Regulation of prodynorphin gene expression in the hippocampus by glucocorticoids

Thai, L.; Lee, Paul H.K.; Ho, Jack; Suh, Hong‐Won; Hong, Jau–Shyong

doi:10.1016/0169-328x(92)90205-p

Cited by 38 publications

(17 citation statements)

References 20 publications

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“…Kappa agonists have been shown to possess anxiolytic properties (Privette and Terrian, 1995) via reducing the activity of the hypothalamic-pituitary-adrenocortical (HPA) axis (Iyengar et al, 1987), and glucocorticoids can regulate the synthesis of dynor-phins in the hippocampal formation (Privette et al, 1994;Thai et al, 1992). These findings support the idea that the IHR would make a useful model to investigate the role of hippocampal dynorphins in blood pressure regulation and hypertension.…”

Section: Introductionsupporting

confidence: 50%

Prevention of isolation‐induced hypertension by intrahippocampal administration of a nonpeptide kappa‐opioid receptor agonist

Wright

Ingenito

2001

Hippocampus

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Previous research in this laboratory showed that hypertension in the spontaneous hypertensive rat (SHR) appears to correlate to insufficient production of hippocampal dynorphins, and that blood pressure could be reduced by intrahippocampal administration of dynorphins and nonpeptide kappa agonists. The purpose of the present study was to investigate whether kappa agonists could prevent the development of hypertension in a different hypertensive model, i.e., the isolated male rat model of hypertension (IHR). Isolation of young male rats for 5-7 days in standard rat cages caused an increase in systolic blood pressure from a mean of 132 to 184 mmHg. The blood pressures of rats grouped 3 per cage remained stable. Rats received the nonpeptide kappa agonist U62, 066E, (Spiradoline, Upjohn), 10 nmoles/0.2 microl or drug vehicle bilaterally into the the hippocampus for 3 days prior to and during isolation or grouping. Animals treated with U62, 066E did not develop hypertension as compared to isolated animals treated with vehicle. The isolation procedure used in these studies appears to induce anxietal stress, as indicated by reduced time spent by the rats in the open arms of the elevated-plus maze. This time is increased by U62, 066E, suggesting that the drug possesses anxiolytic properties and may reduce hypertension in part, by blocking an anxiety/stress component. These data strengthen our previous findings that opioids in the hippocampus may be important in restraining increased blood pressure provoked by environmental stimuli such as isolation.

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Section: Introductionsupporting

confidence: 50%

Prevention of isolation‐induced hypertension by intrahippocampal administration of a nonpeptide kappa‐opioid receptor agonist

Wright

Ingenito

2001

Hippocampus

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“…Recently, it has been shown that glucocorticoids regulate the expression of the prodynorphin gene in the hippocampus. A decrease in dynorphin A(1-8) levels in the hippocampus and in the striatum of adrenalectomized animals was observed [26]. This effect was reversed by dexamethasone administration, and in the striatum, higher dynorphin levels were observed after glucocorticoid treatment in adrenalectomized animals compared with shamadrenalectomized animals.…”

Section: Introductionmentioning

confidence: 58%

“…Several studies showed an involvement of the dynorphinergic system in several epilepsy models [15] and the administration of Î-agonists exerted anticonvulsive activity [15], leading to the hypothesis that dynorphin may act as an endogenous anticonvulsant [15]. Since dexamethasone increases the hippocampal content of dynorphin peptides [26], it may be hypothesized that dexamethasone increases the hippocampal content of dynorphin which in turn would exert an inhibitory action on the EEG and behavioural alterations induced by opioid peptides.…”

Section: Discussionmentioning

confidence: 99%

Dexamethasone Blocking Effects on Mu- and Delta-Opioid-Induced Seizures Involves Kappa-Opioid Activity in the Rabbit

Giannuario

Pieretti²,

Sagratella³

et al. 2001

Neuropsychobiology

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Previous data indicate that intracerebroventricular administration of agonists for µ- and δ-opioid receptors induces limbic seizures in rats, but no data are reported in rabbits. We found that the µ- and δ-opioid peptides [D-Ala²-N,Me-Phe⁴-Gly⁵-ol]enkephalin (DAMGO), β-endorphin and deltorphin II, induced EEG non-convulsive hippocampal seizures, and changes in hippocampal background EEG, physical parameters and overt behaviour after central administration. Dexamethasone pre-treatment prevented DAMGO-, deltorphin II- and β-endorphin-induced seizures as well as changes in background EEG, physical parameters and overt behaviour induced by µ-opioid agonists. Dexamethasone antagonism on opioid action was blocked by pre-treatment with a protein synthesis inhibitor, cycloheximide or by the ĸ-opioid antagonist nor-binaltorphimine. Our data suggest that dexamethasone influences opioid actions at µ- and δ-receptors via a protein synthesis mechanism involving ĸ-opioid receptors.

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“…Thus, GR may either not be involved in PDYN regulation, or loss or gain of interactions in cis and/or trans are required to unmask an effect of glucocorticoid signaling on PDYN expression. Although the cognate response element(s) has not been identified, support for the latter notion comes from studies showing that treatment of rats with dexamethasone or another synthetic glucocorticoid, budesonide, alters hippocampal and spinal cord pdyn expression, respectively [91][92][93]. Moreover, GR binding to PDYN in A549 cells does not correlate with that of RNA polymerase II, suggesting that PDYN is not actively transcribed in these cells [90].…”

Section: Epigenetic Regulation Of Pdyn and Oprk1mentioning

confidence: 96%

The dynorphin/κ-opioid receptor system and its role in psychiatric disorders

Tejeda

Shippenberg

Henriksson

2011

Cell. Mol. Life Sci.

148

144

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The dynorphin/κ-opioid receptor system has been implicated in the pathogenesis and pathophysiology of several psychiatric disorders. In the present review, we present evidence indicating a key role for this system in modulating neurotransmission in brain circuits that subserve mood, motivation, and cognitive function. We overview the pharmacology, signaling, post-translational, post-transcriptional, transcriptional, epigenetic and cis regulation of the dynorphin/κ-opioid receptor system, and critically review functional neuroanatomical, neurochemical, and pharmacological evidence, suggesting that alterations in this system may contribute to affective disorders, drug addiction, and schizophrenia. We also overview the dynorphin/κ-opioid receptor system in the genetics of psychiatric disorders and discuss implications of the reviewed material for therapeutics development.

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Regulation of prodynorphin gene expression in the hippocampus by glucocorticoids

Cited by 38 publications

References 20 publications

Prevention of isolation‐induced hypertension by intrahippocampal administration of a nonpeptide kappa‐opioid receptor agonist

Prevention of isolation‐induced hypertension by intrahippocampal administration of a nonpeptide kappa‐opioid receptor agonist

Dexamethasone Blocking Effects on Mu- and Delta-Opioid-Induced Seizures Involves Kappa-Opioid Activity in the Rabbit

The dynorphin/κ-opioid receptor system and its role in psychiatric disorders

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