Immunohistochemical localization of group I and II metabotropic glutamate receptors in control and amyotrophic lateral sclerosis human spinal cord: upregulation in reactive astrocytes

Aronica, Eleonora; Catania, Maria Vincenza; Geurts, Jeroen J. G.; Yankaya, Bulent; Troost, Dirk

doi:10.1016/s0306-4522(01)00181-6

Cited by 144 publications

(122 citation statements)

References 62 publications

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“…Group II mGluR have been identified with immunohistochemical methods in the spinal cord and brain, and in small to medium size dorsal root ganglia neurons, and in cutaneous sensory nerves that coexpress TRPV1 receptors (5,7,27). Group II mGluR antagonists enhance nociceptive behavior and primary afferent firing induced by intraplantar injection of capsaicin; and a group II mGluR agonist suppressed this enhancement (9).…”

Section: Discussionmentioning

confidence: 99%

Contribution of opioid and metabotropic glutamate receptor mechanisms to inhibition of bladder overactivity by tibial nerve stimulation

Matsuta

Mally

Zhang

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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(mGluR) and opioid receptors to inhibition of bladder overactivity by tibial nerve stimulation (TNS) was investigated in cats under ␣-chloralose anesthesia using LY341495 (a group II mGluR antagonist) and naloxone (an opioid receptor antagonist). Slow infusion cystometry was used to measure the volume threshold (i.e., bladder capacity) for inducing a large bladder contraction. After measuring the bladder capacity during saline infusion, 0.25% acetic acid (AA) was infused to irritate the bladder, activate the nociceptive C-fiber bladder afferents, and induce bladder overactivity. AA significantly (P Ͻ 0.0001) reduced bladder capacity to 26.6 Ϯ 4.7% of saline control capacity. TNS (5 Hz, 0.2 ms) at 2 and 4 times the threshold (T) intensity for inducing an observable toe movement significantly increased bladder capacity to 62.2 Ϯ 8.3% at 2T (P Ͻ 0.01) and 80.8 Ϯ 9.2% at 4T (P ϭ 0.0001) of saline control capacity. LY341495 (0.1-5 mg/kg iv) did not change bladder overactivity, but completely suppressed the inhibition induced by TNS at a low stimulus intensity (2T) and partially suppressed the inhibition at high intensity (4T). Following administration of LY341495, naloxone (0.01 mg/kg iv) completely eliminated the high-intensity TNS-induced inhibition. However, without LY341495 treatment a 10 times higher dose (0.1 mg/kg) of naloxone was required to completely block TNS inhibition. These results indicate that interactions between group II mGluR and opioid receptor mechanisms contribute to TNS inhibition of AA-induced bladder overactivity. Understanding neurotransmitter mechanisms underlying TNS inhibition of bladder overactivity is important for the development of new treatments for bladder disorders.neurotransmitter; neuromodulation; bladder; cat GLUTAMATERGIC NEUROTRANSMISSION involves activation of both ionotropic glutamate receptors (iGluR) and metabotropic glutamate receptors (mGluR) that consist of eight subtypes classified into group I (mGluR 1 and 5), group II (mGluR 2 and 3), and group III (mGluR 4,6,7,and 8). An interaction between iGluR and opioid receptor mechanisms is believed to be important in pain pathways, because block of ionotropic Nmethyl-D-aspartate (NMDA) receptors enhances the antinociceptive effect of morphine (an opioid receptor agonist) (14,28,36,37). Recently, the interaction between mGluR and opioid receptors has also been identified in studies of opioid-induced antinociception (15,16,29,45). Opioid-induced antinociceptive effects were enhanced by antagonists (15,16,45) and agonists (29) of group II mGluR in different types of somatic nociception. Currently, it is unknown whether this interaction between group II mGluR and opioid receptors occurs in visceral nociceptive mechanisms.Recent results from this laboratory (38) revealed that tibial nerve stimulation (TNS) inhibits bladder overactivity elicited by intravesical infusion of acetic acid (AA), which stimulates nociceptive bladder afferent nerves. This TNS-induced antinociceptive effect is completely eliminated by naloxone (an opioid...

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Section: Discussionmentioning

confidence: 99%

Contribution of opioid and metabotropic glutamate receptor mechanisms to inhibition of bladder overactivity by tibial nerve stimulation

Matsuta

Mally

Zhang

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Indeed, the expression of mGluR5 in the ventral spinal cord of ALS patients was reported to be selectively upregulated in astrocytes. 37 Moreover, astrocytes from hSOD1 G93A rats display enhanced mGluR5 expression accompanied by alterations of the coupled signal-transduction pathways. 38 The potential relevance of our observations to ALS pathogenesis was confirmed by the studies in vivo.…”

Section: Discussionmentioning

confidence: 99%

Focal degeneration of astrocytes in amyotrophic lateral sclerosis

et al. 2008

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Astrocytes emerge as key players in motor neuron degeneration in Amyotrophic Lateral Sclerosis (ALS). Whether astrocytes cause direct damage by releasing toxic factors or contribute indirectly through the loss of physiological functions is unclear. Here we identify in the hSOD1 G93A transgenic mouse model of ALS a degenerative process of the astrocytes, restricted to those directly surrounding spinal motor neurons. This phenomenon manifests with an early onset and becomes significant concomitant with the loss of motor cells and the appearance of clinical symptoms. Contrary to wild-type astrocytes, mutant hSOD1-expressing astrocytes are highly vulnerable to glutamate and undergo cell death mediated by the metabotropic type-5 receptor (mGluR5). Blocking mGluR5 in vivo slows down astrocytic degeneration, delays the onset of the disease and slightly extends survival in hSOD1 G93A transgenic mice. We propose that excitotoxicity in ALS affects both motor neurons and astrocytes, favouring their local interactive degeneration. This new mechanistic hypothesis has implications for therapeutic interventions.

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“…For example, DA-DOPAC-HVA levels and TH-DAT immunostaining may reflect functional changes occurring in surviving fibers, whereas the extent of gliosis in knock-out mice may be affected by the absence of mGlu5 receptors in reactive astrocytes (Aronica et al, 2000(Aronica et al, , 2001Ulas et al, 2000;Ferraguti et al, 2001). It is likely that more nigro-striatal dopaminergic terminals are spared in mGlu5 knock-out mice treated with MPTP; however, these terminals are overactive in terms of DA synthesis, release, re-uptake, and metabolism.…”

Section: Discussionmentioning

confidence: 99%

Endogenous Activation of mGlu5 Metabotropic Glutamate Receptors Contributes to the Development of Nigro-Striatal Damage Induced by 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine in Mice

Battaglia¹,

Busceti²,

Molinaro³

et al. 2004

J. Neurosci.

116

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Immunohistochemical localization of group I and II metabotropic glutamate receptors in control and amyotrophic lateral sclerosis human spinal cord: upregulation in reactive astrocytes

Cited by 144 publications

References 62 publications

Contribution of opioid and metabotropic glutamate receptor mechanisms to inhibition of bladder overactivity by tibial nerve stimulation

Contribution of opioid and metabotropic glutamate receptor mechanisms to inhibition of bladder overactivity by tibial nerve stimulation

Focal degeneration of astrocytes in amyotrophic lateral sclerosis

Endogenous Activation of mGlu5 Metabotropic Glutamate Receptors Contributes to the Development of Nigro-Striatal Damage Induced by 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine in Mice

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