen, Mikko R. A.; Sirviö, Jouni; Parsadanian, Alexander; Lindholm, Dan; Thoenen, H.; Riekkinen, Paavo

doi:10.1097/00001756-199307000-00014

Cited by 294 publications

(142 citation statements)

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“…Whereas both BDNF mRNA and protein levels increase in the hippocampus following epileptiform activity, investigations have also shown similar results under a variety of more physiological experimental conditions. Stimulation patterns capable of inducing LTP also increase BDNF mRNA in the hippocampus (Patterson et al 1992;Castren et al 1993). Interestingly, it has been found that bioelectrical activity in general regulates BDNF mRNA levels.…”

Section: Environmental Interactions Modulate Bdnf Expression In the Hmentioning

confidence: 98%

“…Furthermore, spatial training in a complex environment not only improved performance in hippocampal-dependent spatial tasks, but also increased spine density in basal dendrites of hippocampal CA1 pyramidal neurons (Moser et al 1994(Moser et al , 1997. With an intriguing similarity, the induction of LTP in the hippocampus not only increases BDNF mRNA expression (Patterson et al 1992;Castren et al 1993;Dragunow et al 1993), but also increases spine density (Trommald et al 1996), the appearance of new spines (Engert and Bonhoeffer 1999;Maletic-Savatic et al 1999), and/or the formation of multiple spine synapses (Toni et al 1999). Interestingly, NTs themselves are capable of exerting morphological effects on axons (Gallo and Letourneau 1998) and dendrites (McAllister et al 1995) similar to those following the induction of hippocampal LTP.…”

Section: Bdnf/trkb Signaling Mediates Morphological Plasticity In Hipmentioning

confidence: 99%

“…Induction of LTP increases BDNF mRNA levels in hippocampal and dentate neurons (Patterson et al 1992;Castren et al 1993;Dragunow et al 1993;Bramham et al 1996). Furthermore, LTP induction is impaired at CA3-CA1 synapses of hippocampal slices from BDNF knockout mice, despite normal basal synaptic transmission (Korte et al 1995;Patterson et al 1996;Pozzo-Miller et al 1999).…”

Section: The Effects Of Bdnf/trkb Signaling Modulate Ltp and Nmda Recmentioning

confidence: 99%

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From Acquisition to Consolidation: On the Role of Brain-Derived Neurotrophic Factor Signaling in Hippocampal-Dependent Learning

Tyler¹,

Alonso²,

Bramham³

et al. 2002

Learn. Mem.

624

398

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One of the most rigorously investigated problems in modern neuroscience is to decipher the mechanisms by which experience-induced changes in the central nervous system are translated into behavioral acquisition, consolidation, retention, and subsequent recall of information. Brain-derived neurotrophic factor (BDNF) has recently emerged as one of the most potent molecular mediators of not only central synaptic plasticity, but also behavioral interactions between an organism and its environment. Recent experimental evidence indicates that BDNF modulates synaptic transmission and plasticity by acting across different spatial and temporal domains. BDNF signaling evokes both short-and long-term periods of enhanced synaptic physiology in both pre-and postsynaptic compartments of central synapses. Specifically, BDNF/TrkB signaling converges on the MAP kinase pathway to enhance excitatory synaptic transmission in vivo, as well as hippocampal-dependent learning in behaving animals. Emerging concepts of the intracellular signaling cascades involved in synaptic plasticity induced through environmental interactions resulting in behavioral learning further support the contention that BDNF/TrkB signaling plays a fundamental role in mediating enduring changes in central synaptic structure and function. Here we review recent literature showing the involvement of BDNF/TrkB signaling in hippocampal-dependent learning paradigms, as well as in the types of cellular plasticity proposed to underlie learning and memory.

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Section: Environmental Interactions Modulate Bdnf Expression In the Hmentioning

confidence: 98%

Section: Bdnf/trkb Signaling Mediates Morphological Plasticity In Hipmentioning

confidence: 99%

Section: The Effects Of Bdnf/trkb Signaling Modulate Ltp and Nmda Recmentioning

confidence: 99%

See 1 more Smart Citation

From Acquisition to Consolidation: On the Role of Brain-Derived Neurotrophic Factor Signaling in Hippocampal-Dependent Learning

Tyler¹,

Alonso²,

Bramham³

et al. 2002

Learn. Mem.

