Acute nicotine changes dynorphin and prodynorphin mRNA in the striatum

Isola, Raffaella; Zhang, Hailin; Tejwani, Gopi A.; Neff, Norton H.; Hadjiconstantinou, Maria

doi:10.1007/s00213-008-1315-4

Cited by 47 publications

(45 citation statements)

References 74 publications

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“…This is followed by a return to baseline and a rebound elevation of DYN content lasting up to 24 h. Like other drugs of abuse, systemic nicotine administration elevates extracellular NAcc DA levels [156]. Not surprisingly, D1 and NMDA receptor blockade attenuate nicotine-induced DYN elevations [345], again, highlighting the role of D1-NMDA interactions in modulating DYN synthesis in response to various drugs of abuse. Nicotine produces biphasic motivational effects across doses.…”

Section: Nicotinementioning

confidence: 89%

“…Acute nicotine injection produces a dose-dependent increase in pdyn mRNA and DYN immunoreactivity in the striatum and NAcc [345]. PDYN elevations are long-lasting in striatum whereas peptide immunoreactivity is transiently increased (approx.…”

Section: Nicotinementioning

confidence: 96%

“…Low-dose nicotine administration does not alter the number DYN-positive neurons in the CeA or hypothalamus; nor were the number of dual-labeled DYN and C-FOS cells altered suggesting DYN neurons in these regions are not activated by low-dose nicotine administration [348]. Interestingly, doses (1-2 mg/kg; free base) that produce CPA also produce robust elevations of striatal DYN [345]. Thus, future experiments examining a role of KORs in mediating the aversive effects of high-dose nicotine are warranted.…”

Section: Nicotinementioning

confidence: 98%

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The dynorphin/κ-opioid receptor system and its role in psychiatric disorders

Tejeda

Shippenberg

Henriksson

2011

Cell. Mol. Life Sci.

145

144

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The dynorphin/κ-opioid receptor system has been implicated in the pathogenesis and pathophysiology of several psychiatric disorders. In the present review, we present evidence indicating a key role for this system in modulating neurotransmission in brain circuits that subserve mood, motivation, and cognitive function. We overview the pharmacology, signaling, post-translational, post-transcriptional, transcriptional, epigenetic and cis regulation of the dynorphin/κ-opioid receptor system, and critically review functional neuroanatomical, neurochemical, and pharmacological evidence, suggesting that alterations in this system may contribute to affective disorders, drug addiction, and schizophrenia. We also overview the dynorphin/κ-opioid receptor system in the genetics of psychiatric disorders and discuss implications of the reviewed material for therapeutics development.

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Section: Nicotinementioning

confidence: 89%

Section: Nicotinementioning

confidence: 96%

Section: Nicotinementioning

confidence: 98%

See 1 more Smart Citation

The dynorphin/κ-opioid receptor system and its role in psychiatric disorders

Tejeda

Shippenberg

Henriksson

2011

Cell. Mol. Life Sci.

145

144

View full text Add to dashboard Cite

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“…Concomitantly, NIC produces a significant decrease in native methionine-enkephalin (Met-Enk) levels in the central amygdala, flocculo-nodular lobe of the cerebellum, caudal part of the ventrolateral medulla, and the intermediolateral cell column of the spinal cord, reflecting release of the opioid peptide at these sites (11). Furthermore, Isola et al (12) reported that acute NIC (1 mg/kg, s.c.) induces an increase in striatal dynorphin 1-13 content and that prodynorphin mRNA levels were elevated in the striatum for a prolonged time (0.5 -24 h). The content of dynorphin 1-13 increased soon after the rise of prodynorphin mRNA, at 1 h after NIC.…”

Section: Nic and Endogenous Opioid Peptidesmentioning

confidence: 99%

Nicotine Effects and the Endogenous Opioid System

et al. 2014

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Abstract. Nicotine (NIC) is an exogenous ligand of the nicotinic acetylcholine receptor (nAChR), and it influences various functions in the central nervous system. Systemic administration of NIC elicits the release of endogenous opioids (endorphins, enkephalins, and dynorphins) in the supraspinal cord. Additionally, systemic NIC administration induces the release of methionineenkephalin in the spinal dorsal horn. NIC has acute neurophysiological actions, including antinociceptive effects, and the ability to activate the hypothalamic-pituitary-adrenal (HPA) axis. The endogenous opioid system participates in NIC-induced antinociception, but not HPA axis activation. Moreover, NIC-induced antinociception is mediated by a4b2 and a7 nAChRs, while NIC-induced HPA axis activation is mediated by a4b2, not a7, suggesting that the effects of NIC on the endogenous opioid system are mediated by a7, not a4b2. NIC has substantial physical dependence liability. The opioid-receptor antagonist naloxone (NLX) elicits NIC withdrawal after repeated NIC administration, and NLX-induced NIC withdrawal is inhibited by concomitant administration of an opioid-receptor antagonist. NLX-induced NIC withdrawal is also inhibited by concomitant administration of an a7 antagonist, but not an a4b2 antagonist. Taken together, these findings suggest that NIC-induced antinociception and the development of physical dependence are mediated by the endogenous opioid system, via the a7 nAChR.

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“…While the majority of the CREB-regulated genes in the limbic system remain obscured, the precursor of the opioid peptide dynorphin (Dyn), prodynorphin (PD), has been identified as a CREB target . Acute nicotine elevates PD mRNA and enhances the synthesis and release of Dyn in caudate/putamen (CPu) and nucleus accumbens (NAc), an effect that has been associated with the aversive effects of the drug (Isola et al 2009). …”

Section: Introductionmentioning

confidence: 99%