Anterograde transport of endogenous brain-derived neurotrophic factor in hippocampal mossy fibers

Ma, Smith; Lx, Zhang; We, Lyons; La, Mamounas

doi:10.1097/00001756-199705260-00008

Cited by 114 publications

(53 citation statements)

References 10 publications

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“…In addition, antidepressant strategies which do not directly target the monoamine system, such as electroconvulsive shock therapy, transcranial magnetic stimulation, exercise and the novel a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor potentiators and N-methyl-D-aspartic acid (NMDA) antagonists, also increase mRNA or protein BDNF levels in the rat brain. 21,[41][42][43][44][45][46][47][48][49] Although the mechanisms involved in BDNF upregulation remain unknown, SSRI and NARI antidepressants have been reported to increase hippocampal levels of cyclic AMP response binding protein (CREB) in the rat, a nuclear transcription factor known to regulate BDNF expression. 32 …”

Section: Preclinical Evidencementioning

confidence: 99%

Is it time to reassess the BDNF hypothesis of depression?

2007

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The brain-derived neurotrophic factor (BDNF) hypothesis of depression postulates that a loss of BDNF is directly involved in the pathophysiology of depression, and that its restoration may underlie the therapeutic efficacy of antidepressant treatment. While this theory has received considerable experimental support, an increasing number of studies have generated evidence which is not only inconsistent, but also directly contradicts the hypothesis. This article provides a critical review of the clinical and preclinical studies which have been responsible for this controversy, outlining pharmacological, behavioural and genetic evidence which demonstrates the contrasting role of BDNF in regulating mood and antidepressant effects throughout the brain. I will also review key studies, both human and animal, which have investigated the association of a BDNF single-nucleotide polymorphism (Val66Met) with depression pathogenesis, and detail the number of inconsistencies which also afflict this novel area of BDNF research. The article will conclude by discussing why now is a critical time to reassess the original BDNF hypothesis of depression, and look towards the formation of new models that can provide a more valid account of the complex relationships between growth factors, mood disorders and their treatment.

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Section: Preclinical Evidencementioning

confidence: 99%

Is it time to reassess the BDNF hypothesis of depression?

2007

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“…Despite the fact that mRNA levels alone do not always represent protein levels, increases in the amount of BDNF protein have also been found in the hippocampus following seizure activity (Nawa et al 1995;Smith et al 1997;. 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.…”

Section: Environmental Interactions Modulate Bdnf Expression In the Hmentioning

confidence: 99%

“…Most experimental evidence indicates that hippocampal neurons release BDNF via the regulated pathway in an activity-dependent manner. BDNF immunoreactivity has been localized to large dense-core vesicles in hippocampal neurons (Fawcett et al 1997;Smith et al 1997;Haubensak et al 1998;Moller et al 1998). Recently, activity-dependent release of BDNF was shown using optical imaging of a BDNF-green fluorescence protein (GFP) fusion protein in transfected hippocampal neurons maintained in primary culture (Hartmann et al 2001;Kojima et al 2001).…”

Section: Bdnf and Memory Consolidationmentioning

confidence: 99%

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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“…Chronic ECS increases and prolongs the expression of BDNF and its receptor, trkB, in selected areas of rat brain, such as the granule cell layer of the dentate gyrus and the piriform cortex, as do various antidepressant drugs, but not other non-antidepressant psychotropic agents (Nibuya et al 1995;Smith et al 1997;Zetterström et al 1998). In addition, local infusion of high concentrations of BDNF into the midbrain has been reported to exert antidepressant effects in behavioral animal models of depression (Siuciak et al 1997).…”

Section: Chronic Rtms Treatment Increases Bdnf Expression In Specificmentioning

confidence: 99%

Long-Term Repetitive Transcranial Magnetic Stimulation Increases the Expression of Brain-Derived Neurotrophic Factor and Cholecystokinin mRNA, but not Neuropeptide Tyrosine mRNA in Specific Areas of Rat Brain

Müller

Toschi

Kresse

et al. 2000

Neuropsychopharmacology

252

107

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Repetitive transcranial magnetic stimulation (rTMS) is increasingly used as a therapeutic tool in various neurological and psychiatric disorders, and we recently found that it has a neuroprotective effect both in vitro andTranscranial magnetic stimulation (TMS), a technique in which a time-varying strong electric current is applied through a coil held in direct contact with the subject's head, was originally developed for diagnostic use in neurology (for review see Rossini and Rossi 1998). A possible effect of TMS on mood was first reported in 1987 (Bickford et al. 1987) and, although discussed controversially, to date several lines of evidence resulting from both preclinical (Fleischmann et al. 1995;Zyss et al. 1997) and clinical (e.g., Pascual-Leone et al. 1996) studies support the notion that repetitive TMS (rTMS) may have antidepressant properties: rTMS induces transient enhancement of mood in healthy subjects, and daily application alleviates symptoms in patients suffering from treatment-resistant major depression (for review see George et al. 1999).Although rTMS is currently being evaluated as a possible alternative or add-on therapy in the treatment of refractory depression, knowledge concerning its effects at the molecular and cellular level is still very limited. Recently, Ji et al. (1998) reported a specific activation of brain regions in terms of immediate early gene expression in rats in response to rTMS. In addition, we provided a first evidence for a neuroprotective effect of long-term rTMS in vivo and in vitro (Post et al. 1999). The in vitro studies showed that magnetic stimulation analogous to TMS increased the overall viability of mouse monoclonal hippocampal HT22 cells and had a neuroprotective effect against oxidative stressors such as amyloid beta (A ␤ ) and glutamate. Moreover, the treatment increased the release of the potentially neuroprotective secreted amyloid precursor protein (sAPP) into the supernatant of HT22 cells and into cerebrospinal fluid from rats. Accordingly, HT22 cells preincubated with cerebrospinal fluid from long-term rTMStreated rats were found to be protected against A ␤ (Post et al. 1999). However, the neurochemical mechanisms underlying these neuroprotective properties as well as the putative therapeutic effects of rTMS in neurological and psychiatric disorders still remain to be elucidated.Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family and is abundantly expressed in the adult brain. The neurotrophic and also neuroprotective effects of BDNF have been characterized extensively both in vitro and in vivo. In addition, upregulation of BDNF has been implicated in neuronal responses to various kinds of injuries, such as epileptic seizures, cerebral ischemia, and hypoglycemia (for review see Connor and Dragunow 1998). Recent work raised the possibility that one of the many long-term effects of antidepressant treatment may be regulation of neurotrophins: antidepressant drug treatment and electroconvulsive seizures (ECS) were shown to marke...

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Anterograde transport of endogenous brain-derived neurotrophic factor in hippocampal mossy fibers

Cited by 114 publications

References 10 publications

Is it time to reassess the BDNF hypothesis of depression?

Is it time to reassess the BDNF hypothesis of depression?

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

Long-Term Repetitive Transcranial Magnetic Stimulation Increases the Expression of Brain-Derived Neurotrophic Factor and Cholecystokinin mRNA, but not Neuropeptide Tyrosine mRNA in Specific Areas of Rat Brain

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