The role of adenosine A1 and A2A receptors of entorhinal cortex on piriform cortex kindled seizures in rats

Hosseinmardi, Narges; Mirnajafi‐Zadeh, Javad; Fathollahi, Yaghoub; Shahabi, Parviz

doi:10.1016/j.phrs.2007.04.011

Cited by 35 publications

(44 citation statements)

References 51 publications

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“…Increased seizure latency [118] 3-nitropropionic acid-induced (intraperitoneal injection) seizures in mice Anticonvulsant effect [266] 2-CLA (A1 receptor agonist) Mg 2+ -free condition-induced (human neocortical slices) epileptiform activity Decreased/blocked epileptiform activity [219] Kindling (rat piriform cortex, hippocampus, and amygdala) model Anticonvulsant effect [273][274][275][276][277] Lithium-pilocarpine-induced status epilepticus in rats Protective effect [216] Pentylenetetrazole-induced (subcutane, and intraperitoneal injection) seizures in mice Protective effect [237] Pentylenetetrazole-induced (intraperitoneal injection) seizures in mice Increased seizure latency [118] Pentylenetetrazole-induced (intravenous application) seizures in rats Increased seizure threshold [265] Bicuculline-induced (rat prepiriform cortex) seizures Seizure protection [267] Bicuculline-induced (rat hippocampal slices) epileptiform activity Decreased epileptiform activity [168] Kainic acid-induced (intraperitoneal injection) seizures in mice Increased seizure latency [118] 3-mercaptopropionic acid-induced (intraperitoneal injection) seizures in mice Increased seizure latency [118] CHA (A1 receptor agonist)…”

Section: Ado Receptor Agonistsmentioning

confidence: 99%

“…carbamazepine and valproate) [296] Kindling (rat piriform cortex) model Proconvulsant effect [273,276] Audiogenic seizures (audiogenic-seizure-sensitive DBA/2 mice) Seizure prevention [95] CGS 21680 (A2A receptor agonist)…”

Section: -Nitropropionic Acid-induced (Intraperitoneal Injection) Sementioning

confidence: 99%

“…Kindling (rat piriform cortex, hippocampus, and amygdala) model Proconvulsant effect/no effect on seizures [273][274][275][276][277]281] Mg 2+ -free artificial cerebrospinal fluid-evoked epileptiform activity Increased occurrence of seizures/enhanced duration and intensity of epileptiform activity [300] Mg 2+ -free condition-induced (rat hippocampal slices) epileptiform activity Induced persistent epileptiform discharges [303] CPT (A1 receptor antagonist) 4-aminopyridine-induced (rat hippocampal slices; Mg 2+ -free condition) epileptiform activity Enhanced discharge rate [140] Audiogenic seizures (audiogenic-seizure-sensitive DBA/2 mice) Proconvulsant effect…”

Section: Ado Receptor 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%

“…The proconvulsant effect of the selective A 1 receptor antagonist, 8-cyclopentyl-1,3-dimethylxanthine (CPT) ( Table 3), has also been demonstrated in kindled rats [273][274][275][276][277]281]. The antiseizure role of A 1 receptors was recently strengthened because (i) A 1 receptor knockout mice showed spontaneous hippocampal seizures and high sensitivity to status epilepticus [282,283] and (ii) seizure-activity-limiting effects of Ado (A 1 receptor)-induced attenuation of depolarizing GABA A receptor signaling has been demonstrated [284].…”

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: -Nitropropionic Acid-induced (Intraperitoneal Injection) Sementioning

confidence: 99%

Section: Ado Receptor Antagonistsmentioning

confidence: 99%

Section: Adenosine Receptor Agonists and Antagonistsmentioning

confidence: 99%

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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Adenosine modulates the excitability of layer II stellate neurons in entorhinal cortex through A1 receptors

et al. 2011

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Stellate neurons in layer II entorhinal cortex (EC) provide the main output from the EC to the hippocampus. It is believed that adenosine plays a crucial role in neuronal excitability and synaptic transmission in the CNS, however, the function of adenosine in the EC is still elusive. Here, the data reported showed that adenosine hyperpolarized stellate neurons in a concentration-dependent manner, accompanied by a decrease in firing frequency. This effect corresponded to the inhibition of the hyperpolarization-activated, cation nonselective (HCN) channels. Surprisingly, the adenosine-induced inhibition was blocked by 3 μM 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), a selective A(1) receptor antagonists, but not by 10 μM 3,7-dimethyl-1-propargylxanthine (DMPX), a selective A(2) receptor antagonists, indicating that activation of adenosine A(1) receptors were responsible for the direct inhibition. In addition, adenosine reduced the frequency but not the amplitude of miniature EPSCs and IPSCs, suggesting that the global depression of glutamatergic and GABAergic transmission is mediated by a decrease in glutamate and GABA release, respectively. Again the presynaptic site of action was mediated by adenosine A(1) receptors. Furthermore, inhibition of spontaneous glutamate and GABA release by adenosine A(1) receptor activation was mediated by voltage-dependent Ca(2+) channels and extracellular Ca(2+) . Therefore, these findings revealed direct and indirect mechanisms by which activation of adenosine A(1) receptors on the cell bodies of stellate neurons and on the presynaptic terminals could regulate the excitability of these neurons.

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Potential Therapeutic Applications of Adenosine A_2A Receptor Ligands and Opportunities for A_2A Receptor Imaging

Waarde

Dierckx

Zhou

et al. 2017

Medicinal Research Reviews

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Adenosine A 2A receptors (A 2A Rs) are highly expressed in the human striatum, and at lower densities in the cerebral cortex, the hippocampus, and cells of the immune system. Antagonists of these receptors are potentially useful for the treatment of motor fluctuations, epilepsy, postischemic brain damage, or cognitive impairment, and for the control of an immune checkpoint during immunotherapy of cancer. A 2A R agonists may suppress transplant rejection and graft-versus-host disease; be used to treat inflammatory disorders such as asthma, inflammatory bowel disease, and rheumatoid arthritis; be locally applied to promote wound healing and be employed in a strategy for transient opening of the blood-brain barrier (BBB) so that therapeutic drugs and monoclonal antibodies can enter the brain. Increasing A 2A R signaling in adipose tissue is also a potential strategy to combat obesity. Several radioligands for positron emission tomography (PET) imaging of A 2A Rs have been developed in recent years. This review article presents a critical overview of the potential therapeutic applications of A 2A R ligands, the use of A 2A R imaging in drug development, and opportunities and limitations of PET imaging in future research. C

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The role of adenosine A1 and A2A receptors of entorhinal cortex on piriform cortex kindled seizures in rats

Cited by 35 publications

References 51 publications

The Antiepileptic Potential of Nucleosides

The Antiepileptic Potential of Nucleosides

Adenosine modulates the excitability of layer II stellate neurons in entorhinal cortex through A1 receptors

Potential Therapeutic Applications of Adenosine A_2A Receptor Ligands and Opportunities for A_2A Receptor Imaging

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The role of adenosine A1 and A2A receptors of entorhinal cortex on piriform cortex kindled seizures in rats

Cited by 35 publications

References 51 publications

The Antiepileptic Potential of Nucleosides

The Antiepileptic Potential of Nucleosides

Adenosine modulates the excitability of layer II stellate neurons in entorhinal cortex through A1 receptors

Potential Therapeutic Applications of Adenosine A2A Receptor Ligands and Opportunities for A2A Receptor Imaging

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Product

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Potential Therapeutic Applications of Adenosine A_2A Receptor Ligands and Opportunities for A_2A Receptor Imaging