scholarly journals Enhanced synthesis of brain-derived neurotrophic factor in the lesioned peripheral nerve: different mechanisms are responsible for the regulation of BDNF and NGF mRNA.

1992 ◽  
Vol 119 (1) ◽  
pp. 45-54 ◽  
Author(s):  
M Meyer ◽  
I Matsuoka ◽  
C Wetmore ◽  
L Olson ◽  
H Thoenen
Keyword(s):  
Sciatic Nerve ◽  
Schwann Cells ◽  
Neurotrophic Factor ◽  
Time Course ◽  
Interleukin 1 ◽  
Brain Derived Neurotrophic Factor ◽  
Mrna Levels ◽  
Bdnf Mrna ◽  
Rat Sciatic Nerve ◽  
Cultured Schwann Cells

Nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) are molecules which regulate the development and maintenance of specific functions in different populations of peripheral and central neurons, amongst them sensory neurons of neural crest and placode origin. Under physiological conditions NGF is synthesized by peripheral target tissues, whereas BDNF synthesis is highest in the CNS. This situation changes dramatically after lesion of peripheral nerves. As previously shown, there is a marked rapid increase in NGF mRNA in the nonneuronal cells of the damaged nerve. The prolonged elevation of NGF mRNA levels is related to the immigration of activated macrophages, interleukin-1 being the most essential mediator of this effect. Here we show that transsection of the rat sciatic nerve also leads to a very marked increase in BDNF mRNA, the final levels being even ten times higher than those of NGF mRNA. However, the time-course and spatial pattern of BDNF mRNA expression are distinctly different. There is a continuous slow increase of BDNF mRNA starting after day 3 post-lesion and reaching maximal levels 3-4 wk later. These distinct differences suggest different mechanisms of regulation of NGF and BDNF synthesis in non-neuronal cells of the nerve. This was substantiated by the demonstration of differential regulation of these mRNAs in organ culture of rat sciatic nerve and Schwann cell culture. Furthermore, using bioassays and specific antibodies we showed that cultured Schwann cells are a rich source of BDNF- and ciliary neurotrophic factor (CNTF)-like neurotrophic activity in addition to NGF. Antisera raised against a BDNF-peptide demonstrated BDNF-immunoreactivity in pure cultured Schwann cells, but not in fibroblasts derived from sciatic nerve.

scholarly journals Time of Day and Length of Antidepressant Drug Administration Influence Brain-Derived Neurotrophic Factor and TrkB Levels in Rat Brain

2009 ◽  
Vol 3 (1) ◽  
pp. 1-8
Author(s):  
Megan E. Kozisek ◽  
Nidal M. Qutna ◽  
David B. Bylund
Keyword(s):  
Drug Treatment ◽  
Neurotrophic Factor ◽  
Antidepressant Treatment ◽  
Antidepressant Drug ◽  
Brain Derived Neurotrophic Factor ◽  
Time Of Day ◽  
Mrna Levels ◽  
Bdnf Mrna ◽  
Adult Rats ◽  
Antidepressant Drug Treatment

The expression of brain-derived neurotrophic factor (BDNF) mRNA and protein and its primary receptor, TrkB mRNA shows circadian oscillations in adult rats; however it has been unclear if juvenile rats also display a similar pattern in circadian oscillations. We determined the levels of BDNF and TrkB mRNA and of BDNF protein at four separate time points during a 24 hperiod in the hippocampus and frontal cortex. The expression of BDNF and TrkB undergoes diurnal oscillation in adult and postnatal day 21 rats, but no significant variation is present in postnatal day 13 rats. Antidepressant drug treatment also is known to influence BDNF and TrkB levels. However, the reported effects of antidepressant drug treatment on BDNF and TrkB are highly variable and may be influenced by multiple factors, including detection method, class of antidepressant drug, and length of administration. BDNF mRNA levels were decreased significantly in the hippocampus after acute desipramine (a tricyclic antidepressant) treatment compared to control. BDNF mRNA and protein levels, as well as TrkB mRNA levels, were unchanged in adult rats after subchronic and chronic treatment with either desipramine or escitalopram (a selective serotonin reuptake inhibitor) and treatment consistent with several reports in the literature. This study defines several important factors that must be taken into account when comparing BDNF and TrkB levels both within and among studies.

scholarly journals Synthesis and localization of ciliary neurotrophic factor in the sciatic nerve of the adult rat after lesion and during regeneration.

