Opiate and alpha receptor antagonists block the pressor responses of conscious rats given intravenous dynorphin

Thornhill, J. A.; Gregor, L.; Saunders, William S.

doi:10.1016/0196-9781(89)90094-6

Cited by 11 publications

(3 citation statements)

References 16 publications

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“…Our present data extend these effects of prazosin to another stressor that induces reinstatement, the KOR agonist U50,488. Our results also provide the first clear evidence, to our knowledge, for the interaction of alpha-1 adrenoceptors with KOR in drug seeking, as the previous work examining this interaction dealt with feeding, water intake, and locomotor and autonomic responses to KOR activation (Saunders and Thornhill, 1987; Leighton et al, 1988; Thornhill et al, 1989; Nencini et al, 1991).…”

Section: Discussionsupporting

confidence: 62%

Effects of the alpha-1 antagonist prazosin on KOR agonist-induced reinstatement of alcohol seeking

Funk

Coen

Tamadon

et al. 2019

International Journal of Neuropsychopharmacology

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Background Stress is associated with relapse to alcohol seeking during abstinence, but the processes underlying this relationship are poorly understood. Noradrenaline is a key transmitter in stress responses and in stress-induced drug seeking. The alpha-1 adrenoceptor antagonist prazosin has been investigated as a treatment for alcoholism and for chronic stress disorders that are frequently comorbid with alcoholism. In rats, we previously showed that prazosin blocks reinstatement of alcohol seeking induced by footshock and yohimbine stressors, and reduces yohimbine-induced brain activation. The role of alpha-1 adrenoceptors in reinstatement induced by other stressors is not known. Our most recent work is on the role of kappa opioid receptors (KOR) in stress-induced reinstatement of alcohol seeking and have reported that the selective KOR agonist U50,488 induces reinstatement and neuronal activation in stress- and relapse-related brain regions. Here we determine the involvement of alpha-1 receptors in reinstatement and brain activation induced by U50,488. Methods We trained male Long-Evans rats to self-administer alcohol (12% w/v), extinguished alcohol-reinforced responding and then determined the effects of prazosin (1 mg/kg) on U50,488 (2.5 mg/kg)-induced reinstatement and regional Fos expression. Results Prazosin blocked U50,488-induced reinstatement and decreased U50,488-induced Fos expression in the OFC, NAC core, ventral BNST, CeA, BLA and VTA. Conclusions These findings suggest that prazosin may reduce U50,488-induced relapse by inhibiting activity in one or more of these brain areas.

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Section: Discussionsupporting

confidence: 62%

Effects of the alpha-1 antagonist prazosin on KOR agonist-induced reinstatement of alcohol seeking

Funk

Coen

Tamadon

et al. 2019

International Journal of Neuropsychopharmacology

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“…Such an interaction between dynorphinergic and adrenergic transmission has been reported by Szabo et al (1986) and by Thornhill et al (1989). Adrenergic blockade per se facilitated the EFS-induced contractions, which may indicate the existence of adrenergic neurons exerting a tonic inhibition on the excitatory nerves to the bladder.…”

Section: Discussionmentioning

confidence: 72%

Possible regulatory role of dynorphin A in the urinary bladder

Berggren¹,

Dahlström²,

Rubenson³

et al. 1992

J. Neural Transmission

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“…1988. However, some studies have shown pressor responses in conscious cats and rats to dynorphin and enkephalin (Schaz et al 1980, Thornhill et al 1989.…”

Section: Involvement Of 6-and K-opioid Receptors In the Post-stimulatmentioning

confidence: 99%

Role of opioid receptors in the long‐lasting blood pressure depression after electric muscle stimulation in the hind leg of the rat

Hoffmann

Delle

Thorén

1990

Acta Physiologica Scandinavica

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In a previous study, electrically induced contractions of the gastrocnemius muscle in conscious spontaneously hypertensive rats were shown to induce a blood pressure reduction of 15–20 mmHg lasting several hours. We showed in that study that endogenous opioid systems were involved. In this study, drugs with selective affinity for different opioid receptors were used to analyse further the involvement of endogenous opioid systems in the post‐stimulatory drop in blood pressure in spontaneously hypertensive rats. Prestimulatory intra‐cerebroventricular administration of β‐FNA (a preceptor antagonist) did not significantly influence the response at all, nor did a lower intravenous dose of naloxone reverse the post‐stimulatory drop in blood pressure. High‐dose naloxone (15 mg kg‐') increased post‐stimulatory blood pressure by around 10 mmHg. About 50% of the drop thus remained after this treatment. A similar, partial reversal of the decreased blood pressure was seen after intravenous administration of a & receptor antagonist, ICI 154, 129. However, the depressor response was completely reversed by a low intravenous dose of MR 2266 BS (a K‐receptor antagonist). These results suggest that the reduction in blood pressure after muscle stimulation is mainly mediated by the opioid k‐receptor. A certain involvement of the δ‐receptor is also indicated.

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Opiate and alpha receptor antagonists block the pressor responses of conscious rats given intravenous dynorphin

Cited by 11 publications

References 16 publications

Effects of the alpha-1 antagonist prazosin on KOR agonist-induced reinstatement of alcohol seeking

Effects of the alpha-1 antagonist prazosin on KOR agonist-induced reinstatement of alcohol seeking

Possible regulatory role of dynorphin A in the urinary bladder

Role of opioid receptors in the long‐lasting blood pressure depression after electric muscle stimulation in the hind leg of the rat

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