Signal transduction mechanisms mediating rapid, nongenomic effects of cortisol on prolactin release

Borski, Russell J.; Hyde, Gregory N.; Fruchtman, Shira

doi:10.1016/s0039-128x(01)00197-0

Cited by 58 publications

(22 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, (1) interactions between GRs and activating protein-1 or nuclear factor B have been shown to be involved in the process of immunosuppression and anti-inflammation (Barrett and Vedeckis, 1996;Refojo et al, 2001); (2) GRs mediate the inhibition of bradykinin-induced Ca 2ϩ influx in PC12 cells (Qiu et al, 2003); (3) the regulatory role of cortisol in prolactin release is mediated through GRs (Borski et al, 2002); (4) GRs regulate spinal glutamate binding to glutamate receptors after spinal cord injury (Gonzalez et al, 1995); (5) GRs mediate acute elevation of the intracellular Ca 2ϩ concentration induced by corticosterone in hippocampal neurons (Takahashi et al, 2002); and (6) activation of GRs potentiates NMDAR-mediated responses in dopamine-sensitive neurons within the ventral tegmental area (Cho and Little, 1999) as well as long-term depression (Coussens et al, 1997). Collectively, these previous studies strongly indicate that activation of GRs could directly interact with cellular components through nongenomic regulation, thereby modulating cellular events.…”

Section: Discussionmentioning

confidence: 99%

Central Glucocorticoid Receptors Modulate the Expression and Function of Spinal NMDA Receptors after Peripheral Nerve Injury

Wang¹,

Lim²,

Zeng³

et al. 2005

J. Neurosci.

124

116

View full text Add to dashboard Cite

Central glucocorticoid receptors (GRs) and NMDA receptors (NMDARs) have been shown to play a significant role in the mechanisms of neuropathic pain after peripheral nerve injury; however, how central GRs and NMDARs interact in this process remains unknown. Here we show that the expression and function of spinal NMDARs after peripheral nerve injury were modulated by central GRs. Chronic constriction nerve injury (CCI) in rats induced a time-dependent upregulation of NR1 and NR2 subunits of the NMDAR within the spinal cord dorsal horn ipsilateral to CCI. The upregulation of NMDARs was significantly diminished by intrathecal administration (twice daily for postoperative days 1-6) of either the GR antagonist RU38486 or an antisense oligonucleotide against GRs. Moreover, this CCI-induced expression of NMDARs was significantly attenuated in rats receiving intrathecal treatment with an interleukin-6 (IL-6) antiserum and in mice with protein kinase C␥ (PKC␥) knock-out. Because IL-6 and PKC␥ mediated the upregulation of central GRs after CCI as demonstrated previously, the results suggest that IL-6 and PKC␥ served as cellular mediators contributing to the GR-mediated expression of NMDARs after CCI. Functionally, nociceptive behaviors induced by NMDAR activation and CCI were reversed by a single intrathecal administration of the GR antagonist RU38486. Conversely, a single intrathecal injection with the noncompetitive NMDAR antagonist MK-801 reversed neuropathic pain behaviors exacerbated by the GR agonist dexamethasone in CCI rats. These data suggest that interactions between central GRs and NMDARs through genomic and nongenomic regulation may be an important mechanism critical to neuropathic pain behaviors in rats.

show abstract

Section: Discussionmentioning

confidence: 99%

Central Glucocorticoid Receptors Modulate the Expression and Function of Spinal NMDA Receptors after Peripheral Nerve Injury

