Increase inω3 (peripheral type benzodiazepine) binding sites in the rat cortex and striatum after local injection of interleukin-1, tumour necrosis factor-α and lipopolysaccharide

Bourdiol, F.; Toulmond, Sylvie; Serrano, A.; Bénavidès, J.; Scatton, B.

doi:10.1016/0006-8993(91)90028-t

Cited by 77 publications

(42 citation statements)

References 27 publications

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“…The kinetics of the inflammatory reaction following intracerebral LPS infusion have been previously described in murine (Andersson et al,l992b) and rat (Bourdiol et al, 1991;Montero-Menei et al, 1994Szczepanik et al, 1996) CNS. Similarly, the aim of our study was to determine whether glial activation by a single LPS injection into the SN could have any effect on the viability of the dopaminergic neurons in vivo.…”

Section: Discussionmentioning

confidence: 97%

“…Andersson et al (1992b) described pyramidal cell loss in the CAl field in mice following an acute intrahippocampal infusion of 2.0 ‚ug of LPS. Also, a slight but significant loss of neuronal NMDA receptors was reported following a single LPS infusion into the striatum (Bourdiol et al, 1991).…”

Section: Discussionmentioning

confidence: 98%

“…Taking into account that intracerebral injection of LPS activates glial cells in vivo (Bourdiol et al, 1991;Andersson et al, 1992b;Montero-Menei et al, 1994Szczepanik at al., 1996) and that, recently, in vitro studies (Bronstein et al, 1995) have described that dopaminergic neurons were twice as sensitive to the toxic effects of LPS as were tyrosine hydroxylase (TH)-negative neurons, we consider that LPS provides an interesting model to study the re-sponse of the dopaminergic system to inflammation and to help clarify how brain cells can be involved in neurotoxic processes.…”

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confidence: 99%

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Lipopolysaccharide Intranigral Injection Induces Inflammatory Reaction and Damage in Nigrostriatal Dopaminergic System

Castaño

Herrera

Cano

et al. 1998

Journal of Neurochemistry

365

270

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Abstract:The pathogenesis of Parkinson's disease is still poorly understood. To address the hypothesis that immunemediated events, such as microglial activation, may be involved in the dopaminergic neurodegeneration, we have studied the effect that intranigral injection of the immunostimulant lipopolysaccharide has on monoaminergic neurotransmitters in rats. Activation of microglial cells, visualized by immunohistochemistry with a specific monoclonal antibody, was already obvious 2 days after injection. In relation to the biochemical parameters studied, we found a significant decrease of dopamine levels in both the substantia nigra and striatum up to at least 21 days after intranigral injection of lipopolysaccharide. This result was supported by the decrease in tyrosine hydroxylase activity and the loss of tyrosine hydroxylase-positive neuronal bodies, shown by immunohistochemistry. These alterations of the dopaminergic system did not reverse during the interval studied (21 days); conversely, the serotoninergic system suffered only transient damage. In addition, we found that the neurotoxic effect of lipopolysaccharide was not mediated by nitric oxide. Based on our results we suggest that the nigrostriatal dopaminergic system is susceptible to damage by inf lammatory events and that these may be implicated in neurodegeneration processes such as Parkinson's disease.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 98%

mentioning

confidence: 99%

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Lipopolysaccharide Intranigral Injection Induces Inflammatory Reaction and Damage in Nigrostriatal Dopaminergic System

Castaño

Herrera

Cano

et al. 1998

Journal of Neurochemistry

365

270

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“…Feedback regulations between cytokines and PBR may also be considered. Indeed, data from in vivo experiments have shown that cytokines, like interleukin-1 and TNF␣, induce an up-regulation of PBR sites in the rat brain (Bourdiol et al, 1991). Identification of these relationships may help to understand the mechanisms responsible for the neuroprotective effects of PBR ligands.…”

Section: Discussionmentioning

confidence: 99%

SSR180575 (7-Chloro-N,N,5-trimethyl-4-oxo-3-phenyl-3,5-dihydro-4H-pyridazino[4,5-b]indole-1-acetamide), a Peripheral Benzodiazepine Receptor Ligand, Promotes Neuronal Survival and Repair

