Effects of chronic morphine and N6-cyclopentyl-adenosine administration on kainic acid-induced status epilepticus

Cano-Martı́nez, Agustina; Villalobos‐Molina, Rafael; Rocha, Luísa

doi:10.1016/s0920-1211(01)00187-5

Cited by 12 publications

(8 citation statements)

References 44 publications

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“…, 2002) and epileptic seizures (Snead & Bearden, 1982; Snead, 1986; Velisek et al. , 2000; Cano‐Martinez et al. , 2001), the expression and transcription of the GABA‐synthesizing enzyme GAD‐67 in response to morphine treatment were quantified.…”

Section: Alteration Of Glutamate Decarboxylase‐67 Mrna and Protein Lesupporting

confidence: 75%

Repeated morphine treatment alters polysialylated neural cell adhesion molecule, glutamate decarboxylase‐67 expression and cell proliferation in the adult rat hippocampus

Kahn

Alonso

Normand

et al. 2005

Eur J of Neuroscience

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Altered synaptic transmission and plasticity in brain areas involved in reward and learning are thought to underlie the long-lasting effects of addictive drugs. In support of this idea, opiates reduce neurogenesis [A.J. Eisch et al. (2000) Proceedings of the National Academy of Sciences USA, 97, 7579-7584] and enhance long-term potentiation in adult rodent hippocampus [J.M. Harrison et al. (2002) Journal of Neurophysiology, 87, 2464-2470], a key structure of learning and memory processes. Here we studied how repeated morphine treatment and withdrawal affect cell proliferation and neuronal phenotypes in the dentate gyrus-CA3 region of the adult rat hippocampus. Our data showed a strong reduction of cellular proliferation in morphine-dependent animals (54% of control) that was followed by a rebound increase after 1 week withdrawal and a return to normal after 2 weeks withdrawal. Morphine dependence was also associated with a drastic reduction in the expression levels of the polysialylated form of neural cell adhesion molecule (68% of control), an adhesion molecule expressed by newly generated neurons and involved in cell migration and structural plasticity. Polysialylated neural cell adhesion molecule levels quickly returned to normal following withdrawal. In morphine-dependent rats, we found a significant increase of glutamate decarboxylase-67 mRNA transcription (170% of control) in dentate gyrus granular cells which was followed by a marked rebound decrease after 1 week withdrawal and a return to normal after 4 weeks withdrawal. Together, the results show, for the first time, that, in addition to reducing cell proliferation and neurogenesis, chronic exposure to morphine dramatically alters neuronal phenotypes in the dentate gyrus-CA3 region of the adult rat hippocampus.

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Section: Alteration Of Glutamate Decarboxylase‐67 Mrna and Protein Lesupporting

confidence: 75%

Repeated morphine treatment alters polysialylated neural cell adhesion molecule, glutamate decarboxylase‐67 expression and cell proliferation in the adult rat hippocampus

Kahn

Alonso

Normand

et al. 2005

Eur J of Neuroscience

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“…Pentylenetetrazole-induced (intraperitoneal injection) seizures in rats and in mice Seizure reduction, anticonvulsant effect [254,256] Pentylenetetrazole-induced seizures in rats Suppressed/abolished tonic phase of generalized tonicclonic seizures [255] Bicuculline-induced (intraperitoneal injection) seizures in mice Anticonvulsant effect [254] Audiogenic seizures (audiogenic-seizure-sensitive DBA/2 mice) Seizure prevention [95] PPS (perforant path stimulation) rat model of status epilepticus Decreased progression from self-terminating seizures to selfsustaining status epilepticus (SSSE) and decreased severity of SSSE [68] Kainic acid-induced (intraperitoneal injection) seizures in rats Delayed status epilepticus presentation [235] 4-aminopyridine-induced (rat hippocampal slices) epileptiform activity Decreased epileptiform bursting duration [269] 3-mercaptopropionic acid-induced seizures Increased seizure latency [271] Aminophylline-induced (intraperitoneal application) seizures in mice Delayed time to onset of clonic convulsions [279] Bicuculline-induced (rat prepiriform cortex) seizures Seizure protection [267] Electrical stimulation rat models of status epilepticus Seizure suppression [257] CPA (A1 receptor agonist)…”

Section: Ado Receptor Agonistsmentioning

confidence: 99%

“…Activation of A 2B receptors by elevated Ado levels may induce the release of proinflammatory interleukin-6 (IL-6) from astrocytes leading to increased expression of A 1 receptors and their functions in the brain [229,230], which may explain (i) the increase of A 1 receptor expression after seizures parallel with increasing Ado level and (ii) the higher level of IL-6 in the brain areas (e.g., in the hippocampus and cortex) of epileptic patients and rats [186,[231][232][233], which may have a protective effect against subsequent seizures [230]. In addition, an increase in A 1 receptor density has been demonstrated in the epileptic tissue, for example, in PTZ kindling mice and kainic-acid-treated rats, which may also be an adaptive/protective mechanism against hyperexcitability-induced seizures and convulsions [96,230,[234][235][236][237][238][239].…”

