Opioid Modulation of Scratching and Spinal c-<i>fos</i>Expression Evoked by Intradermal Serotonin

Nishimura, Hiroshi; Simons, Christopher T.; Cuéllar, Jason M.; Carstens, Mirela Iodi; Moore, Justin A.; Carstens, Earl

doi:10.1523/jneurosci.23-34-10784.2003

Cited by 52 publications

(35 citation statements)

References 52 publications

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“…Cheek injection of 5-HT was presently found to elicit dose-dependent hindlimb scratching, consistent with previous reports that 5-HT evoked hindlimb scratch bouts directed to the injection site in the nape of the neck in rats (Hachisuka et al 2010;Jinks and Carstens 2002;Carstens 2003a, 2003b;Nojima et al 2003;Thomsen et al 2001Thomsen et al , 2002 and mice (Inagaki et al 2001;Maekawa et al 2000;Yamaguchi et al 1999). Rat mast cells contain higher concentrations of 5-HT than histamine (Purcell et al 1989), possibly related to the scratch-inducing capacity of 5-HT in this species.…”

Section: Discussionsupporting

confidence: 90%

Facial injections of pruritogens or algogens elicit distinct behavior responses in rats and excite overlapping populations of primary sensory and trigeminal subnucleus caudalis neurons

Klein

Carstens

2011

Journal of Neurophysiology

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Klein A, Carstens MI, Carstens E. Facial injections of pruritogens or algogens elicit distinct behavior responses in rats and excite overlapping populations of primary sensory and trigeminal subnucleus caudalis neurons. J Neurophysiol 106: 1078 -1088. First published June 8, 2011 doi:10.1152/jn.00302.2011In the present study, we investigated whether intradermal cheek injection of pruritogens or algogens differentially elicits hindlimb scratches or forelimb wipes in Sprague-Dawley rats, as recently reported in mice. We also investigated responses of primary sensory trigeminal ganglion (TG) and dorsal root ganglion (DRG) cells, as well as second-order neurons in trigeminal subnucleus caudalis (Vc), to pruritic and algesic stimuli. 5-HT was the most effective chemical to elicit dose-dependent bouts of hindlimb scratches directed to the cheek, with significantly less forelimb wiping, consistent with itch. Chloroquine also elicited significant scratching but not wiping. Allyl isothiocyanate (AITC; mustard oil) elicited dose-dependent wiping with no significant scratching. Capsaicin elicited equivalent numbers of scratch bouts and wipes, suggesting a mixed itch and pain sensation. By calcium imaging, ϳ6% of cultured TG and DRG cells responded to 5-HT. The majority of 5-HT-sensitive cells also responded to chloroquine, AITC, and/or capsaicin, and one-third responded to histamine. Using a chemical search strategy, we identified single units in Vc that responded to intradermal cheek injection of 5-HT. Most were wide dynamic range (WDR) or nociceptive specific (NS), and a few were mechanically insensitive. The large majority additionally responded to AITC and/or capsaicin and thus were not pruritogen selective. These results suggest that primary and second-order neurons responsive to pruritogens and algogens may utilize a population coding mechanism to distinguish between itch and pain, sensations that are behaviorally manifested by distinct hindlimb scratching and forelimb wiping responses.

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Section: Discussionsupporting

confidence: 90%

Facial injections of pruritogens or algogens elicit distinct behavior responses in rats and excite overlapping populations of primary sensory and trigeminal subnucleus caudalis neurons

Klein

Carstens

2011

Journal of Neurophysiology

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“…The subcutaneous dose of morphine we used (4 mg ⅐ kg Ϫ1 ) has been shown to reduce noxious stimulus-induced Fos expression in the spinal and medullary dorsal horns consistently (Presley et al, 1990;Nozaki et al, 1992;Nojima et al, 2003). Our findings are thus in coherence with the suggestion that glycine inhibition in the dorsal horn is selective for A␤ input.…”

Section: Discussionsupporting

confidence: 85%

Glycine Inhibitory Dysfunction Induces a Selectively Dynamic, Morphine-Resistant, and Neurokinin 1 Receptor- Independent Mechanical Allodynia

