Chapter 6 Regulation of brain-derived neurotrophic factor mRNA levels in hippocampus by neuronal activity

Ċastrén, Eero; Berninger, Benedikt; Leingärtner, Axel; Lindholm, Dan

doi:10.1016/s0079-6123(08)64007-8

Cited by 83 publications

(55 citation statements)

References 27 publications

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“…However, the present results indicate that hippocampal and cortical neurons quickly regain their responsiveness to ampakines upon washout of the drugs; i.e., a 24-h drugfree period was sufficient to restore the full effect of ampakine treatment on BDNF expression. Previous results demonstrated that BDNF mRNA levels decline (Ϫ40%) between 12 and 24 h after the onset of continuous ampakine treatment , suggesting that the refractory period occurs well in advance of 24 h. Indeed, refractory mechanisms probably emerge hours before the decline in BDNF mRNA is detected but are masked by the half-life of BDNF transcripts (estimated as 0.5 to 2.5 h for longer and shorter transcripts, respectively, Sano et al, 1996;Castren et al, 1998). Thus, it is likely the refractory state develops during the 24-h drug-on intervals and reverses during the 24-h drug-off periods.…”

Section: Discussionmentioning

confidence: 99%

Chronic Elevation of Brain-Derived Neurotrophic Factor by Ampakines

Lauterborn

Truong²,

Baudry³

et al. 2003

J Pharmacol Exp Ther

124

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The ampakine CX614 positively modulates ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor-gated currents and increases brain-derived neurotrophic factor (BDNF) expression. In rat hippocampal slice cultures, CX614 rapidly increases BDNF gene expression but with time, mRNA levels fall despite the continued presence of active drug. The present study examined this apparent refractory period and the possibility that spaced ampakine treatments could sustain elevated BDNF protein levels. In cultured hippocampal slices, CX614, a second ampakine CX546, and the cholinergic agonist carbachol each increased BDNF mRNA levels with acute (3-h) treatment. After 4-day pretreatment with CX614, fresh ampakine (CX614 or CX546) did not induce BDNF mRNA, whereas carbachol did. Western blots confirmed that after an extended period of ampakine treatment, AMPA receptor protein levels are indeed reduced, suggesting that with longer treatments receptor down-regulation mediates ampakine insensitivity. Finally, using a "24-h on/24-h off" CX614 treatment protocol, the ampakine refractory state was circumvented, BDNF mRNA was induced with each ampakine application, and elevated BDNF protein levels were maintained through 5 days in vitro. These results suggest that spaced ampakine treatments can be used to sustain elevated neurotrophin levels and to test the utility of this manipulation for neuroprotection by endogenous neurotrophins.

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Section: Discussionmentioning

confidence: 99%

Chronic Elevation of Brain-Derived Neurotrophic Factor by Ampakines

Lauterborn

Truong²,

Baudry³

et al. 2003

J Pharmacol Exp Ther

124

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“…This most probably occurs because BDNF gene expression is induced with very brief increases in neuronal activity (seconds) (Castren et al, 1998) after which mRNA levels remain elevated for hours and elevated BDNF protein levels persist for days (Gall and Lauterborn, 2000). Combining these features results in a system in which a transient increase in EPSPs can quickly increase BDNF mRNA levels for hours and BDNF protein content for days.…”

Section: Modulatorsmentioning

confidence: 99%

Synaptic plasticity in early aging

Lynch

Rex

Gall

2006

Ageing Research Reviews

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Studies of how aging affects brain plasticity have largely focused on old animals. However, deterioration of memory begins well in advance of old age in animals, including humans; the present review is concerned with the possibility that changes in synaptic plasticity, as found in the long-term potentiation (LTP) effect, are responsible for this. Recent results indicate that impairments to LTP are in fact present by early middle age in rats but only in certain dendritic domains. The search for the origins of these early aging effects necessarily involves ongoing analyses of how LTP is induced, expressed, and stabilized. Such work points to the conclusion that cellular mechanisms responsible for LTP are redundant and modulated both positively and negatively by factors released during induction of potentiation. Tests for causes of the localized failure of LTP during early aging suggest that the problem lies in excessive activity of a negative modulator. The view of LTP as having redundant and modulated substrates also suggests a number of approaches for reversing age-related losses. Particular attention will be given to the idea that induction of brain-derived neurotrophic factor, an extremely potent positive modulator, can be used to provide long periods of normal plasticity with very brief pharmacological interventions. The review concludes with a consideration of how the selective, regional deficits in LTP found in early middle age might be related to the global phenomenon of brain aging. #

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“…n.s., non significant. duced by electrolytic lesion or kainic acid strongly increase BDNF mRNA in adult hippocampus and cortex (for review see Castrén et al 1998). Furthermore, ischemia induces BDNF expression in brain regions outside the ischemic area (Kokaia et al 1995).…”

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

254

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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Chapter 6 Regulation of brain-derived neurotrophic factor mRNA levels in hippocampus by neuronal activity

Cited by 83 publications

References 27 publications

Chronic Elevation of Brain-Derived Neurotrophic Factor by Ampakines

Chronic Elevation of Brain-Derived Neurotrophic Factor by Ampakines

Synaptic plasticity in early aging

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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