INT66040

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Context Info
Confidence 0.69
First Reported 1996
Last Reported 2010
Negated 5
Speculated 1
Reported most in Body
Documents 114
Total Number 116
Disease Relevance 67.67
Pain Relevance 51.81

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

extracellular region (Bdnf) cytoplasmic membrane-bounded vesicle (Bdnf)
Anatomy Link Frequency
brain 21
hippocampus 12
neurons 7
PFC 5
dorsal horn 3
Bdnf (Mus musculus)
Pain Link Frequency Relevance Heat
Hippocampus 1203 100.00 Very High Very High Very High
Nerve growth factor 535 100.00 Very High Very High Very High
Dopamine 429 100.00 Very High Very High Very High
bDMF 426 100.00 Very High Very High Very High
amygdala 99 100.00 Very High Very High Very High
c fibre 12 100.00 Very High Very High Very High
substance P 12 100.00 Very High Very High Very High
Hsan 3 100.00 Very High Very High Very High
spinal dorsal horn 3 100.00 Very High Very High Very High
antidepressant 2768 99.98 Very High Very High Very High
Disease Link Frequency Relevance Heat
Hereditary Sensory And Autonomic Neuropathies 3 100.00 Very High Very High Very High
Familial Dysautonomia 1 100.00 Very High Very High Very High
Injury 256 99.98 Very High Very High Very High
Targeted Disruption 494 99.96 Very High Very High Very High
Suicidal Behaviour 2502 99.84 Very High Very High Very High
Neurodegenerative Disease 444 99.76 Very High Very High Very High
Colitis 2 99.70 Very High Very High Very High
Virus Diseases 94 99.68 Very High Very High Very High
Pain 69 99.66 Very High Very High Very High
Asthma 12 99.66 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Thus, the hippocampus and the spinal cord respond in distinct ways to wheel running and fluoxetine, and a prior induction of BDNF, IGF-1 or cytogenesis is unlikely to be the mechanism for wheel running providing a margin of protection against SCI.
Positive_regulation (induction) of BDNF in margin associated with frailty, hippocampus, fluoxetine and spinal cord
1) Confidence 0.69 Published 2007 Journal Neuroscience Section Abstract Doc Link 17137724 Disease Relevance 0.38 Pain Relevance 1.33
However, the overall observation was that all the antidepressants increased the level of total BDNF mRNA in the brain of corticosterone-treated rats.
Positive_regulation (increased) of BDNF in brain associated with antidepressant
2) Confidence 0.69 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2732010 Disease Relevance 0.57 Pain Relevance 1.00
However, upregulation of a molecular target of CREB, BDNF, is abolished in the CREB-deficient mice after chronic administration of DMI.
Positive_regulation (upregulation) of BDNF associated with desipramine
3) Confidence 0.64 Published 2002 Journal J. Neurosci. Section Abstract Doc Link 11943827 Disease Relevance 0.10 Pain Relevance 0.87
In inflammatory state of colitis, TNBS induced upregulation of BDNF in dorsal root ganglia of both genotypes while BDNF(+/-) mice showing significantly lower sensitivity in the colon at 30 mm Hg and lower sensitivity in bladder than BDNF(+/+) mice.
Positive_regulation (upregulation) of BDNF in colon associated with colitis and inflammation
4) Confidence 0.61 Published 2010 Journal Eur J Pain Section Abstract Doc Link 19932037 Disease Relevance 0.94 Pain Relevance 0.30
In summary, animal studies have shown that an increase in brain BDNF plays an important role in antidepressant action and that the antidepressant response is attenuated in mutant mice with BDNF deficit.
Positive_regulation (increase) of BDNF in brain associated with antidepressant
5) Confidence 0.61 Published 2010 Journal Psychiatry Investigation Section Body Doc Link PMC3022309 Disease Relevance 0.34 Pain Relevance 0.72
Similarly, increases in serum BDNF level by amitriptyline after 36 days, paroxetine after 4 or 8 weeks, or venalfaxine after 12 weeks of treatment to depressed patients were reported.145–147 Not only antidepressants but vagus nerve stimulation, repetitive transcranial magnetic stimulation,148 or electroconvulsive therapy149 to depressed patients also cause an increase in serum BDNF level in depressed patients.