624

398

View full text Add to dashboard Cite

show abstract

“…BDNF, the most widely distributed growth factor within the brain, has profound influences on the survival and function of several neurotransmitter systems. The expression of BDNF is responsive to a variety of stimuli which enhance neuronal activity (Boatell et al 1992;Castrén et al 1993;Gall 1993;Gwag and Springer 1993). In our Institute, general physical exercise has been shown to lead to rapid increases in rat hippocampal BDNF mRNA levels (Neeper et al 1995(Neeper et al , 1996, opening the possibility that this physiological behavior can lead to enhanced trophic support in key brain areas.…”

mentioning

confidence: 93%

Exercise, Antidepressant Medications, and Enhanced Brain Derived Neurotrophic Factor Expression

Russo-Neustadt

Beard

Cotman

1999

Neuropsychopharmacology

353

192

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Physical activity and antidepressant treatment have each separately been of significant interest for the management of Alzheimer's disease (AD);In recent years, great strides have been made in understanding the regulation of growth factors at the molecular level. We report, for the first time, an apparent interaction between two distinct interventions, a pharmacological agent and a behavioral change, leading to a potentiation of brain-derived neurotrophic factor (BDNF) expression. As discussed below, this observation may have important applications to neurodegenerative/behavioral disorder treatment investigation and development.

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“…BDNF was originally identified as a neurotrophin that plays key roles in development of the nervous system, and has since been shown that BDNF and the high affinity BDNF receptor trkB are widely expressed in neurons throughout the brain and spinal cord (158). BDNF levels have been shown to be increase upon LTP induction (28) and BDNF promotes changes at dendritic spine structure (157). Suppression of BDNF production can block dendritic structural changes (157), and mice lacking BDNF in their forebrain neurons exhibit impaired LTP (89,90) and learning and memory (59).…”

Section: Molecular Mechanisms Of Adaptive Responses To Oxidative Stressmentioning

confidence: 99%

Impaired Adaptive Cellular Responses to Oxidative Stress and the Pathogenesis of Alzheimer's Disease

Texel

Mattson

2011

Antioxidants & Redox Signaling

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As is generally true with other age-related diseases, Alzheimer's disease (AD) involves oxidative damage to cellular components in the affected tissue, in this case the brain. The causes and consequences of oxidative stress in neurons in AD are not fully understood, but considerable evidence points to important roles for accumulation of amyloid b-peptide upstream of oxidative stress and perturbed cellular Ca 2+ homeostasis and energy metabolism downstream of oxidative stress. The identification of mutations in the b-amyloid precursor protein and presenilin-1 as causes of some cases of early onset inherited AD, and the development of cell culture and animal models based on these mutations has greatly enhanced our understanding of the AD process, and has greatly expanded opportunities for preclinical testing of potential therapeutic interventions. In this regard, and of particular interest to us, is the elucidation of adaptive cellular stress response pathways (ACSRP) that can counteract multiple steps in the AD neurodegenerative cascades, thereby limiting oxidative damage and preserving cognitive function. ACSRP can be activated by factors ranging from exercise and dietary energy restriction, to drugs and phytochemicals. In this article we provide an overview of oxidative stress and AD, with a focus on ACSRP and their potential for preventing and treating AD. Antioxid. Redox Signal. 14, 1519-1534.

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The induction of LTP increases BDNF and NGF mRNA but decreases NT-3 mRNA in the dentate gyrus

Cited by 294 publications

References 0 publications

From Acquisition to Consolidation: On the Role of Brain-Derived Neurotrophic Factor Signaling in Hippocampal-Dependent Learning

From Acquisition to Consolidation: On the Role of Brain-Derived Neurotrophic Factor Signaling in Hippocampal-Dependent Learning

Exercise, Antidepressant Medications, and Enhanced Brain Derived Neurotrophic Factor Expression

Impaired Adaptive Cellular Responses to Oxidative Stress and the Pathogenesis of Alzheimer's Disease

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