Current Research on Opioid Receptor Function

Feng, Yuan; He, Xiaozhou; Yang, Yilin; Chao, Dongman; Lazarus, Lawrence H.; Xia, Ying

doi:10.2174/138945012799201612

Cited by 287 publications

(200 citation statements)

References 276 publications

(262 reference statements)

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“…94 The exact cause of withdrawal-related seizure is unknown, although the threshold for seizure activity may be decreased due to upregulation of sodium channels as a result of receptor instability. 75 Heart rate, respiratory rate, muscle tone, and other physiologic responses to stimuli are impaired in these neonates with NAS as a result of the dysregulation and instability of the autonomic nervous system. 95 Other autonomic nervous system signs include temperature instability, sweating, sneezing, and mottling.…”

Section: Clinical Presentationmentioning

confidence: 97%

“…75 The density and affinity of m-receptors in neonates are as good as those in adults; however, evidence failed to show similar development of k-and d-receptors, as well as other receptors, in the neonatal brain. 76 A lack of opioids in a chronically stimulated state increases activity in the opioid receptors, leading to increased adenyl cyclase activity, and cellular ionic imbalance.…”

Section: Pathophysiologymentioning

confidence: 99%

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Neonatal Abstinence Syndrome

2014

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Neonatal abstinence syndrome (NAS) is a result of the sudden discontinuation of fetal exposure to substances that were used or abused by the mother during pregnancy. Withdrawal from licit or illicit substances is becoming more common among neonates in both developed and developing countries. NAS continues to be an important clinical entity throughout much of the world. NAS leads to a constellation of signs and symptoms involving multiple systems. The pathophysiology of NAS is not completely understood. Urine or meconium confirmation may assist the diagnosis and management of NAS. The Finnegan scoring system is commonly used to assess the severity of NAS; scoring can be helpful for initiating, monitoring, and terminating treatment in neonates. Nonpharmacological care is the initial treatment option, and pharmacological treatment is required if an improvement is not observed after nonpharmacological measures or if the infant develops severe withdrawal. Morphine is the most commonly used drug in the treatment of NAS secondary to opioids. An algorithmic approach to the management of infants with NAS is suggested. Breastfeeding is not contraindicated in NAS, unless the mother is taking street drugs, is involved in polydrug abuse, or is infected with HIV. Future studies are required to assess the long-term effects of NAS on children after prenatal exposure.

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Section: Clinical Presentationmentioning

confidence: 97%

Section: Pathophysiologymentioning

confidence: 99%

Neonatal Abstinence Syndrome

2014

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“…Certainly, in some animal models of MS and PD, opioid agonists may be effective. However, there are cases of movement disorders occurring in patients after anesthesia and use of opioid drugs, which can be reversed by the opioid antagonist naloxone and so suggests that the role of the opioid system in neuroprotection might be more complex [210]. Thus, the potential role of CBD in modulating neuroprotection via the opioid system remains unclear.…”

