Effects of glucose and diabetes on binding of naloxone and dihydromorphine to opiate receptors in mouse brain

Brase, David A.; Han, Y. H.; Dewey, William L.

doi:10.2337/diabetes.36.10.1173

Cited by 34 publications

(12 citation statements)

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“…This finding suggests that the effect of diabetes on in vivg responses to opiates is due to elevated glucose levels rather than to some other changes associated with diabetes. This possibility is supported by the work of Brase et al (8), which demonstrated that glucose decreases high affinity binding of naloxone in mouse brain membranes. However, these authors indicate that decreased binding affinity cannot completely explain the in vivo effects of hyperglycemia on opioid responses; they suggest that glucose metabolism, glucoseendogenous opioid interactions or an interaction of glucose with ion transport mechanisms may also be important.…”

mentioning

confidence: 74%

Effects of streptozotocin-induced diabetes on feeding stimulated by centrally administered opioid agonists

et al. 1989

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The potencies of several opioid agonists are reduced in diabetic animals and in animals made hyperglycemic via injections of glucose. In this report we examined the effects of streptozotocin-induced diabetes on the feeding responses to centrally administered opioid agonists with differing receptor selectivities. The selective mu receptor agonist Tyr-D-Ala-Gly-(Me)Phe-Gly-ol (DAGO) caused a larger increase in intake in diabetic rats than in controls. In both groups feeding responses were greater on the fourth day of daily injections than on the first day. The delta receptor agonist [D-Ser2,Leu5]-enkephalin-Thr6 (DSLET) stimulated intake in controls but not in diabetics. However, the elevated baseline and large variability in intake of the diabetics in this experiment prevent drawing a conclusion on diabetes-induced changes in the potency of this peptide. No differences between controls and diabetics were apparent in the feeding responses to U50, 488H, a selective kappa receptor agonist. These data suggest that diabetes may differentially affect the classes of opioid receptors or the binding of ligands to these receptors.

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confidence: 74%

Effects of streptozotocin-induced diabetes on feeding stimulated by centrally administered opioid agonists

et al. 1989

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“…Moreover, the differences observed in the memory tasks between morphine injections into the septum and amygdala indicate that these two anatomical systems are involved in dif-jections by intra-amygdala glucose treatment adds to other findings, indicating that glucose attenuates the effects of morphine on several measures (Simon and Dewey, 1981;Shook et al, 1986;Stone et al, 1990Stone et al, ,1992Arankowsky-Sandoval and Gold, unpublished observations). Glucose attenuation of the behavioral effects of morphine may be due to a decrease in opioidreceptor affinity because increasing glucose concentrations decrease receptor affinities for 3H-naloxone and 3H-dihydromorphine in the brain (Brase et al, 1987). If glucose acts by decreasing opioid receptor affinity, then glucose should produce effects similar to those of an opioid antagonist.…”

Section: Discussionmentioning

confidence: 99%

“…The amygdala binds high levels of opioid ligands (Zamir et al,, 1985). Behavioral and pharmacological studies indicate that glucose interacts with opioids (Brase et al, 1987;Stone et al, 1990Stone et al, , 1991. Because glucose reduces the mnemonic deficits induced by intraseptal morphine treatment (Ragozzino et al, 1992), glucose may interact with opioids in other brain areas to alter mnemonic functioning.…”

Section: Lntraseptalmentioning

confidence: 99%

Task-dependent effects of intra-amygdala morphine injections: attenuation by intra-amygdala glucose injections

Ragozzino

Gold

1994

J. Neurosci.

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Intraseptal injections of morphine impair learning and memory in rats, and these impairments are reversed by intraseptal injections of glucose. With evidence that injections of morphine into the amygdala also impair memory for some tasks, the present experiment determined whether (1) intra-amygdala morphine injections impair performance in inhibitory avoidance and spontaneous alternation tasks, and (2) intra-amygdala glucose injections attenuate the effects of intra-amygdala morphine injections. Rats receiving bilateral injections of morphine (4.0 nmol) into the amygdala, 30 min prior to training in inhibitory avoidance, had retention latencies significantly lower than those of unoperated and CSF controls when tested 24 hr later. Bilateral morphine injections (4.0 or 8.0 nmol) 30 min prior to testing in a spontaneous alternation task did not alter performance. The morphine-induced impairment observed in inhibitory avoidance was not due to diffusion up the cannulas, altered sensitivity to shock, or seizure activity. A glucose dose of 16.67 nmol, but not 8.33 nmol, injected into the amygdala attenuated the morphine-induced deficit in inhibitory avoidance. Rats receiving CSF into the amygdala exhibited decreased retention latencies in inhibitory avoidance compared to those of unoperated controls. This decrease was not attenuated by glucose at doses of 8.33 and 16.67 nmol. Therefore, these findings suggest that the amygdala is another brain region in which glucose affects brain functions, possibly by interacting with the opioid system and/or other neurotransmitter systems.

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“…It is well known that endogenous opioids play a role in the regulation of LH release during the normal menstrual cycle [29,30]. Even although experiments in vitro have demonstrated that diabetes does not change naloxone binding to opiate receptors [31], considerable evidence of various opioid receptor changes in diabetes mellitus has been obtained [32][33][34][35].…”

Section: Discussionmentioning

confidence: 99%

Influence of residual insulin secretion and duration of diabetes mellitus on the control of luteinizing hormone secretion in women

Volpi

Chiodera

Gramellini

et al. 1998

Eur J Clin Investigation

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Effects of glucose and diabetes on binding of naloxone and dihydromorphine to opiate receptors in mouse brain

Cited by 34 publications

References 0 publications

Effects of streptozotocin-induced diabetes on feeding stimulated by centrally administered opioid agonists

Effects of streptozotocin-induced diabetes on feeding stimulated by centrally administered opioid agonists

Task-dependent effects of intra-amygdala morphine injections: attenuation by intra-amygdala glucose injections

Influence of residual insulin secretion and duration of diabetes mellitus on the control of luteinizing hormone secretion in women

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