1992 ◽  
Vol 118 (1) ◽  
pp. 139-148 ◽  
Author(s):  
M Sendtner ◽  
K A Stöckli ◽  
H Thoenen
Keyword(s):  
Sciatic Nerve ◽  
Schwann Cells ◽  
Neurotrophic Factor ◽  
Immunohistochemical Analysis ◽  
Ciliary Neurotrophic Factor ◽  
Immunohistochemical Localization ◽  
Biologically Active ◽  
Nerve Lesion ◽  
Mrna Levels ◽  
Western Blots

Ciliary neurotrophic factor (CNTF) is expressed in high quantities in Schwann cells of peripheral nerves during postnatal development of the rat. The absence of a hydrophobic leader sequence and the immunohistochemical localization of CNTF within the cytoplasm of these cells indicate that the factor might not be available to responsive neurons under physiological conditions. However, CNTF supports the survival of a variety of embryonic neurons, including spinal motoneurons in culture. Moreover we have recently demonstrated that the exogenous application of CNTF protein to the lesioned facial nerve of the newborn rat rescued these motoneurons from cell death. These results indicate that CNTF might indeed play a major role in assisting the survival of lesioned neurons in the adult peripheral nervous system. Here we demonstrate that the CNTF mRNA and protein levels and the manner in which they are regulated are compatible with such a function in lesioned peripheral neurons. In particular, immunohistochemical analysis showed significant quantities of CNTF at extracellular sites after sciatic nerve lesion. Western blots and determination of CNTF biological activity of the same nerve segments indicate that extracellular CNTF seems to be biologically active. After nerve lesion CNTF mRNA levels were reduced to less than 5% in distal regions of the sciatic nerve whereas CNTF bioactivity decreased to only one third of the original before-lesion levels. A gradual reincrease in Schwann cells occurred concomitant with regeneration.

Three markers of adult non-myelin-forming Schwann cells, 217c(Ran-1), A5E3 and GFAP: development and regulation by neuron-Schwann cell interactions

Development ◽  
1990 ◽  
Vol 109 (1) ◽  
pp. 91-103 ◽  
Author(s):  
K.R. Jessen ◽  
L. Morgan ◽  
H.J. Stewart ◽  
R. Mirsky
Keyword(s):  
Sciatic Nerve ◽  
Schwann Cell ◽  
Schwann Cells ◽  
Cell Signalling ◽  
Surface Proteins ◽  
Developmental Changes ◽  
Rat Sciatic Nerve ◽  
Ngf Receptor ◽  
Cultured Schwann Cells ◽  
Do So

Immunohistochemical methods are used to investigate in detail the development and regulation of three proteins (217c(Ran-1), A5E3 and GFAP) specifically associated with adult non-myelin-forming Schwann cells in the rat sciatic nerve, from embryo day 15 to maturity. 217c(Ran-1), which is probably the NGF-receptor, and A5E3 are expressed by the majority of cells in the nerve at embryo day 15 and by essentially all cells at embryo day 18. GFAP first appears at embryo day 18; this is an intrinsically programmed developmental event which occurs in cultured Schwann cells even in the absence of serum. Postnatally, the expression of 217c(Ran-1), A5E3 and GFAP is suppressed in cells that form myelin but retained in non-myelin-forming Schwann cells. Mature myelin-forming cells nevertheless maintain the potential to express all three proteins but will only do so if removed from contact with myelinated axons. In neuron-free cultures Schwann cells express all three proteins. This work, together with our previous observations on N-CAM, shows that removal of a diverse set of surface proteins and a change in intermediate filament expression is one of the major consequences of axon to Schwann cell signalling during myelination in the rat sciatic nerve. Unlike myelin-forming cells, adult non-myelin-forming Schwann cells remain very similar to embryonic and newborn cells with respect to expression of surface proteins, in contrast to the previously established developmental changes that occur in their surface lipids.