Wang¹,

Lim²,

Zeng³

et al. 2005

J. Neurosci.

124

116

View full text Add to dashboard Cite

show abstract

“…A GR-homodimer binds to nuclear-specific DNA responsive elements and regulates gene transcription and translation for a number of cellular elements (Drouin et al, 1992;Karst et al 2002). In addition, GR action could take place through nongenomic mechanisms (Barrett and Vedeckis, 1996;Refojo et al, 2001), including (1) the GR-mediated inhibition of bradykinin-induced Ca 2ϩ influx in PC12 cells (Qiu et al, 2003), (2) the effect of cortisol through GRs on prolactin release (Borski et al, 2002), (3) regulation by GRs of glutamate binding in the injured spinal cord (Gonzalez et al, 1995), and (4) a corticosterone-induced acute elevation of intracellular Ca 2ϩ concentration in hippocampal neurons (Takahashi et al, 2002). Of interest is that a number of previous studies have suggested that GRs may have modulatory effects on the expression and function of NMDAR.…”

Section: Discussionmentioning

confidence: 99%

Expression of Central Glucocorticoid Receptors after Peripheral Nerve Injury Contributes to Neuropathic Pain Behaviors in Rats

Wang¹,

Lim²,

Zeng³

et al. 2004

J. Neurosci.

114

121

View full text Add to dashboard Cite

Peripheral glucocorticoid receptors (GRs) play a significant role in the anti-inflammatory effects of glucocorticoids; however, the role of central GRs in nociceptive behaviors after peripheral nerve injury (neuropathic pain behaviors) remains unknown. Here we show that the development of neuropathic pain behaviors (thermal hyperalgesia and mechanical allodynia) induced by chronic constriction nerve injury (CCI) in rats was attenuated by either the GR antagonist RU38486 (4 ϭ 2 Ͼ 1 ϭ 0.5 g) or a GR antisense oligonucleotide administered intrathecally twice daily for postoperative days 1-6. The development of thermal hyperalgesia and mechanical allodynia after CCI also was prevented in adrenalectomized rats, whereas the GR agonist dexamethasone (100 g/kg) given subcutaneously twice daily for postoperative day 1-6 restored CCI-induced neuropathic pain behaviors in the adrenalectomized rats. Mechanistically, CCI induced a time-dependent and region-specific expression of neuronal GRs primarily within the spinal cord dorsal horn ipsilateral to nerve injury, which showed a time course parallel to that of the development of neuropathic pain behaviors. Moreover, the expression of neuronal GR after CCI was mediated in part through an elevated spinal level of interleukin-6 (IL-6) and protein kinase C␥ (PKC␥), because intrathecal treatment with an IL-6 antiserum, a PKC inhibitor (cheryrithrine), or PKC␥ knock-out substantially reduced the expression of neuronal GRs as well as neuropathic pain behaviors after CCI. These findings indicate a central role of neuronal GRs in the mechanisms of neuropathic pain behaviors in rats and suggest a potential role for GR antagonists in clinical management of neuropathic pain.

show abstract

“…First, cortisol decreases membrane adenylyl cyclase activity and cAMP levels (39). The ubiquitous second messenger cAMP has an important role in maintaining endothelial function and prevention of atherosclerosis in addition to decreasing endothelial permeability and promoting cadherin-dependent cell adhesion and inhibiting hyperpermeability evoked by inflammatory reactions (99).…”

Section: Cortisolmentioning

confidence: 99%

Chronic stress impacts the cardiovascular system: animal models and clinical outcomes

Golbidi

Frisbee

Laher

2015

American Journal of Physiology-Heart and Circulatory Physiology

178

132

View full text Add to dashboard Cite

show abstract

Signal transduction mechanisms mediating rapid, nongenomic effects of cortisol on prolactin release

Cited by 58 publications

References 48 publications

Central Glucocorticoid Receptors Modulate the Expression and Function of Spinal NMDA Receptors after Peripheral Nerve Injury

Central Glucocorticoid Receptors Modulate the Expression and Function of Spinal NMDA Receptors after Peripheral Nerve Injury

Expression of Central Glucocorticoid Receptors after Peripheral Nerve Injury Contributes to Neuropathic Pain Behaviors in Rats

Chronic stress impacts the cardiovascular system: animal models and clinical outcomes

Contact Info

Product

Resources

About