Section: Cbd Receptor Targets In Neurodegenerationmentioning

confidence: 99%

Molecular Targets of Cannabidiol in Neurological Disorders

Bih

Chen

Nunn³

et al. 2015

Neurotherapeutics

462

323

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Cannabis has a long history of anecdotal medicinal use and limited licensed medicinal use. Until recently, alleged clinical effects from anecdotal reports and the use of licensed cannabinoid medicines are most likely mediated by tetrahydrocannabinol by virtue of: 1) this cannabinoid being present in the most significant quantities in these preparations; and b) the proportion:potency relationship between tetrahydrocannabinol and other plant cannabinoids derived from cannabis. However, there has recently been considerable interest in the therapeutic potential for the plant cannabinoid, cannabidiol (CBD), in neurological disorders but the current evidence suggests that CBD does not directly interact with the endocannabinoid system except in vitro at supraphysiological concentrations. Thus, as further evidence for CBD's beneficial effects in neurological disease emerges, there remains an urgent need to establish the molecular targets through which it exerts its therapeutic effects. Here, we conducted a systematic search of the extant literature for original articles describing the molecular pharmacology of CBD. We critically appraised the results for the validity of the molecular targets proposed. Thereafter, we considered whether the molecular targets of CBD identified hold therapeutic potential in relevant neurological diseases. The molecular targets identified include numerous classical ion channels, receptors, transporters, and enzymes. Some CBD effects at these targets in in vitro assays only manifest at high concentrations, which may be difficult to achieve in vivo, particularly given CBD's relatively poor bioavailability. Moreover, several targets were asserted through experimental designs that demonstrate only correlation with a given target rather than a causal proof. When the molecular targets of CBD that were physiologically plausible were considered for their potential for exploitation in neurological therapeutics, the results were variable. In some cases, the targets identified had little or no established link to the diseases considered. In others, molecular targets of CBD were entirely consistent with those already actively exploited in relevant, clinically used, neurological treatments. Finally, CBD was found to act upon a number of targets that are linked to neurological therapeutics but that its actions were not consistent withmodulation of such targets that would derive a therapeutically beneficial outcome. Overall, we find that while >65 discrete molecular targets have been reported in the literature for CBD, a relatively limited number represent plausible targets for the drug's action in neurological disorders when judged by the criteria we set. We conclude that CBD is very unlikely to exert effects in neurological diseases through modulation of the endocannabinoid system. Moreover, a number of other molecular targets of CBD reported in the literature are unlikely to be of relevance owing to effects only being observed at supraphysiological concentrations. Of interest and after excludin...

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“…Met-enkephalin peptide sequence is coded for by the preproenkephalin gene; the leu-enkephalin peptide sequence is coded for by both the preproenkephalin gene and the preprodynorphin gene [106]. The third family of opioid peptides, the endorphins, has not been significantly implicated in the generation and control of seizures even though all opioid peptides are present in several brain regions [107]. In the hippocampus, enkephalins are present in mossy fibers, the perforant path, and in scattered GABAergic interneurons while dynorphins are present in granule cells, as well as perforant path and supramammillary afferents [108].…”

Section: Dynorphin and Enkephalinmentioning

confidence: 99%

Receptors of Peptides as Therapeutic Targets in Epilepsy Research

Dobolyi¹,

Kékesi²,

Juhász³

et al. 2014

CMC

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Neuropeptides are signaling molecules participating in the modulation of synaptic transmission. Neuropeptides are stored in dense core synaptic vesicles, the release of which requires profound excitation. Only in the extracellular space, neuropeptides act on G-protein coupled receptors to exert a relatively slow action both pre-and postsynaptically. Consequently, neuropeptide modulators are ideal candidates to influence epileptic tissue overexcited during seizures. Indeed, a number of neuropeptides have been implicated in epilepsy and many of them are considered to have endogenous neuroprotective actions. Neuropeptides, present in the hippocampus, the most frequent focus of seizures in temporal lobe epilepsy, received the largest attention as potential anti-epileptic substances. Hippocampal neuropeptides, somatostatin, neuropeptide Y, galanin, dynorphin, enkephalin, substance P, cholecystokinin, vasoactive intestinal polypeptide, and some neuropeptides, which are also hormones such as ghrelin, angiotensins, corticotropin-releasing hormone, adrenocorticotropin, thyrotropin-releasing hormone, oxytocin and vasopressin involved in epilepsy are discussed in the review article. Oral application of neuropeptides as drugs is typically not efficient because of low bioavailability: rapid degradation and insufficient penetration through the blood-brain barrier. Recent progress in the development of non-peptide agonists and antagonists of neuropeptide receptors as well as gene therapeutic approaches leading to the local production of neuropeptides within the central nervous system will also be discussed.

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Current Research on Opioid Receptor Function

Cited by 287 publications

References 276 publications

Neonatal Abstinence Syndrome

Neonatal Abstinence Syndrome

Molecular Targets of Cannabidiol in Neurological Disorders

Receptors of Peptides as Therapeutic Targets in Epilepsy Research

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