Regulation of neurofibromin expression in rat sciatic nerve and cultured Schwann cells

Glia ◽  
1995 ◽  
Vol 15 (1) ◽  
pp. 22-32 ◽  
Author(s):  
Lawrence Wrabetz ◽  
Maria Laura Feltri ◽  
Haesun Kim ◽  
Maryellen Daston ◽  
John Kamholz ◽  
...  
Keyword(s):  
Sciatic Nerve ◽  
Schwann Cells ◽  
Rat Sciatic Nerve ◽  
Cultured Schwann Cells

scholarly journals Brain-derived neurotrophic factor enhances spontaneous sleep in rats and rabbits

1999 ◽  
Vol 276 (5) ◽  
pp. R1334-R1338 ◽  
Author(s):  
Tetsuya Kushikata ◽  
Jidong Fang ◽  
James M. Krueger
Keyword(s):  
Growth Factors ◽  
Neurotrophic Factor ◽  
Brain Temperature ◽  
Brain Derived Neurotrophic Factor ◽  
Normal Brain ◽  
Sprague Dawley ◽  
Sleep Regulation ◽  
Bdnf Mrna ◽  
Sprague Dawley Rats ◽  
Intracerebroventricular Injections

Various growth factors are involved in sleep regulation. Brain-derived neurotrophic factor (BDNF) belongs to the neurotrophin family; it and its receptors are found in normal brain. Furthermore, cerebral cortical levels of BDNF mRNA have a diurnal variation and increase after sleep deprivation. Therefore, we investigated whether BDNF would promote sleep. Twenty-four male Sprague-Dawley rats (320–380 g) and 25 male New Zealand White rabbits (4.5–5.5 kg) were surgically implanted with electroencephalographic (EEG) electrodes, a brain thermistor, and a lateral intracerebroventricular cannula. The animals were injected intracerebroventricularly with pyrogen-free saline and, on a separate day, one of the following doses of BDNF: 25 or 250 ng in rabbits; 10, 50, or 250 ng in rats. The EEG, brain temperature, and motor activity were recorded for 23 h after the intracerebroventricular injections. BDNF increased time spent in non-rapid eye movement sleep (NREMS) in rats and rabbits and REMS in rabbits. Current results provide further evidence that various growth factors are involved in sleep regulation.

Dose-related effects of venlafaxine on pCREB and brain-derived neurotrophic factor (BDNF) in the hippocampus of the rat by chronic unpredictable stress

2011 ◽  
Vol 23 (1) ◽  
pp. 20-30 ◽  
Author(s):  
Jing-Jing Li ◽  
Yong-Gui Yuan ◽  
Gang Hou ◽  
Xiang-Rong Zhang
Keyword(s):  
Neurotrophic Factor ◽  
Sucrose Solution ◽  
Brain Derived Neurotrophic Factor ◽  
Rat Hippocampus ◽  
Antidepressant Effect ◽  
High Dose ◽  
Sprague Dawley ◽  
Bdnf Mrna ◽  
Adult Rat ◽  
Element Binding Protein

Background: The molecular pathogenesis of depression and psychopharmacology of antidepressants remain elusive. Recent hypotheses suggest that changes in neurogenesis and plasticity may underlie the aetiology of depression. The hippocampus is affected by depression and shows neuronal remodelling during adulthood.Objective: The present study on the adult rat hippocampus, was to evaluate the dose-related effects of chronic venlafaxine on the expression of brain-derived neurotrophic factor (BDNF) and phosphorylated cyclic-AMP response element binding protein (pCREB).Methods: Sprague-Dawley rats were exposed to a variety of chronic unpredictable stressors (CUSs) to establish a depression model. Rats were treated for either 14 or 28 days with venlafaxine (5 and 10 mg/kg, respectively). The hippocampal expression of pCREB and BDNF mRNA and protein was assessed by using immunohistochemistry, western blotting and reverse transcription polymerase chain reaction (RT-PCR).Results: Rats subjected to CUS procedure consumed less sucrose solution compared with non-stressed rats. The CUS influenced exploratory activity resulting in a reduction of the motility counts. Chronic low dose (5 mg/kg, 14 and 28 days), but not high dose (10 mg/kg, 14 and 28 days) of venlafaxine treatment increased the expression of pCREB and BDNF mRNA and protein in the CUS rat hippocampus.Conclusion: Neuronal plasticity-associated proteins such as pCREB and BDNF play an important role both in stress-related depression and in antidepressant effect.

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