Positive_regulation (increase) of BDNF in vagus nerve associated with antidepressant, transcranial magnetic stimulation, vagus nerve and endep
6) Confidence 0.60 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2732010 Disease Relevance 0.22 Pain Relevance 0.50
On the other hand, Gonul et al142 reported that depressed patients show increased BDNF level in serum after treatment with a variety of antidepressants for 8 weeks, including venalfaxine, sertraline, fluoxetine, paroxetine, and citalopram.
Positive_regulation (increased) of BDNF associated with antidepressant and fluoxetine
7) Confidence 0.60 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2732010 Disease Relevance 0.10 Pain Relevance 0.37
Similarly, increases in serum BDNF level by amitriptyline after 36 days, paroxetine after 4 or 8 weeks, or venalfaxine after 12 weeks of treatment to depressed patients were reported.145–147 Not only antidepressants but vagus nerve stimulation, repetitive transcranial magnetic stimulation,148 or electroconvulsive therapy149 to depressed patients also cause an increase in serum BDNF level in depressed patients.
Positive_regulation (increases) of BDNF in vagus nerve associated with antidepressant, transcranial magnetic stimulation, vagus nerve and endep
8) Confidence 0.60 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2732010 Disease Relevance 0.09 Pain Relevance 0.44
To examine how BDNF is regulated in response to antidepressants, we administered different classes of antidepressants (serotonin uptake blocker, fluoxetine, norepinephrine blocker, desipramine, monoamine oxidase inhibitor, or phenelzine) to healthy rats and examined whether antidepressants regulate the expression of BDNF via specific BDNF transcript(s).92 We observed very interesting results such that treatment of healthy rats with desipramine or phenelzine increased mRNA levels of total BDNF in both the frontal cortex and hippocampus, whereas fluoxetine increased the mRNA level of BDNF only in the hippocampus.92 More interestingly, when we examined the effects of antidepressants on the expression of individual exons containing BDNF transcripts, we found that desipramine specifically increased exons I and III in both the frontal cortex and hippocampus; fluoxetine increased only exon II in the hippocampus; and phenelzine effectively increased exons I and IV in the hippocampus but only exon I in the frontal cortex.
Positive_regulation (increased) of BDNF in hippocampus associated with desipramine, antidepressant, urological neuroanatomy, hippocampus, serotonin, monoamine and fluoxetine
9) Confidence 0.60 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2732010 Disease Relevance 0.27 Pain Relevance 1.37
They found that BDNF level was much lower in the midbrain (nonpreganglionic Edinger-Westphal nucleus) of male suicide subjects, whereas female suicide subjects showed an increased level of BDNF in this brain area, suggesting a possible sex effect in the regulation of BDNF expression in suicide subjects.
Positive_regulation (increased) of BDNF in brain associated with suicidal behaviour and midbrain
10) Confidence 0.60 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2732010 Disease Relevance 1.10 Pain Relevance 0.29
To examine how BDNF is regulated in response to antidepressants, we administered different classes of antidepressants (serotonin uptake blocker, fluoxetine, norepinephrine blocker, desipramine, monoamine oxidase inhibitor, or phenelzine) to healthy rats and examined whether antidepressants regulate the expression of BDNF via specific BDNF transcript(s).92 We observed very interesting results such that treatment of healthy rats with desipramine or phenelzine increased mRNA levels of total BDNF in both the frontal cortex and hippocampus, whereas fluoxetine increased the mRNA level of BDNF only in the hippocampus.92 More interestingly, when we examined the effects of antidepressants on the expression of individual exons containing BDNF transcripts, we found that desipramine specifically increased exons I and III in both the frontal cortex and hippocampus; fluoxetine increased only exon II in the hippocampus; and phenelzine effectively increased exons I and IV in the hippocampus but only exon I in the frontal cortex.
