Effects of brain-derived neurotrophic factor and neurotrophin-3 on expression of mRNAs encoding c-Fos, neuropeptides and glutamic acid decarboxylase in cultured spinal neurons

Kim, Hyo-Sin; Lee, Sang-Ji; Kim, Dong–Sun; Cho, Hee-Jung

doi:10.1097/00001756-200011270-00053

Cited by 21 publications

(17 citation statements)

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“…According with our results, the up-regulation of the BDNF mature protein has been observed in the ACC during inflammatory pain. 27 In this view, our results suggest that the interplay between BDNF and dynorphin may also occur in an in vivo model of neuropathic pain, precisely at cortical level. Relative gene expression was calculated by the Delta-Delta Ct (DDCt) method and normalized to the reference gene Gapdh.…”

Section: Discussionmentioning

confidence: 56%

“…[19][20][21] The brain-derived neurotrophic factor (BDNF) is an important modulator of neuropathic pain. 27 Neuroimaging studies revealed that morphological and functional changes are induced by neuropathic pain in several brain regions. 24,25 Moreover, rats subjected to chronic constriction injury (CCI) showed typical neuropathic pain signs, together with a higher BDNF immunoreactivity in the ipsilateral dorsal horn.…”

mentioning

confidence: 99%

“…[28][29][30] Plastic alterations developing after nerve injury involve cortical and subcortical structures, such as the thalamus (TH) and the brainstem (BS). Because of the relationship between BDNF and dynorphin in spinal neurons, 27 the expression levels of the brain-derived neurotrophic factor gene (Bdnf ) were also measured in the areas where Pdyn and Oprk1 gene expression was found to be altered. This evidence suggests that alterations of the functional connectivity in the corticostriatal circuitry are implicated in the transition from acute to chronic pain.…”

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confidence: 99%

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Dynorphinergic system alterations in the corticostriatal circuitry of neuropathic mice support its role in the negative affective component of pain

Palmisano

Caputi

Mercatelli

et al. 2018

Genes Brain and Behavior

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The dynorphinergic system is involved in pain transmission at spinal level, where dynorphin exerts antinociceptive or pronociceptive effects, based on its opioid or non-opioid actions. Surprisingly, little evidence is currently available concerning the supraspinal role of the dynorphinergic system in pain conditions. The present study aimed to investigate whether neuropathic pain is accompanied by prodynorphin (Pdyn) and κ-opioid receptor (Oprk1) gene expression alterations in selected mouse brain areas. To this end, mice were subjected to chronic constriction injury of the right sciatic nerve and neuropathic pain behavioral signs were ascertained after 14 days. At this interval, a marked increase in Pdyn mRNA in the anterior cingulate cortex (ACC) and prefrontal cortex (PFC) was observed. Oprk1 gene expression was increased in the PFC, and decreased in the ACC and nucleus accumbens (NAc). No changes were observed in the other investigated regions. Because of the relationship between dynorphin and the brain-derived neurotrophic factor, and the role of this neurotrophin in chronic pain-related neuroplasticity, we investigated brain-derived neurotrophic factor gene (Bdnf) expression in the areas showing Pdyn or Oprk1 mRNAs changes. Bdnf mRNA levels were increased in both the ACC and PFC, whereas no changes were assessed in the NAc. Present data indicate that the dynorphinergic system undergoes quite selective alterations involving the corticostriatal circuitry during neuropathic pain, suggesting a contribution to the negative affective component of pain. Moreover, parallel increases in Pdyn and Bdnf mRNA at cortical level suggest the occurrence of likely interactions between these systems in neuropathic pain maladaptive neuroplasticity.

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Section: Discussionmentioning

confidence: 56%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Dynorphinergic system alterations in the corticostriatal circuitry of neuropathic mice support its role in the negative affective component of pain

Palmisano

Caputi

Mercatelli

et al. 2018

Genes Brain and Behavior

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“…Furthermore, NT-3 has been shown to induce c-fos (Marsh & Palfrey, 1996;Nonomura et al, 1996), with a time-course relevant to our study. More specifically, in neuronal cultures treated with NT-3 the levels of c-fos mRNA had increased by 3 hr and the increase was maintained up to 6 hr (Bilsland & Harper, 1998;Kim, Lee, Kim, & Cho, 2000). Another possible molecule that could mediate the increase in Fos expression may be the transcription factor pCREB, the increase of which precedes that of Fos, being observed at 4 hr following ''handling'' on PND1 (Garoflos, Stamatakis, Mantelas, Philippidis, & Stylianopoulou, 2005).…”

