Noradrenergic stimulation of BDNF synthesis in astrocytes: Mediation via α1- and β1/β2-adrenergic receptors

Jurič, Damijana Mojca; Loncar, Darja; Carman-Krzan, M

doi:10.1016/j.neuint.2007.06.035

Cited by 101 publications

(69 citation statements)

References 64 publications

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“…Thus, we assessed the direct effects of monoamines on BDNF expression in cultured astrocytes. Consistent with previous research in astrocytes (43), noradrenalin increased BDNF mRNA expression (Fig. 6C).…”

Section: Discussionsupporting

confidence: 93%

Imipramine Induces Brain-Derived Neurotrophic Factor mRNA Expression in Cultured Astrocytes

et al. 2012

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Abstract. Depression is one of the most prevalent and livelihood-threatening forms of mental illnesses and the neural circuitry underlying depression remains incompletely understood. Recent studies suggest that the neuronal plasticity involved with brain-derived neurotrophic factor (BDNF) plays an important role in the recovery from depression. Some antidepressants are reported to induce BDNF expression in vivo; however, the mechanisms have been considered solely in neurons and not fully elucidated. In the present study, we evaluated the effects of imipramine, a classic tricyclic antidepressant drug, on BDNF expression in cultured rat brain astrocytes. Imipramine dose-dependently increased BDNF mRNA expression in astrocytes. The imipramine-induced BDNF increase was suppressed with inhibitors for protein kinase A (PKA) or MEK/ERK. Moreover, imipramine exposure activated transcription factor cAMP response element binding protein (CREB) in a dose-dependent manner. These results suggested that imipramine induced BDNF expression through CREB activation via PKA and/or ERK pathways. Imipramine treatment in depression might exert antidepressant action through BDNF production from astrocytes, and glial BDNF expression might be a target of developing novel antidepressants.

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Section: Discussionsupporting

confidence: 93%

Imipramine Induces Brain-Derived Neurotrophic Factor mRNA Expression in Cultured Astrocytes

et al. 2012

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“…There is evidence that a1 adrenergic receptors in astroglia produce long-ranging fast calcium waves which are blocked by adrenergic receptor a1 antagonists (Ding et al 2013). Also a1 adrenergic receptors are involved in the noradrenergic stimulation of brainderived neurotrophic factor (BDNF) synthesis in astrocytes (Juric et al 2008). Thus, ADRA1A/B-CXCR4 heteroreceptor complexes on astrocytes can have major consequences for function of neural-glial networks through CXCR4-mediated modulation of a1 receptor actions on long-distance astroglial communication of calcium waves and increased trophism through release of BDNF (Fuxe et al 2015).…”

Section: Discussionmentioning

confidence: 99%

The triplet puzzle theory indicates extensive formation of heteromers between opioid and chemokine receptor subtypes

Tarakanov

Fuxé

2015

J Neural Transm

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Biochemical studies had previously demonstrated examples of heteromerization between opioid and chemokine receptors. Based on the triplet puzzle theory, it has been discovered that opioid receptors are structurally more closely related to chemokine receptors than to other class A G-protein-coupled receptors. Their similarity is established in terms of the number of triplet homologies Asn-Leu-Ala, Thr-Leu-Pro, and Tyr-Ala-Phe in the amino acid code of extensive numbers of members of these two receptor groups. Such widespread similarities probably mean that many opioid and chemokine receptor subtypes utilize some of these mutual triplets to form heteromers. The findings underline that heteromerization among these two receptor groups can represent a major general mechanism for significant interactions between opioid peptides and chemokines in pain and neuroinflammation within the neural-glial networks of the CNS including immune cells.

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“…The nucleus together with the myelinated axon give rise to a signet ring configuration and a collar of cytoplasm external to the myelinated axon that are characteristic of Schwann cells. Scale bar=1 μm activates neuronal CREB [15] and may be released by astrocytes in which β 2 -receptors are activated by clenbuterol [20]. Another factor that can be released via astrocytic β 2 -receptor stimulation is IL-6 [26] which can directly promote axonal regeneration via gp130 receptors in the central nervous system [7].…”

Section: Discussionmentioning

confidence: 99%

“…Clenbuterol was used since it can cross the blood-brain barrier and stimulate neuronal β 2 -receptors thereby elevating cAMP levels that potentially can promote axonal regrowth. In addition, stimulation of astrocytic β 2 -receptors releases brain-derived neurotrophic factor (BDNF) [20] and interleukin-6 (IL-6) [26] which are both known to promote axonal regeneration. We hypothesized that clenbuterol may also enhance axonal regrowth in the central nervous system (CNS), as in the peripheral nervous system [14], provided that CSPGs are sufficiently eliminated.…”

Section: Introductionmentioning

confidence: 99%

Partial functional recovery after complete spinal cord transection by combined chondroitinase and clenbuterol treatment

Fu-sheng

Peng

Etlinger

et al. 2010

Pflugers Arch - Eur J Physiol

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Spinal cord injury not only disrupts axonal tracts but also causes gliotic, fibrotic, and Schwannotic scarring with resulting deposition of chondroitin sulfate proteoglycans (CSPGs) which prevent axonal reconnection and recovery of locomotor function. Here, we determined whether recovery of locomotor function could be promoted after complete transection, by degrading CSPGs enzymatically within the injury site with chondroitinase ABC (chABC) together with treatment with the beta(2)-adrenoceptor agonist, clenbuterol, a neuroprotective agent which can promote regrowth of lower motoneurons. Partial recovery of locomotor function was observed 8-12 weeks postinjury only after combined chABC and clenbuterol treatment. The recovery of locomotor function coincided with the presence of axons caudal to the injury site arising from neurons of the reticular, vestibular, and red nuclei also only with combined chABC and clenbuterol treatment. Axons myelinated by Schwann cells were most prominent in the transection site in the combined treatment group. Clenbuterol treatment activated cAMP response element binding protein within retrogradely traced neurons which has been associated with axonal regrowth. ChABC treatment decreased scarring due to both CSPG and collagen deposition as well as the gap between intact regions of the spinal cord. ChABC also increased numbers of phagocytic cells which remove myelin debris as well as populations of astrocytes thereby aiding blood-spinal cord barrier reformation. Together the results suggest that chABC and clenbuterol can act synergistically to promote recovery of locomotor function.

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Noradrenergic stimulation of BDNF synthesis in astrocytes: Mediation via α1- and β1/β2-adrenergic receptors

Cited by 101 publications

References 64 publications

Imipramine Induces Brain-Derived Neurotrophic Factor mRNA Expression in Cultured Astrocytes

Imipramine Induces Brain-Derived Neurotrophic Factor mRNA Expression in Cultured Astrocytes

The triplet puzzle theory indicates extensive formation of heteromers between opioid and chemokine receptor subtypes

Partial functional recovery after complete spinal cord transection by combined chondroitinase and clenbuterol treatment

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