Positive_regulation (increased) of BDNF in hippocampus associated with desipramine, antidepressant, urological neuroanatomy, hippocampus, serotonin, monoamine and fluoxetine
11) Confidence 0.60 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2732010 Disease Relevance 0.27 Pain Relevance 1.30
We determined mRNA and protein expression of BDNF in the PFC (Brodmann’s area 9) and hippocampus from specimens obtained from 21 fully characterized suicide subjects and 27 nonpsychiatric healthy control subjects.181 We observed that mRNA level of BDNF was significantly reduced, independently and as a ratio to neuron-specific enolase (a housekeeping gene), in both the PFC and hippocampus of suicide subjects compared with nonpsychiatric healthy control subjects.
Positive_regulation (level) of BDNF in neuron associated with suicidal behaviour and hippocampus
12) Confidence 0.60 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2732010 Disease Relevance 1.48 Pain Relevance 0.35
We further examined whether antidepressants reverse the corticosterone-mediated decrease in BDNF and whether similar BDNF exons are involved in this mechanism by which antidepressants upregulate BDNF expression.92 We observed that long-term treatment with desipramine completely reversed the corticosterone-induced decrease in BDNF in both the frontal cortex and hippocampus.
Positive_regulation (upregulate) of BDNF in hippocampus associated with desipramine, antidepressant, urological neuroanatomy and hippocampus
13) Confidence 0.60 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2732010 Disease Relevance 0.32 Pain Relevance 0.88
There was a negative correlation between increase in BDNF level and decrease in Hamilton Depression Rating Scale score.
Positive_regulation (increase) of BDNF associated with depression
14) Confidence 0.60 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2732010 Disease Relevance 0.15 Pain Relevance 0.36
However, the cause and effect relationship among the induction of CREB and BDNF, the neurogenesis, and behavioral effects of antidepressants remains to be further investigated.
Positive_regulation (induction) of BDNF associated with antidepressant, neurodegenerative disease and bdmf
15) Confidence 0.57 Published 2010 Journal Mol Brain Section Body Doc Link PMC2848031 Disease Relevance 0.68 Pain Relevance 0.72
By contrast, the measured BDNF concentration was significantly increased to 92.4 ± 13.0 ng/ml (n = 3, P < 0.002) after 6 d exposure of cultures to medium containing 200 ng/ml BDNF.
Positive_regulation (increased) of BDNF associated with bdmf
16) Confidence 0.53 Published 2010 Journal Mol Pain Section Body Doc Link PMC2918544 Disease Relevance 0.07 Pain Relevance 0.57
Conversely, a chronic treatment with antidepressants not only enhances the BDNF level but also increases the stress resistance in animals [40,41].
Positive_regulation (enhances) of BDNF associated with stress, antidepressant and bdmf
17) Confidence 0.50 Published 2010 Journal Mol Brain Section Body Doc Link PMC2848031 Disease Relevance 0.81 Pain Relevance 0.68
Enhanced BDNF signaling is associated with an antidepressant-like behavioral response and changes in brain monoamines.
Positive_regulation (Enhanced) of BDNF in brain associated with antidepressant and monoamine
18) Confidence 0.49 Published 2005 Journal Cell. Mol. Neurobiol. Section Title Doc Link 16392030 Disease Relevance 0.23 Pain Relevance 0.51
The segregation of polymorphic alleles at and around loci for p75NGFR, TRKA, TRKB, BDNF, and familial dysautonomia (another hereditary sensory neuropathy having features in common with HSN II) virtually excluded these genes as the cause of HSN II in this family.
Positive_regulation (cause) of BDNF associated with familial dysautonomia and hsan
19) Confidence 0.49 Published 1996 Journal Pain Section Abstract Doc Link 8895241 Disease Relevance 0.56 Pain Relevance 0.40
docking sites (referred to as TrkBD mice) [13] results in a loss of vestibular neurons that is essentially indistinguishable from that of Trkb null mice (Trkb-/-), suggesting that the survival function of BDNF/TrkB is mediated predominantly through the cooperative action of these two docking sites, whereas the PLC?
Positive_regulation (mediated) of BDNF in neurons
20) Confidence 0.48 Published 2010 Journal BMC Dev Biol Section Body Doc Link PMC2964534 Disease Relevance 0 Pain Relevance 0

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