Antinociceptive action of intrathecally administered IGF-I and the expression of its receptor in rat spinal cord

Bitar, Milad S.; Al-Bustan, Mahmoud; Nehme, Cheryl L.; Pilcher, C.W.T.

doi:10.1016/0006-8993(96)00747-0

Cited by 22 publications

(15 citation statements)

References 16 publications

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“…Similarly, deficiency of insulin and IGF-1 may secondarily deplete gastric ICCs in the NOD mouse (Horvath et al, 2005). Local synthesis of IGF-1 and perikaryal, axonal, and nerve terminal IGF-1 receptors in the rat SCG suggest a possible autocrine or paracrine role for IGF-1 in sympathetic ganglia (Bitar et al, 1996;Singhal et al, 1997;Carroll et al, 2004). Although the diabetic male rat MPG showed no significant change in IGF-1 gene and receptor expression, increased ganglionic IGF binding proteins (IGFBP-3, 4, 5) add another layer of complexity to the analysis (Abdelbaky et al, 1998).…”

Section: Insulin-like Growth Factorsmentioning

confidence: 96%

Autonomic neuropathy in experimental models of diabetes mellitus

Schmidt

2014

Handbook of Clinical Neurology

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Section: Insulin-like Growth Factorsmentioning

confidence: 96%

Autonomic neuropathy in experimental models of diabetes mellitus

Schmidt

2014

Handbook of Clinical Neurology

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“…If gene regulations were not after a simple "on/off" pattern (i.e., that formalin was modulating gene expression toward a pronociceptive phenotype and that acetaminophen was reversing it to the basal state), some evidence suggests that the activity of those up-regulated receptors could be involved in producing antinoception. GHR stimulation provokes IGF-1 synthesis (Schwartzbauer and Menon, 1998) and spinal IGF-1R stimulation produces a dose-dependent antinociception in the rat tail-flick reflex (Bitar et al, 1996). It is noteworthy that reduced GH and IGF-1 secretions are observed in fibromyalgic patients (Leal-Cerro et al, 1999).…”

Section: New Spinal Mediators In Acetaminophen-elicited Analgesiamentioning

confidence: 99%

Acetaminophen Recruits Spinal p42/p44 MAPKs and GH/IGF-1 Receptors to Produce Analgesia via the Serotonergic System

Bonnefont

Daulhac²,

Etienne³

et al. 2006

Mol Pharmacol

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The mechanism of action of acetaminophen is currently widely discussed. Direct inhibition of cyclooxygenase isoforms remains the commonly advanced hypothesis. We combined behavioral studies with molecular techniques to investigate the mechanism of action of acetaminophen in a model of tonic pain in rats. We show that acetaminophen indirectly stimulates spinal 5-hydroxytryptamine (5-HT) 1A receptors in the formalin test, thereby increasing transcript and protein levels of low-affinity neurotrophin receptor, insulin-like growth factor-1 (IGF-1) receptor ␣ subunit, and growth hormone receptor and reducing the amount of somatostatin 3 receptor (sst3R) mRNA. Those cellular events seem to be important for the antinociceptive activity of acetaminophen. Indeed, down-regulation of sst3R mRNA depends on acetaminophen-elicited, 5-HT 1A receptordependent increase in neuronal extracellular signal-regulated kinase 1/2 (ERK1/2) activities that mediate antinociception. In addition, spinal growth hormone (GH) and IGF-1 receptors would also be involved in the antinociceptive activity of the analgesic at different degrees. Our results show the involvement of specific 5-HT 1A receptor-dependent cellular events in acetaminophen-produced antinociception and consequently indicate that inhibition of cyclooxygenase activities is not the exclusive mechanism involved. Furthermore, we propose that the mechanisms of 5-HT 1A receptor-elicited antinociception and the role of the spinal ERK1/2 pathway in nociception are more intricate than suspected so far and that the GH/IGF-1 axis is an interesting new player in the regulation of spinal nociception.

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“…Indeed, it was reported that IGF-1 impairs glutamate and depolarization-induced release of GABA and acetylcholine, respectively, in several brain areas including the cerebellum, cortex and hippocampus [20,21]. Moreover, IGF-1, but not insulin, elevated nociceptive thresholds as reflected by the increased tail flick latency of the tail immersion test in a doseand time-dependent manner [2]. Overall, the above findings are consistent with the concept that IGF-1 may be a trophic factor during neurogenesis and a neuromodulator and/or plasticity mediator in the adult nervous system.…”

Section: Introductionmentioning

confidence: 99%

“…Insulin-like growth factor I (IGF-1) is a trophic and neuromodulatory polypeptide with structural and functional homology to insulin [1]. It is localized to discrete areas of the embryonic and adult nervous system including brain, spinal motor neurons and spinal and autonomic ganglia [2][3][4]. In these specific neuronal tissues, IGF-1 appears to be important for embryonic and early postnatal growth and development 15].…”

Section: Introductionmentioning

confidence: 99%

Insulin-Like Growth Factor 1-Induced Alterations in Lumbospinal Monoamine Dynamics

Ms¹,

Im²,

Cw³

2000

Horm Metab Res

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A wealth of evidence indicates that insulin-like growth factor (IGF-1) is involved in neurotransmitter release, synaptic plasticity, morphogenesis and regulation of gene expression. RT-PCR and immunocytochemical-based techniques revealed that IGF-1 and its receptor are highly expressed by different neuronal elements of the spinal cord lumbar enlargement. Accordingly, the present study intended to examine lumbospinal monoamine dynamics in the context of the neurotrophic factor IGF-1. Spinal release of norepinephrine (NE) represented by 3-methoxy-4-hydroxyphenylglycol (MHPG)/NE ratio was enhanced by IGF-1. This action of IGF-1 was associated with a similar increase in both tyrosine hydroxylase (TH) immunoreactivity and the level of its mRNA. In contrast, neuronal contents of serotonin and its metabolite 5-hydroxyindoleacetic acid in IGF-1-treated animals remained at control level. Genistein, a tyrosine kinase inhibitor, which by itself had no effect on NE metabolism, abolished the induction effect of IGF-1 on TH and MHPG/NE ratio. Our results suggest that IGF-1 augments the lumbospinal noradrenergic system by an intracellular mechanism involving a receptor-linked tyrosine kinase. The physiological consequences of the IGF-1 actions are discussed in terms of neuroprotection and nociception.

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Antinociceptive action of intrathecally administered IGF-I and the expression of its receptor in rat spinal cord

Cited by 22 publications

References 16 publications

Autonomic neuropathy in experimental models of diabetes mellitus

Autonomic neuropathy in experimental models of diabetes mellitus

Acetaminophen Recruits Spinal p42/p44 MAPKs and GH/IGF-1 Receptors to Produce Analgesia via the Serotonergic System

Insulin-Like Growth Factor 1-Induced Alterations in Lumbospinal Monoamine Dynamics

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