FMRF-NH2-like mammalian octapeptide: Possible role in opiate dependence and abstinence

Malin, David H.; Lake, John R.; Hammond, Maria V.; Fowler, David E.; Rogillio, Robert B.; Brown, Sharon L.; Sims, Jamie L.; Leecraft, Bert M.; Yang, Hyunwon

doi:10.1016/0196-9781(90)90018-z

Cited by 144 publications

(49 citation statements)

References 20 publications

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“…These results suggest that the basal level of activation of this system is low under normal conditions. In keeping with this notion, it has been shown that NPFF levels in the spinal fluid of morphine-treated rats are elevated significantly (33) and that antisense oligonucleotides to human SQA-NPFF attenuate tolerance to analgesic effect of morphine in mice (34). Our data showing that coadministration of the NPFF receptor antagonist RF9 with heroin prevents the development of tolerance are in good agreement with these results and suggest that the NPFF system is triggered by activation of the opioid system as observed in in vitro studies (23).…”

Section: Discussionmentioning

confidence: 59%

“…Thus, i.c.v. administration of NPFF reverses morphineinduced analgesia in rats (33), whereas intrathecal administration induces a long-lasting opioid-induced analgesia and prolongs morphine-induced analgesia (35). Recently, a novel family of G protein-coupled receptors specifically expressed in neurons of trigeminal and dorsal root ganglia was identified (36).…”

Section: Discussionmentioning

confidence: 99%

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RF9, a potent and selective neuropeptide FF receptor antagonist, prevents opioid-induced tolerance associated with hyperalgesia

Simonin

Schmitt

Laulin

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

201

221

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Fig. 3. Decision tree for hybrid sequencing strategy. For organisms with a small genome size (Ͻ3 Mb) and͞or a small number of gaps and͞or high levels of repetitive structure inducing physical ends, we found 8ϫ Sanger sequencing to be the most cost-effective approach. For organisms with a large genome size, many sequencing gaps, and͞or hard stops, we found initial sequencing of 5.3ϫ Sanger data followed by the addition of two 454 runs to be the most cost-effective approach.

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Section: Discussionmentioning

confidence: 59%

Section: Discussionmentioning

confidence: 99%

RF9, a potent and selective neuropeptide FF receptor antagonist, prevents opioid-induced tolerance associated with hyperalgesia

Simonin

Schmitt

Laulin

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

201

221

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“…We also showed that large concentrations of RFRP-1 had no effect on HaFaNaC-expressing neurons. Finally, because neuropeptides are released from nonsynaptic locations (Salio et al, 2006) and are normally found in the CNS at concentrations approximately 1000 to 10000 fold lower than required for the full agonist to activate HaFaNaC (Malin et al, 1990;Sundblom et al, 1997;Zangen et al, 1999;Kiyashchenko et al, 2002;Burlet-Schiltz et al, 2002;Guan et al, 2005;Hilke et al, 2005;Pallis et al, 2006), physiologically released RFamide peptides will have no effect on heterologously expressed HaFaNaC. Therefore, endogenous RFamides of the mammalian CNS will have no effect on heterologously expressed HaFaNaC.…”

Section: Discussionmentioning

confidence: 99%

Heterologous expression of the invertebrate FMRFamide–gated sodium channel as a mechanism to selectively activate mammalian neurons

Schanuel¹,

Bell²,

Henderson³

et al. 2008

Neuroscience

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Considerable effort has been directed toward the development of methods to selectively activate specific subtypes of neurons. Focus has been placed on the heterologous expression of proteins that are capable of exciting neurons in which they are expressed. Here we describe the heterologous expression of the invertebrate FMRFamide-gated sodium channel from Helix aspersa (HaFaNaC) in hippocampal slice cultures. HaFaNaC was co-expressed with a fluorescent protein (GFP, dsRed or tdTomato) in CA3 pyramidal neurons of rat hippocampal slice cultures using single cell electroporation. Pressure application of the agonist FMRFamide to HaFaNaC-expressing neuronal somata produced large prolonged depolarizations and bursts of action potentials (AP). FMRFamide responses were inhibited by amiloride (100 µM). In contrast, pressure application of FMRFamide to the axons of neurons expressing HaFaNaC produced no response. Fusion of GFP to the N-terminus of HaFaNaC showed that GFP-HaFaNaC was absent from axons. Bath application of FMRFamide produced persistent AP firing in HaFaNaC-expressing neurons. This FMRFamide-induced increase in the frequency of APs was dose-dependent. The concentrations of FMRFamide required to activate HaFaNaC-expressing neurons were below that required to activate the homologous acid sensing ion channel normally found in mammalian neurons. Furthermore, the mammalian neuropeptides neuropeptide FF and RFRP-1, which have amidated RF C-termini, did not affect HaFaNaCexpressing neurons. Antagonists of NPFF receptors (BIBP3226) also had no effect on HaFaNaC. Therefore, we suggest that heterologous-expression of HaFaNaC in mammalian neurons could be a useful method to selectively and persistently excite specific subtypes of neurons in intact nervous tissue.

