Anticonvulsant action of 2-chloroadenosine injected focally into the perirhinal cortex in amygdaloid kindled rats

Mirnajafi‐Zadeh, Javad; Pourgholami, Mohammad H.; Palizvan, Mohammad Reza; Rostampour, Mohammad; Fallahi, Mansour

doi:10.1016/s0920-1211(99)00025-x

Cited by 17 publications

(6 citation statements)

References 31 publications

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“…Kindling (rat amygdala, and hippocampus) model Seizure suppression, seizure prevention [115,116,213,[258][259][260] Pilocarpine-induced (intraperitoneal injection) seizures in rats Blocked seizure appearance [258,261] Pilocarpine-induced (hippocampus) seizures in rats Seizure protection [262] Lithium-pilocarpine-induced status epilepticus in rats Protective effect [216] Pentylenetetrazole-induced (intravenous application) seizures in rats Increased seizure threshold [265] Pentylenetetrazole-induced (intraperitoneal injection) seizures in rats Partial seizure protection [204] Pentylenetetrazole-induced (intraperitoneal injection) seizures in mice Increased seizure latency [118] Pentylenetetrazole-induced seizures in rats Suppressed/abolished tonic phase of generalized tonicclonic seizures [255] Kainic acid-induced (intraperitoneal injection) seizures in mice Increased seizure latency [118] Electroshock-induced seizures in rats Protective effect [263] Bicuculline-induced (rat prepiriform cortex) seizures Seizure protection [267] Bicuculline-induced (rat hippocampal slices) epileptiform activity Decreased epileptiform activity [168] 3-mercaptopropionic acid-induced (intraperitoneal injection) seizures in mice…”

Section: Ado Receptor Agonistsmentioning

confidence: 99%

“…Both A 1 receptor agonists N 6 -cyclohexyl-adenosine (CHA) and N 6 -cyclopentyl-adenosine (CPA) (Table 3) suppressed the development of status epilepticus in electrical stimulation mod-els in rats [257]. An Ado analogue A 1 receptor agonist 2-chloroadenosine (2-CLA) ( Table 3) showed antiseizure effects in amygdaloid and hippocampal kindled rats [115,116,213,[258][259][260], pilocarpine-induced seizures [216,258,261,262], electroshock-induced seizures [263], Mg 2+ -free conditions [219,264], PTZ-induced seizures [118,204,255,265], 3-nitropropionic-acid-induced seizures [266], kainic-acidand 3-mercaptopropionic-acid-induced seizures [118] and bicuculline-induced seizures [168,267].…”

Section: Adenosine Receptor Agonists and Antagonistsmentioning

confidence: 99%

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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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Section: Ado Receptor Agonistsmentioning

confidence: 99%

Section: Adenosine Receptor Agonists and Antagonistsmentioning

confidence: 99%

The Antiepileptic Potential of Nucleosides

Kovács¹,

Kékesi²,

Juhász³

et al. 2014

CMC

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“…In line with this view, in vivo studies have shown that kindling within the perirhinal cortex promotes seizure activity more rapidly than stimulation of the piriform cortex, amygdala or dorsal hippocampus (McIntyre et al, 1993, 1999; Sato et al, 1998). Moreover, lesioning the perirhinal cortex (Kelly and McIntyre, 1996; Fukumoto et al, 2002) or applying glutamatergic receptor antagonists (Tortorella et al, 1997) or adenosine A1 receptor agonists (Mirnajafi-Zadeh et al, 1999) to the perirhinal cortex attenuated and even prevented the appearance of seizure activity following amygdala kindling.…”

Section: Epileptiform Synchronization In Vitromentioning

confidence: 99%

Perirhinal cortex and temporal lobe epilepsy

Biagini¹,

D’Antuono²,

Benini³

et al. 2013

Front. Cell. Neurosci.

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The perirhinal cortex-which is interconnected with several limbic structures and is intimately involved in learning and memory-plays major roles in pathological processes such as the kindling phenomenon of epileptogenesis and the spread of limbic seizures. Both features may be relevant to the pathophysiology of mesial temporal lobe epilepsy that represents the most refractory adult form of epilepsy with up to 30% of patients not achieving adequate seizure control. Compared to other limbic structures such as the hippocampus or the entorhinal cortex, the perirhinal area remains understudied and, in particular, detailed information on its dysfunctional characteristics remains scarce; this lack of information may be due to the fact that the perirhinal cortex is not grossly damaged in mesial temporal lobe epilepsy and in models mimicking this epileptic disorder. However, we have recently identified in pilocarpine-treated epileptic rats the presence of selective losses of interneuron subtypes along with increased synaptic excitability. In this review we: (i) highlight the fundamental electrophysiological properties of perirhinal cortex neurons; (ii) briefly stress the mechanisms underlying epileptiform synchronization in perirhinal cortex networks following epileptogenic pharmacological manipulations; and (iii) focus on the changes in neuronal excitability and cytoarchitecture of the perirhinal cortex occurring in the pilocarpine model of mesial temporal lobe epilepsy. Overall, these data indicate that perirhinal cortex networks are hyperexcitable in an animal model of temporal lobe epilepsy, and that this condition is associated with a selective cellular damage that is characterized by an age-dependent sensitivity of interneurons to precipitating injuries, such as status epilepticus.

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“…The PRH can also influence seizure generalization from other limbic sites. Prior PRH kindling can promote kindling in another site (Buchanan & Bilkey, 1997), and inhibitory agonists applied focally to the PRH can either block or suppress generalized seizures evoked from another site (Halonen et al ., 1994; Mirnajafi‐Zadeh et al ., 1999).…”

Section: Introductionmentioning

confidence: 99%

Kindling of claustrum and insular cortex: comparison to perirhinal cortex in the rat

Mohapel¹,

Zhang

Gillespie

et al. 2001

Eur J of Neuroscience

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The perirhinal cortex has recently been implicated in the kindling of limbic generalized seizures. The following experiments in rats tested the selectivity of the perirhinal cortex's epileptogenic properties by comparing its kindling profile with those of the adjacent insular cortex, posterior (dorsolateral) claustrum and amygdala. The first experiment examined the kindling and EEG profiles, and found that both the claustrum and insular cortex demonstrated rapid epileptogenic properties similar to the perirhinal cortex, including very rapid kindling rates and short latencies to convulsion. Furthermore, electrical stimulation of all three structures led to a two-phase progression through stage-5 seizures which had characteristics of both neocortical and amygdaloid kindling. In a second experiment rats were suspended in a harness to allow for more detailed documentation of both forelimb and hindlimb convulsions. With this procedure we were able to detect subtle yet unique differences in convulsion characteristics from each of the kindled sites and stage-5 seizure phases. Some of these convulsive parameters were correlated with changes in FosB/DeltaFosB protein and BDNF mRNA expression measured two hours after the last convulsion. Overall, it appears that the perirhinal cortex is not unique in its property of rapid epileptogenesis. Moreover, the posterior claustrum exhibited the fastest kindling and most vigorous patterns of clonus, suggesting that it may be even more intimately associated with the motor substrates responsible for limbic seizure generalization than is the perirhinal cortex.

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Anticonvulsant action of 2-chloroadenosine injected focally into the perirhinal cortex in amygdaloid kindled rats

Cited by 17 publications

References 31 publications

The Antiepileptic Potential of Nucleosides

The Antiepileptic Potential of Nucleosides

Perirhinal cortex and temporal lobe epilepsy

Kindling of claustrum and insular cortex: comparison to perirhinal cortex in the rat

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