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Modulation of hippocampal theta rhythm by the opioid system of the pedunculopontine tegmental nucleus

100%
Leszkowicz E., Kusmierczak M., Matulewicz P., Trojniar W.
Acta Neurobiologiae Experimentalis
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2007
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vol. 67
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issue 4
447-460
EN
The pedunculopontine tegmental nucleus (PPN) belongs to the brainstem system which synchronizes hippocampal activity. Theta relevant intra-PPN circuitry involves its cholinergic, GABA-ergic and glutamatergic neurons and Substance P as neuromodulator. Evidence that PPN opioid elements also modulate the hippocampal theta is provided here. In urethane-anesthetized rats a unilateral microinjection of morphine (MF) (1.5 and 5 micrograms) increased the maximal peak power of tail pinch-induced theta. The higher dose also increased the corresponding frequency. When the theta was evoked by intra-PPN injection of carbachol (10 micrograms), the addition of MF (5 micrograms) prolonged theta latency and shortened the duration of the theta. These effects of MF were blocked by naloxone (5 micrograms). The results obtained suggest that the PPN opioid system can enhance or suppress the hippocampal theta depending on the actual level of PPN activation.
2

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

88%
Michalska E., Malec D.
Polish Journal of Pharmacology
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1993
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vol. 45
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issue 1
1-9
EN
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.
3
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Effect of opioids on Ca2+/cAMP responsive element binding protein

75%
Bilecki W., Przewlocki P. R., Przewlocki R.
Acta Neurobiologiae Experimentalis
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2000
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vol. 60
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issue 4
557-567
EN
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.
4

Opiate abuse, innate immunity, and bacterial infectious diseases

63%
Wang J., Barke R. A., Ma J., Charboneau R., Roy S.
Archivum Immunologiae et Therapiae Experimentalis
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2008
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vol. 56
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issue 5
299-309
EN
The first line of defense against invading bacteria is provided by the innate immune system. Morphine and other opiates can immediately disrupt the body's first line of defense against harmful external bacteria. Opiate, for example morphine, abuse degrades physical and physiologic barriers, and modulates phagocytic cells (macrophages, neutrophils) and, nonspecific cytotoxic T cells (gd T), natural killer cells, and dendritic cells, that are functionally important for carrying out a rapid immune reaction to invading pathogens. In vitro studies with innate immune cells from experimental animals and humans and in vivo studies with animal models have shown that opiate abuse impairs innate immunity and is responsible for increased susceptibility to bacterial infection. However, to better understand the complex interactions between opiates, innate immunity, and bacterial infection and develop novel approaches to treat and even prevent bacterial infection in the opiate-abuse population, there is an urgent need to fill the numerous gaps in our understanding of the cellular and molecular mechanisms by which opiate abuse increases susceptibility to bacterial infection.
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