Seizures and sensory stimulation result in different patterns of brain derived neurotrophic factor protein expression in the barrel cortex and hippocampus

Nanda, Steven A.; Mack, Kenneth J.

doi:10.1016/s0169-328x(00)00054-1

Cited by 45 publications

(26 citation statements)

References 52 publications

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“…Combined with our ChIP data, these results suggest that E 2 induces a transcriptionally permissive state at the Bdnf promoter within 30 min, which may increase levels of Bdnf transcripts and BDNF protein within 4 h. Evidence that BDNF is transcribed within 30-60 min and translated within 4-6 h is supported by other studies demonstrating that visual experience affects BDNF synthesis in visual cortex (Schwartz et al 2011) and that vibrissae stimulation affects BDNF synthesis in somatosensory cortex and hippocampus (Nanda and Mack 2000). Although protein changes in the order of hours could suggest regulation of the BDNF gene by classic genomic signaling through nuclear estrogen receptors at the BDNF ERE (Sohrabji et al 1995), the present data instead implicate rapid nonclassical epigenetic regulation of BDNF.…”

Section: Discussionsupporting

confidence: 85%

17β-Estradiol regulates histone alterations associated with memory consolidation and increases Bdnf promoter acetylation in middle-aged female mice

et al. 2014

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Histone acetylation is essential for hippocampal memory formation in young adult rodents. Although dysfunctional histone acetylation has been associated with age-related memory decline in male rodents, little is known about whether histone acetylation is altered by aging in female rodents. In young female mice, the ability of 17b-estradiol (E 2 ) to enhance object recognition memory consolidation requires histone H3 acetylation in the dorsal hippocampus. However, the extent to which histone acetylation is regulated by E 2 in middle-aged females is unknown. The mnemonic benefits of E 2 in aging females appear to be greatest in middle age, and so pinpointing the molecular mechanisms through which E 2 enhances memory at this age could lead to the development of safer and more effective treatments for maintaining memory function without the side effects of current therapies. Here, we show that dorsal hippocampal infusion of E 2 rapidly enhanced object recognition and spatial memory, and increased histone H3 acetylation in the dorsal hippocampus, while also significantly reducing levels of histone deacetylase (HDAC2 and HDAC3) proteins. E 2 specifically increased histone H3 acetylation at Bdnf promoters pII and pIV in the dorsal hippocampus of both young and middle-aged mice, despite age-related decreases in pI and pIV acetylation. Furthermore, levels of mature BDNF and pro-BDNF proteins in the dorsal hippocampus were increased by E 2 in middle-aged females. Together, these data suggest that the middle-aged female dorsal hippocampus remains epigenetically responsive to E 2 , and that E 2 may enhance memory in middle-aged females via epigenetic regulation of Bdnf.

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Section: Discussionsupporting

confidence: 85%

17β-Estradiol regulates histone alterations associated with memory consolidation and increases Bdnf promoter acetylation in middle-aged female mice

et al. 2014

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“…First, a number of NTs, including BDNF and NT-3, are known to be widely distributed in the cochlear nucleus (Hafidi, 1999;Lefebvre et al, 1994;Tierney et al, 2001) and are thought to exert a trophic influence on SGNs (Lefebvre et al, 1994). Second, neural activity -including patterned ES -is known to up-regulate the secretion of endogenous BDNF in various neurons by regulating the transcription of the BDNF gene (Balkowiec et al, 2000;Balkowiec et al, 2002;Gartner et al, 2002;Hansen et al, 2001a;Lever et al, 2001;Lu, 2003;Nanda et al, 2000;Rocamora et al, 1996;Tan et al, In Press). Thus chronic intracochlear ES could be expected to increase endogenous levels of BDNF in SGNs; this mechanism may contribute to the reduced SGN degeneration following ES reported in some studies.…”

Section: Discussionmentioning

confidence: 99%

Neurotrophins and electrical stimulation for protection and repair of spiral ganglion neurons following sensorineural hearing loss