Section: Adenosine Receptor Agonists and Antagonistsmentioning

confidence: 99%

“…3B) [143,168,214,256] and/or CPA [204,235], CHA (Fig. 3A) [118,168,216,237] and D-, L-, R-and S-N 6 -(2-phenylisopropyl) adenosine (D-, L-, R-and S-PIA; A 1 agonists) ( Table 3; Fig.…”

Section: Adenosine Receptor Agonists and Antagonistsmentioning

confidence: 99%

“…3A) [118,168,216,237] and D-, L-, R-and S-N 6 -(2-phenylisopropyl) adenosine (D-, L-, R-and S-PIA; A 1 agonists) ( Table 3; Fig. 3A) [118,168,180] were effective against bicuculline-and/or kainicacid-, pilocarpin-, 3-nitropropionic-acid-, 3-mercaptopropionicacid-and PTZ-induced seizures/epileptiform activity as well as 4-aminopyridine-induced epileptiform bursting activity [235,[265][266][267][268][269][270][271] and in the rat kindling model [119,[272][273][274][275][276][277]. It has also been demonstrated that R-PIA prolonged the latency to convulsions in a hypoxia-induced model [278] and CPA delayed the time onset of clonic convulsions in aminophylline-induced seizures [279].…”

Section: Adenosine Receptor Agonists and Antagonistsmentioning

confidence: 99%

See 2 more Smart Citations

The Antiepileptic Potential of Nucleosides

Kovács¹,

Kékesi²,

Juhász³

et al. 2014

CMC

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Despite newly developed antiepileptic drugs to suppress epileptic symptoms, approximately one third of patients remain drug refractory. Consequently, there is an urgent need to develop more effective therapeutic approaches to treat epilepsy. A great deal of evidence suggests that endogenous nucleosides, such as adenosine (Ado), guanosine (Guo), inosine (Ino) and uridine (Urd), participate in the regulation of pathomechanisms of epilepsy. Adenosine and its analogues, together with non-adenosine (non-Ado) nucleosides (e.g., Guo, Ino and Urd), have shown antiseizure activity. Adenosine kinase (ADK) inhibitors, Ado uptake inhibitors and Ado-releasing implants also have beneficial effects on epileptic seizures. These results suggest that nucleosides and their analogues, in addition to other modulators of the nucleoside system, could provide a new opportunity for the treatment of different types of epilepsies. Therefore, the aim of this review article is to summarize our present knowledge about the nucleoside system as a promising target in the treatment of epilepsy.

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GABA and opioid binding distribution in the brain of the seizure-resistantProechimys guyannensis: An autoradiography study

Rocha¹,

Arida

Carvalho

et al. 2006

Synapse

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Proechimys guyannensis rodents present resistance to epilepsy. Autoradiography was used to map GABA(A) ((3)H-Muscimol), benzodiazepine ((3)H-Flunitrazepam), mu ((3)H-DAMGO), and delta ((3)H-DPDPE) opioid receptor binding in adult Proechimys guyannensis brain under normal conditions. Results were compared with values obtained from adult Wistar rats. Proechimys presented reduced (3)H-Muscimol binding in several cortices, thalamus, medial amygdala nucleus, and dorsal dentate gyrus. (3)H-Flunitrazepam binding was reduced in periaqueductal gray, frontal and entorhinal cortices, and enhanced in piriform cortex and ventral CA2 field of Ammons horn. Concerning (3)H-DAMGO binding, high values were found in several cortices, medial amygdala nucleus, dorsal dentate gyrus, and periaqueductal gray, whereas reduced binding was detected in anterior olfactory tubercle, cingulated cortex, thalamus, basolateral amygdala, substantia nigra, and dorsal and ventral CA fields. High (3)H-DPDPE binding was noticed in CA1 field from dorsal hippocampus, while reduced values were found in cingulate cortex, olfactory tubercle, thalamus, and substantia nigra. These findings provide the first description of receptor binding distribution of the Proechimys brain and suggest natural endogenous anticonvulsant mechanisms of theses rodents under normal conditions.

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Effects of chronic morphine and N6-cyclopentyl-adenosine administration on kainic acid-induced status epilepticus

Cited by 12 publications

References 44 publications

Repeated morphine treatment alters polysialylated neural cell adhesion molecule, glutamate decarboxylase‐67 expression and cell proliferation in the adult rat hippocampus

Repeated morphine treatment alters polysialylated neural cell adhesion molecule, glutamate decarboxylase‐67 expression and cell proliferation in the adult rat hippocampus

The Antiepileptic Potential of Nucleosides

GABA and opioid binding distribution in the brain of the seizure-resistantProechimys guyannensis: An autoradiography study

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