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Modulation of Ca2+ channel current by mu opioid receptors in prefrontal cortex pyramidal neurons in rats

100%

Rola R. , Jarkiewicz M. , Szulczyk P.

Acta Neurobiologiae Experimentalis

2008

tom 68

nr 1

10-25

Our work assesses the effects of ? opioid receptor activation on high-threshold Ca2+/Ba2+ currents in freshly dispersed pyramidal neurons of the medial prefrontal cortex in rats. Application of the specific ? receptor agonist (D-Ala2, N-Me-Phe4, Gly5-ol)-enkephalin (DAMGO) at 1 muM decreased Ca2+ current amplitudes from 0.72 to 0.49 nA. The effect was abolished by naloxone and ?-Conotoxin GVIA. Inhibition was not abolished by strong depolarisation of the cell membrane. In addition, a macroscopic Ba2+ current recorded in cell-attached configuration was inhibited when DAMGO was applied outside the patch pipette. An adenylyl cyclase inhibitor (SQ 22536) and a protein kinase A inhibitor (H-89) decreased Ca2+ current amplitude. Moreover, the inhibitory effect of mu opioid receptors on Ca2+ currents required the activation of protein kinase A. We conclude that activation of mu opioid receptors in medial prefrontal cortex pyramidal neurons inhibits N type Ca2+ channel currents, and that protein kinase A is involved in this transduction pathway.

Endogenous opioid peptides in physiological and pathological states with particular regard to kidneys

100%

Trelewicz P. , Grzeszczyk W. , Drabczyk R.

Postępy Higieny i Medycyny Doświadczalnej

1993

tom 47

nr 5

325-344

Agonists and antagonists of adenosine receptors and morphine withdrawal syndrome in rats

88%

Michalska E. , Malec D.

Polish Journal of Pharmacology

1993

tom 45

nr 1

1-9

The compounds activating adenosine system alleviated morphine withdrawal syndrome (the number of escape attempts and body shakes) in rats. Body shakes were decreased mostly by N-ethylcarboxamidoadenosine, cyclohexyladenosine, dipyridamole and 2-chloroadenosine, while R-phenylisopropyladenosine very strongly decreased the number of escape attempts. Adenosine receptor antagonists (caffeine and theophylline) increased the number of escape attempts in morphine-dependent rats. Caffeine (10 mg/kg), administered preventively, antagonized the ingibitory effects of adenosine analogs. These results suggest the existence of relation between opioid receptors and the adenosine system.

Effect of opioids on Ca2+/cAMP responsive element binding protein

75%

Bilecki W. , Przewlocki P. R. , Przewlocki R.

Acta Neurobiologiae Experimentalis

2000

tom 60

nr 4

557-567

Ca2+/cAMP response element binding protein (CREB) is an important factor linking the opioid-regulated secondary messenger systems to alterations in gene expression. Opioids regulate CREB level, its phosphorylation and binding to its corresponding response element in the promoters of several genes implicated in drug addiction. CREB mediates the action of opioids on the expression of several genes in brain regions responsible for drug-seeking behavior and manifestation of signs of dependence. Moreover, alterations in CREB level can affect the rewarding properties of morphine and regulate the self-administration of cocaine. At the cellular level CREB acts as convergence point for different cellular pathways. Opioids affect two different intracellular mediator systems: inhibitory - connected with cAMP, and stimulatory - involving calcium and the PKC pathway. Both can affect CREB but in different phases of opiate action. The presence of this biphasic mechanism can explain the phenomenon of the induction of some CRE-controlled genes after both acute and chronic morphine administration. Cellular studies also highlight the relevance of other ATF/CREB family members which can affect Ca2+/cAMP response element (CRE) controlled transcription as well as other transcription factors which make the opioid induction longer lasting.