Opioid neurotransmission in the post-ictal analgesia: Involvement of μ1-opioid receptor

Coimbra, Norberto Cysne; Freitas, Renato Leonardo de; Savoldi, Marcela; Castro-Souza, C.; Segato, E.N.; Kishi, Renato; Weltson, Alfredo; Resende, Gisele Cristina

doi:10.1016/s0006-8993(01)02366-6

Cited by 37 publications

(24 citation statements)

References 16 publications

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“…PTZ is an antagonist of the type A receptor of γ-aminobutyric acid (GABA A ) (Stone, 1970). As with other GABA A antagonists, administration of low doses of PTZ can result in absence seizures in animal models (Snead et al, 2000), whereas higher doses result in generalized tonic-clonic seizures (Woodbury et al, 1980; Panagopoulos et al, 1998; Coimbra et al, 2001a,b; Erakovic et al, 2001; Eloqayli et al, 2003). In this study, we used PTZ at both sub-convulsive and convulsive doses to analyze seizure thresholds in an attempt to elucidate the molecular mechanisms underlying altered neuronal excitability in Epm2a −/− and Epm2b −/− mice and to further evaluate novel therapeutic strategies to treat epileptic symptoms.…”

Section: Introductionmentioning

confidence: 99%

Enhanced sensitivity of laforin- and malin-deficient mice to the convulsant agent pentylenetetrazole

et al. 2014

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Lafora disease is a rare form of inherited progressive myoclonus epilepsy caused by mutations in the EPM2A gene encoding laforin, or in the EPM2B gene, which encodes malin. It is characterized by the presence of polyglucosan inclusion bodies (Lafora bodies) in brain and other tissues. Genetically engineered mice lacking expression of either the laforin (Epm2a−/−) or malin (Epm2b−/−) genes display a number of neurological and behavioral abnormalities that resemble those found in patients suffering from Lafora disease; of these, both Epm2a−/− and Epm2b−/− mice have shown altered motor activity, impaired motor coordination, episodic memory deficits, and different degrees of spontaneous epileptic activity. In this study, we analyze the sensitivity of Epm2a−/− and Epm2b−/− mice to the convulsant drug pentylenetetrazol (PTZ), an antagonist of the γ-aminobutyric acid type A (GABAA) receptor, commonly used to induce epileptic tonic-clonic seizures in laboratory animals. PTZ-induced epileptic activity, including myoclonic jerks and tonic-clonic seizures, was analyzed in 2 age groups of mice comprising representative samples of young adult and aged mice, after administration of PTZ at sub-convulsive and convulsive doses. Epm2a−/− and Epm2b−/− mice showed a lower convulsive threshold after PTZ injections at sub-convulsive doses. A lower convulsive threshold and shorter latencies to develop epileptic seizures were observed after PTZ injections at convulsive doses. Different patterns of generalized seizures and of discharges were observed in Epm2a−/− and Epm2b−/− mice. Epm2a−/− and Epm2b−/− mice present an increased sensitivity to the convulsant agent PTZ that may reflect different degrees of increased GABAA receptor-mediated hyperexcitability.

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Section: Introductionmentioning

confidence: 99%

Enhanced sensitivity of laforin- and malin-deficient mice to the convulsant agent pentylenetetrazole

et al. 2014

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“…Several studies have demonstrated that post-ictal analgesia is induced, following electroshock or drug-induced generalized seizures in rats (Coimbra et al, 2001; De Oliveira et al, 2006; Portugal-Santana et al, 2004; Urca et al, 1981). Reduced responsiveness to pain is also known to occur in certain forms of human epilepsy (Guieu et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

Post-ictal analgesia in genetically epilepsy-prone rats is induced by audiogenic seizures and involves cannabinoid receptors in the periaqueductal gray

2011

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Post-ictal depression of consciousness occurs after generalized convulsive seizures, and includes analgesia, lasting for hours after electrically- or chemically-induced seizures in animals. The brain sites and mechanisms, mediating post-ictal analgesia, are unclear. The ventrolateral periaqueductal gray (PAG) is an important neuronal network site for mediating analgesia and also in generalized seizures, particularly in genetically epilepsy-prone rats (GEPRs). Endocannabinoids are implicated in mediating analgesia in several brain sites, including the PAG, and generalized seizures result in endocannabinoid release. This study evaluated if post-ictal analgesia occurs in GEPRs, following audiogenic seizures (AGS), and whether this analgesia involves endocannabinoid actions in PAG. Analgesia was evaluated, using thermal stimulation to evoke nociception, measuring changes in paw withdrawal latencies (PWLs) induced by AGS. Endocannabinoid involvement in post-ictal analgesia in GEPRs was evaluated, using focal bilateral microinjection of a cannabinoid (CB1) receptor antagonist (AM251) into PAG. AGS induced a significant increase in PWLs, lasting for ≥120 min. Microinjection of AM251 (100 and 200, but not 50 pmoles/side) into PAG significantly decreased post-ictal analgesia in GEPRs. Endocannabinoids are also known to activate transient receptor potential vanilloid (TRPV1) receptors, but PAG microinjection of a TRPV1 receptor antagonist (capsazepine) did not affect post-ictal analgesia in GEPRs. These results indicate that AGS in GEPRs induce post-ictal analgesia, which is the first observation of this phenomenon in a genetic epilepsy model. These findings suggest an important role of PAG in post-ictal analgesia. The results also suggest that CB1 receptors in PAG are critical for mediating post-ictal analgesia in GEPRs.