Miraucourt¹,

Moisset²,

Dallel³

et al. 2009

J. Neurosci.

118

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Dynamic mechanical allodynia is a widespread and intractable symptom of neuropathic pain for which there is a lack of effective therapy. We recently provided a novel perspective on the mechanisms of this symptom by showing that a simple switch in trigeminal glycine synaptic inhibition can turn touch into pain by unmasking innocuous input to superficial dorsal horn nociceptive specific neurons through a local excitatory, NMDA-dependent neural circuit involving neurons expressing the gamma isoform of protein kinase C. Here, we further investigated the clinical relevance and processing of glycine disinhibition. First, we showed that glycine disinhibition with strychnine selectively induced dynamic but not static mechanical allodynia. The induced allodynia was resistant to morphine. Second, morphine did not prevent the activation of the neural circuit underlying allodynia as shown by study of Fos expression and extracellularsignal regulated kinase phosphorylation in dorsal horn neurons. Third, in contrast to intradermal capsaicin injections, light, dynamic mechanical stimuli applied under disinhibition did not produce neurokinin 1 (NK1) receptor internalization in dorsal horn neurons. Finally, light, dynamic mechanical stimuli applied under disinhibition induced Fos expression only in neurons that did not express NK1 receptor. To summarize, the selectivity and morphine resistance of the glycine-disinhibition paradigm adequately reflect the clinical characteristics of dynamic mechanical allodynia. The present findings thus reveal the involvement of a selective dorsal horn circuit in dynamic mechanical allodynia, which operates through superficial lamina nociceptive-specific neurons that do not bear NK1 receptor and provide an explanation for the differences in the pharmacological sensitivity of neuropathic pain symptoms.

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“…Naïve mice were perfused transcardially with phosphate-buffered saline (PBS) followed by 4% paraformaldehyde. Similar to other studies (Nojima et al, 2003;Nakano et al, 2008), the collected cervical (C3-C5) and lumbar (L4-L6) spinal cord and dorsal root ganglion (DRG, L4-6) were then postfixed for 2 hours and cryoprotected in a 25% sucrose solution at 4°C overnight. Frozen tissues embedded in optimal cutting temperature compound (Sakura Finetek USA, Torrance, CA) were cut at 12 mm (spinal cord) or 10 mm (DRG) with a cryostat, and thaw-mounted on glass slides.…”

Section: Methodsmentioning

confidence: 99%

Spinal Functions of B-Type Natriuretic Peptide, Gastrin-Releasing Peptide, and Their Cognate Receptors for Regulating Itch in Mice

Kiguchi

Sukhtankar

Ding

et al. 2015

Journal of Pharmacology and Experimental Therapeutics

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B-type natriuretic peptide (BNP)-natriuretic peptide receptor A (NPRA) and gastrin-releasing peptide (GRP)-GRP receptor (GRPR) systems contribute to spinal processing of itch. However, pharmacological and anatomic evidence of these two spinal ligandreceptor systems are still not clear. The aim of this study was to determine the spinal functions of BNP-NPRA and GRP-GRPR systems for regulating scratching activities in mice by using pharmacological and immunohistochemical approaches. Our results showed that intrathecal administration of BNP (0.3-3 nmol) dose dependently elicited scratching responses, which could be blocked by the NPRA antagonist (Arg6,b-cyclohexyl-Ala8,D-Tic16, Arg17,Cys18)-atrial natriuretic factor(6-18) amide (A71915). However, A71915 had no effect on intrathecal GRP-induced scratching. In contrast, pretreatment with a GRPR antagonist (D-Tpi6,Leu13c (CH2-NH)-Leu14)bombesin(6-14) (RC-3095) inhibited BNPinduced scratching. Immunostaining revealed that NPRA proteins colocalize with GRP, but not GRPR, in the superficial area of dorsal horn, whereas BNP proteins do not colocalize with either GRP or GRPR in the dorsal horn. Intradermal administration of ligands including endothelin-1, U-46619, bovine adrenal medulla 8-22, and Ser-Leu-Ile-Gly-Arg-Leu-NH 2 (SLIGRL) increased scratching bouts at different levels of magnitude. Pretreatment with intrathecal A71915 did not affect scratching responses elicited by all four pruritogens, whereas pretreatment with RC-3095 only inhibited SLIGRL-induced scratching. Interestingly, immunostaining showed that RC-3095, but not A71915, inhibited SLIGRLelicited c-Fos activation in the spinal dorsal horn, which was in line with behavioral outcomes. These findings demonstrate that: 1) BNP-NPRA system may function upstream of the GRP-GRPR system to regulate itch in the mouse spinal cord, and 2) both NPRA and GRPR antagonists may have antipruritic efficacy against centrally, but not peripherally, elicited itch.

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Opioid Modulation of Scratching and Spinal c-fosExpression Evoked by Intradermal Serotonin

Cited by 52 publications

References 52 publications

Facial injections of pruritogens or algogens elicit distinct behavior responses in rats and excite overlapping populations of primary sensory and trigeminal subnucleus caudalis neurons

Facial injections of pruritogens or algogens elicit distinct behavior responses in rats and excite overlapping populations of primary sensory and trigeminal subnucleus caudalis neurons

Glycine Inhibitory Dysfunction Induces a Selectively Dynamic, Morphine-Resistant, and Neurokinin 1 Receptor- Independent Mechanical Allodynia

Spinal Functions of B-Type Natriuretic Peptide, Gastrin-Releasing Peptide, and Their Cognate Receptors for Regulating Itch in Mice

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