Section: Discussionmentioning

confidence: 99%

Neonatal handling on the first postnatal day leads to increased maternal behavior and fos levels in the brain of the newborn rat

Garoflos

Stamatakis

Rafrogianni

et al. 2008

Developmental Psychobiology

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In the present work we employed Fos expression, an index of neuronal activity, to identify brain areas activated by a single exposure to "neonatal handling" on postnatal Day 1. Eight hours following "handling" there was an increase in the number of Fos positive cells in the hippocampus, the parietal and occipital cortex. We also recorded maternal behavior during the 8 hr following "handling." "Handled" pups received increased maternal licking during the 4 hr following the end of "handling." Furthermore, the number of Fos positive cells detected in each of the three brain areas 8 hr following "handling" was positively correlated with the amount of licking up to 8 hr following "handling." These results indicate that the increased maternal care could underlie the handling-induced increase in Fos. The Fos protein, acting as a transcription factor, controls the expression of downstream genes, whose products may mediate the effects of "neonatal handling" on the developing rat brain.

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“…Interneuron development is considered neurotrophin-dependent as many cells express trkB receptors (Gorba & Wahle, 1999). TrkB signalling promotes, in particular, interneuronal synaptogenesis (Huang et al, 1999;Marty et al, 2000;Seil & Drake-Baumann, 2000) and in¯uences inhibitory markers, as in dissociated cultures of cortex, striatum, substantia nigra and spinal cord, GAD-67 mRNA expression, GAD activity and GABA uptake are increased by trkB ligands (Widmer & Hefti, 1994;Carnahan & Nawa, 1995 for review;Spenger et al, 1995;Arenas et al, 1996;Kim et al, 2000). Furthermore, neuronal activity regulates cortical inhibitory markers.…”

Section: Introductionmentioning

confidence: 99%

Neuronal activity and neurotrophic factors regulate GAD‐65/67 mRNA and protein expression in organotypic cultures of rat visual cortex

Patz

Wirth

Gorba

et al. 2003

Eur J of Neuroscience

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Environmental factors are known to regulate the molecular differentiation of neocortical interneurons. Their class-defining transmitter synthetic enzymes are the glutamic acid decarboxylases (GAD); yet, fairly little is known about the developmental regulation of transcription and translation of the GAD-65/67 isoforms. We have characterized the role of neuronal activity, neurotrophins and afferent systems for GAD-65/67 expression in visual cortex in organotypic cultures (OTC) compared with in vivo in order to identify cortex-intrinsic regulatory mechanisms. Spontaneously active OTC prepared at postnatal day 0 displayed from 10 days in vitro (DIV) onwards 12-14% GAD-65/GAD-67 neurons similar to in vivo. However, GAD-65 mRNA was higher, whereas GAD-67 protein was lower, than in vivo. During the first week neurotrophins increased whereas the Trk receptor inhibitor K252a and MEK inhibitors decreased both GAD mRNAs and proteins. After 10 DIV GAD expression no longer depended on neurotrophin signalling. Activity-deprived OTC revealed only 6% GAD-67 neurons and mRNA and protein were reduced by 50%. GAD-65 mRNA was less reduced, but protein was reduced by half, suggesting translational regulation. Upon recovery of activity GAD mRNAs, cell numbers, and both proteins quickly returned to normal and these 'adult' levels were resistant to late-onset deprivation. In 20 DIV activity-deprived OTC, only neurotrophin 4 increased GAD-65/67 mRNAs, rescued the percentage of GAD-67 neurons and increased both proteins in a TrkB-dependent manner. Activity deprivation had thus shifted the period of neurotrophin sensitivity to older ages. The results suggested neuronal activity as a major regulator differentially affecting transcription and translation of the GAD isoforms. The early presence of neuronal activity promoted the GAD expression in OTC to a neurotrophin-independent state suggesting that neurotrophins play a context-dependent role.

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Effects of brain-derived neurotrophic factor and neurotrophin-3 on expression of mRNAs encoding c-Fos, neuropeptides and glutamic acid decarboxylase in cultured spinal neurons

Cited by 21 publications

References 2 publications

Dynorphinergic system alterations in the corticostriatal circuitry of neuropathic mice support its role in the negative affective component of pain

Dynorphinergic system alterations in the corticostriatal circuitry of neuropathic mice support its role in the negative affective component of pain

Neonatal handling on the first postnatal day leads to increased maternal behavior and fos levels in the brain of the newborn rat

Neuronal activity and neurotrophic factors regulate GAD‐65/67 mRNA and protein expression in organotypic cultures of rat visual cortex

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