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“…Anti-opiate activities also have been hypothesized for NPFF, previously called F8Fa, based on the effects of intracerebroventricular injection of NPFFrelated peptides. Administration of NPFF attenuates morphine-and stress-induced analgesia (Kavaliers 1990), and precipitates morphine withdrawal (Malin et al 1990). More compelling, NPFF antagonists can increase both morphine-and stress-induced analgesia, reverse morphine tolerance (Lake et al 1992), and attenuate the naloxone-precipitated withdrawal syndrome in morphine-dependent rats.…”

Section: Neural Substrates Of Motivational Withdrawalmentioning

confidence: 99%

Drug Addiction, Dysregulation of Reward, and Allostasis

Koob

Moal

2001

Neuropsychopharmacology

2,544

1,962

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This paper reviews recent developments in the neurocircuitry and neurobiology of addiction from a perspective of allostasis. A model is proposed for brain changes that occur during the development of addiction that explain the persistent vulnerability to relapse long after drug-taking has ceased. Addiction is presented as a cycle of spiralling dysregulation of brain reward systems that progressively increases, resulting in the compulsive use and loss of control over drug-taking. The development of addiction recruits different sources of reinforcement, different neuroadaptive mechanisms, and different neurochemical changes to dysregulate the brain reward system. Counteradaptive processes such as opponent-process that are part of normal homeostatic limitation of reward function fail to return within the normal homeostatic range and are hypothesized to form an allostatic state. Allostasis from the addiction perspective is defined as the process of maintaining apparent reward function stability by changes in brain reward mechanisms. The allostatic state represents a chronic deviation of reward set point and is fueled not only by dysregulation of reward circuits per se, but also by the activation of brain and hormonal stress responses. The manifestation of this allostatic state as compulsive drugtaking and loss of control over drug-taking is hypothesized to be expressed through activation of brain circuits involved in compulsive behavior such as the cortico-striatal-thalamic loop. The view that addiction is the pathology that results from an allostatic mechanism using the circuits established for natural rewards provides a realistic approach to BACKGROUNDDrug addiction is a chronically relapsing disorder that is defined by two major characteristics: a compulsion to take the drug with a narrowing of the behavioral repertoire toward excessive drug intake, and a loss of control in limiting intake (American Psychiatric Association 1994; World Health Organization 1992). An important challenge for neurobiological research is to understand the neuroadaptive differences between controlled drug use and loss of control, and by extension, the molecular, cellular and system processes that lead to addiction (Koob and Le Moal 1997).Animal models are critical for understanding the neuropharmacological mechanisms involved in the development of addiction. While there are no complete animal models of addiction, animal models do exist for many elements of the syndrome. These elements can be derived from symptoms or diagnostic criteria for addiction or conceptual frameworks such as different sources of reinforcement (American Psychiatric Association 1994; World Health Organization 1992). Linking neu- 24 , NO . 2 ropharmacological events to animal models can occur at multiple levels of analysis -molecular, cellular and system -and it will only be the integration of these changes across dimensions of analysis that will allow a full understanding of the neurobiology of drug addiction.Advances in neuroscience research are rapidly unr...

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FMRF-NH2-like mammalian octapeptide: Possible role in opiate dependence and abstinence

Cited by 144 publications

References 20 publications

RF9, a potent and selective neuropeptide FF receptor antagonist, prevents opioid-induced tolerance associated with hyperalgesia

RF9, a potent and selective neuropeptide FF receptor antagonist, prevents opioid-induced tolerance associated with hyperalgesia

Heterologous expression of the invertebrate FMRFamide–gated sodium channel as a mechanism to selectively activate mammalian neurons

Drug Addiction, Dysregulation of Reward, and Allostasis

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