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“…Another study did not detect correspondence between the behavioral and histopathological effects provoked by coagulation of the MCA in rats 6 . Using the open fi eld test according to the criteria established at our institution 16 , we observed reduction of exploratory activity (rearing and sniffing) and of defecation on the 1st postoperative day in all animals of the ischemic groups. Despite differences in the elaboration and execution of the tests, our results agree with those reported by Wahl et al 6 regarding the absence of a correlation between the behavioral and histopathological changes.…”

Section: Discussionmentioning

confidence: 86%

“…This was used in this study because it was the only way we fi nd to assess behaviors as crossing, defecation, sniffi ng, resting, rearing, half rotation, and grooming and because it was available and validated in our facility 16 . The time of observation was arbitrarily fi xed in 15 minutes after some previous observations that the exploratory activity of the animals decreased progressively after 5 to 10 minutes.…”

Section: Discussionmentioning

confidence: 99%

“…Before surgery, 24 animals from group A and 44 from group B were observed and fi lmed in an open fi eld 16 for 15 minutes for behavioral evaluation. The following items were analyzed: a) number of crossings (passing from one section of the open fi eld to another), number of defecations (number of fecal boluses during the period), number of rearings of the front paws and of half rotations (180º turns); b) rates of sniffi ng (exploration of the environment by olfaction), of grooming (selfcleaning) and resting (immobility in the same place).…”

Section: Methodsmentioning

confidence: 99%

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Evaluation of the neuroprotective effect of ketoprofen on rats submitted to permanent focal brain ischemia

Silva

Colli

Coimbra

et al. 2007

Arq. Neuro-Psiquiatr.

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-Objective: To study the neurobehavioral, biochemical and histopathological consequences of permanent focal brain ischemia, and the putative neuroprotective action of ketoprofen. Method: Onehundred-and-three Wistar rats divided into groups A and B were respectively submitted to 48 hours and 15 days of ischemia. Each group was divided into 4 subgroups: ischemic not treated, ischemic treated, sham not treated, and sham treated. Ischemic animals had the left middle cerebral artery coagulated. Ketoprofen was administered to treated subgroups 15 minutes before arterial coagulation (manipulation in the sham group). Results: Exploratory activity and defecation were reduced in all ischemic animals in the first postoperative days and constant histopathological changes were observed in each group. The total brain glutamate levels were higher in treated animals 48 hours after surgery. Conclusion: No clear parallelism among behavioral, biochemical and histopathological findings was observed. Ketoprofen demonstrated no neuroprotective effect on the behavioral or histopathological aspects of focal permanent brain ischemia.KEY WORDS: focal brain ischemia, rat, open field, glutamate, histopathology, neuroprotection, ketoprofen. Avaliação do efeito neuroprotetor do cetoprofeno em ratos submetidos à isquemia cerebral focal permanenteRESUMO -Objetivo: Estudar as conseqüências comportamentais, bioquímicas e histopatológicas da isquemia cerebral focal permanente e o possível efeito neuroprotetor do cetoprofeno. Método: Foram utilizados 103 ratos Wistar, divididos em grupos A e B, submetidos, respectivamente, a 48 horas e a 15 dias de isquemia. Cada grupo foi dividido em 4 subgrupos: isquêmico não tratado; isquêmico tratado; sham não tratado; sham tratado. Nos animais isquêmicos foi coagulada a artéria cerebral média esquerda. Os subgrupos tratados receberam cetoprofeno 15 minutos antes da oclusão ou manipulação arterial. Resultados: Os animais isquêmicos reduziram a atividade exploratória e as evacuações nos primeiros dias pós-operatórios e mostraram alterações histopatológicas constantes em cada grupo. As concentrações do glutamato total 48 horas após a cirurgia foram maiores nos animais tratados. Conclusão: Não houve um paralelismo entre os achados comportamentais, bioquímicos e histopatológicos. O cetoprofeno não apresentou efeito protetor contra isquemia cerebral focal permanente, nos aspectos comportamentais e histopatológicos.

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Opioid neurotransmission in the post-ictal analgesia: Involvement of μ1-opioid receptor

Cited by 37 publications

References 16 publications

Enhanced sensitivity of laforin- and malin-deficient mice to the convulsant agent pentylenetetrazole

Enhanced sensitivity of laforin- and malin-deficient mice to the convulsant agent pentylenetetrazole

Post-ictal analgesia in genetically epilepsy-prone rats is induced by audiogenic seizures and involves cannabinoid receptors in the periaqueductal gray

Evaluation of the neuroprotective effect of ketoprofen on rats submitted to permanent focal brain ischemia

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