Ferzaz

Brault²,

Bourliaud³

et al. 2002

J Pharmacol Exp Ther

114

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In the present study, we have investigated the potential neuroprotective effects of a novel peripheral benzodiazepine binding site (PBR) ligand,N,indole-1-acetamide (SSR180575), in models of central and peripheral neurodegeneration in vivo and its effect on steroid concentrations in plasma and nervous tissue. SSR180575 shows high affinity (IC 50 , 2.5-3.5 nM) and selectivity for the rat and human PBR and potently inhibits the in vivo binding of [ 3 H]alpidem to PBR in the rat brain and spleen after oral or i.p. administration (ID 50 , 0.1-0.3 mg/kg). In an experimental model of motoneuron degeneration induced by facial nerve axotomy in the immature rat, SSR180575 given i.p. or orally for 8 days rescued facial motoneurons, increasing their survival by 40 to 72% at 6 and 10 mg/kg p.o. b.i.d. Moreover, in this model, SSR180575 (10 mg/kg p.o. b.i.d.) increased by 87% the number of motoneurons immunoreactive to peripherin, a type III intermediate filament, whose expression is up-regulated during nerve regeneration. SSR180575 also improved functional recovery in acrylamide-induced neuropathy in the rat when given therapeutically at 2.5 to 10 mg/kg/day p.o. Furthermore, SSR180575 (3 mg/kg i.p. b.i.d.) accelerated functional recovery of the blink reflex after local injury of the facial nerve in the rat. SSR180575 increased pregnenolone accumulation in the brain and sciatic nerve (ϩ100% at 3 mg/kg i.p.), suggesting that its neuroprotective effects are steroid-mediated. These results indicate that PBR ligands (e.g., SSR180575) promote neuronal survival and repair in axotomy and neuropathy models and have potential for the treatment of neurodegenerative diseases (e.g., peripheral neuropathies or amyotrophic lateral sclerosis).

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“…PBRs are associated with mitochondrial fractions although their function is still unclear (see Moreno-Sanchez et al, 1991;Gavish et al, 1992). There are now numerous reports of studies using ligands for the PBR binding site (PK 11195 and Ro54864), which have confirmed a significant increase in PBR binding associated with neurodegeneration, (Schoemaker et al, 1982;Benavides et al, 1987;Altar & Baudry, 1990;Bourdiol et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

Inhibition by the adenosine analogue, (R‐)‐N⁶‐phenylisopropyl‐adenosine, of kainic acid neurotoxicity in rat hippocampus after systemic administration

MacGregor

Stone

1993

British J Pharmacology

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Binding of the peripheral benzodiazepine receptor ligand, [3H]‐PK 11195, to rat hippocampal membranes has been used to quantify the reactive gliosis resulting from neuronal death induced by intraperitoneally administered kainic acid. Intraperitoneal administration of kainic acid (10 mg kg−1) caused a 350–500% increase in [3H]‐PK 11195 binding measured in rat hippocampal P2 membranes 7 days later. Co‐treatment with the adenosine derivative R‐phenylisopropyladenosine (R‐PIA) (100, 25 or 10 μg kg−1, i.p.) abolished this elevation. The protective action of R‐PIA could itself be abolished by co‐treatment with 8‐phenyltheophylline (1 mg kg−1). Body temperatures were recorded in the antagonist experiments and no significant changes were recorded, suggesting that the protective action of R‐PIA was not mediated by hypothermia. Since systemic kainic acid‐induced neurotoxicity has been claimed as a good model of neuronal death in temporal lobe epilepsy, the results suggest that the systemic administration of purines in low doses may provide protection against certain neurodegenerative insults.

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Increase inω3 (peripheral type benzodiazepine) binding sites in the rat cortex and striatum after local injection of interleukin-1, tumour necrosis factor-α and lipopolysaccharide

Cited by 77 publications

References 27 publications

Lipopolysaccharide Intranigral Injection Induces Inflammatory Reaction and Damage in Nigrostriatal Dopaminergic System

Lipopolysaccharide Intranigral Injection Induces Inflammatory Reaction and Damage in Nigrostriatal Dopaminergic System

SSR180575 (7-Chloro-N,N,5-trimethyl-4-oxo-3-phenyl-3,5-dihydro-4H-pyridazino[4,5-b]indole-1-acetamide), a Peripheral Benzodiazepine Receptor Ligand, Promotes Neuronal Survival and Repair

Inhibition by the adenosine analogue, (R‐)‐N⁶‐phenylisopropyl‐adenosine, of kainic acid neurotoxicity in rat hippocampus after systemic administration

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Increase inω3 (peripheral type benzodiazepine) binding sites in the rat cortex and striatum after local injection of interleukin-1, tumour necrosis factor-α and lipopolysaccharide

Cited by 77 publications

References 27 publications

Lipopolysaccharide Intranigral Injection Induces Inflammatory Reaction and Damage in Nigrostriatal Dopaminergic System

Lipopolysaccharide Intranigral Injection Induces Inflammatory Reaction and Damage in Nigrostriatal Dopaminergic System

SSR180575 (7-Chloro-N,N,5-trimethyl-4-oxo-3-phenyl-3,5-dihydro-4H-pyridazino[4,5-b]indole-1-acetamide), a Peripheral Benzodiazepine Receptor Ligand, Promotes Neuronal Survival and Repair

Inhibition by the adenosine analogue, (R‐)‐N6‐phenylisopropyl‐adenosine, of kainic acid neurotoxicity in rat hippocampus after systemic administration

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Inhibition by the adenosine analogue, (R‐)‐N⁶‐phenylisopropyl‐adenosine, of kainic acid neurotoxicity in rat hippocampus after systemic administration