2008

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Exogenous neurotrophins (NTs) have been shown to rescue spiral ganglion neurons (SGNs) from degeneration following a sensorineural hearing loss (SNHL). Furthermore, chronic electrical stimulation (ES) has been shown to retard SGN degeneration in some studies but not others. Since there is evidence of even greater SGN rescue when NT administration is combined with ES, we examined whether chronic ES can maintain SGN survival long after cessation of NT delivery. Young adult guinea pigs were profoundly deafened using ototoxic drugs; five days later they were unilaterally implanted with an electrode array and drug delivery system. Brain derived neurotrophic factor (BDNF) was continuously delivered to the scala tympani over a four week period while the animal simultaneously received ES via bipolar electrodes in the basal turn (i.e. turn 1) scala tympani. One cohort (n=5) received ES for six weeks (i.e. including a two week period after the cessation of BDNF delivery; ES 6 ); a second cohort (n=5) received ES for 10 weeks (i.e. a six week period following cessation of BDNF delivery; ES 10 ). The cochleae were harvested for histology and SGN density determined for each cochlear turn for comparison with normal hearing controls (n=4). The withdrawal of BDNF resulted in a rapid loss of SGNs in turns 2-4 of the deafened/BDNF-treated cochleae; this was significant as early as two weeks following removal of the NT when compared with normal controls (p<0.05). Importantly, there was not a significant reduction in SGNs in turn 1 (i.e. adjacent to the electrode array) two and six weeks after NT removal, as compared with normal controls. This result suggests that chronic ES can prevent the rapid loss of SGNs that occurs after the withdrawal of exogenous NTs. Implications for the clinical delivery of NTs are discussed.

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“…In the visual cortex, the expression of BDNF, but not NGF, in the visual cortex is regulated by visual inputs Schoups et al 1995;Pollock et al 2001), and monocular activity blockade elicits a striking decrease in BDNF mRNA and protein in the visual cortex corresponding the deprived eye (Bozzi et al 1995;Rossi et al 1999;Lein and Shatz 2000). Sensory stimulation of whiskers enhances the expression of BDNF in the barrel cortex (Rocamora et al 1996;Nanda and Mack 2000). Other physiologically relevant stimuli, such as physical activity and running (Neeper et al 1996;Oliff et al 1998;Russo-Neustadt et al 1999;…”

Section: Activity-dependent Bdnf Transcription and Local Translationmentioning

confidence: 99%

BDNF and Activity-Dependent Synaptic Modulation: Figure 1.

Lu¹

2003

Learn. Mem.

828

589

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It is widely accepted that neuronal activity plays a pivotal role in synaptic plasticity. Neurotrophins have emerged recently as potent factors for synaptic modulation. The relationship between the activity and neurotrophic regulation of synapse development and plasticity, however, remains unclear. A prevailing hypothesis is that activity-dependent synaptic modulation is mediated by neurotrophins. An important but unresolved issue is how diffusible molecules such as neurotrophins achieve local and synapse-specific modulation. In this review, I discuss several potential mechanisms with which neuronal activity could control the synapse-specificity of neurotrophin regulation, with particular emphasis on BDNF. Data accumulated in recent years suggest that neuronal activity regulates the transcription of BDNF gene, the transport of BDNF mRNA and protein into dendrites, and the secretion of BDNF protein. There is also evidence for activity-dependent regulation of the trafficking of the BDNF receptor, TrkB, including its cell surface expression and ligand-induced endocytosis. Further study of these mechanisms will help us better understand how neurotrophins could mediate activity-dependent plasticity in a local and synapse-specific manner.Much of the brain's ability to adapt or modify itself in response to experience and environment lies in the plasticity of synaptic connections, both short-and long-terms. Substantial evidence indicates that the number and the strength of synapses can be changed by neuronal activity (Bliss and Collingridge 1993;Linden 1994;Malenka and Nicoll 1999;McEwen 1999). It is now widely accepted that activity-dependent modulation of synapses is critical for brain development as well as many cognitive functions in the adult. Molecular mechanisms that translate patterns of neuronal activity into specific changes in the structures and function of synapses, however, remain largely unknown. A hypothesis was put forward several years ago that neurotrophins may serve as molecular mediators for synaptic plasticity based on two observations: (1) The expression of neurotrophins is regulated by neuroelectric activity; and (2) neurotrophins could modulate the efficacy of synaptic transmission or the growth of dendrites and axons, the structural elements necessary for synaptogenesis

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Seizures and sensory stimulation result in different patterns of brain derived neurotrophic factor protein expression in the barrel cortex and hippocampus

Cited by 45 publications

References 52 publications

17β-Estradiol regulates histone alterations associated with memory consolidation and increases Bdnf promoter acetylation in middle-aged female mice

17β-Estradiol regulates histone alterations associated with memory consolidation and increases Bdnf promoter acetylation in middle-aged female mice

Neurotrophins and electrical stimulation for protection and repair of spiral ganglion neurons following sensorineural hearing loss

BDNF and Activity-Dependent Synaptic Modulation: Figure 1.

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