Adenosine A1 and A2A receptors of hippocampal CA1 region have opposite effects on piriform cortex kindled seizures in rats.
In this study the role of adenosine A1 and A2A receptors of the hippocampal CA1 region on piriform cortex-kindled seizures was investigated in rats. Animals were kindled by daily electrical stimulation of piriform cortex. In fully kindled rats, N6-cyclohexyladenosine (CHA; a selective A1 receptor agonist), 1,3-dimethyl-8-cyclopenthylxanthine (CPT; a selective A1 receptor antagonist), CGS21680 hydrochloride (CGS, a selective A2A receptor agonist) and, ZM241385 (ZM, a selective A2A receptor antagonist) were microinfused bilaterally into the hippocampal CA1 region. Rats were stimulated and seizure parameters were measured. Obtained results showed that microinjection of CHA (10 and 100 microM) decreased the afterdischarge duration (ADD), stage 5 seizure duration (S5D) and seizure duration (SD), and significantly increased the latency to stage 4 (S4L). Intra-hippocampal CPT increased ADD at the dose of 20 microM. Pretreatment of rats with CPT (10 microM) before CHA (10 microM), significantly reduced the effect of CHA on seizure parameters. On the other hand, microinjection of CGS (200 and 500 microM) increased ADD, but of ZM had no effect on seizure parameters. Pretreatment of rats with ZM (50 microM) before CGS (500 microM), significantly reduced the effect of CGS on seizure parameters. The results suggest that the facilitatory role of the hippocampal CA1 region in relaying or spreading of piriform cortex kindled seizures is decreased by the activation of adenosine A1 receptors and increased by A2A receptors.
Zeraati
Maryam
M
Department of Physiology, School of Medical Sciences, Tarbiat Modares University, P.O. Box 14115-111, Tehran, Iran.
Mirnajafi-Zadeh
Javad
J
Fathollahi
Yaghoub
Y
Namvar
Simin
S
Rezvani
Mohammad Ebrahim
ME
D000241:Adenosine / Q000031:analogs & derivatives / Q000494:pharmacology; D058907:Adenosine A1 Receptor Agonists; D058916:Adenosine A1 Receptor Antagonists; D058908:Adenosine A2 Receptor Agonists; D058917:Adenosine A2 Receptor Antagonists; D000818:Animals; D002540:Cerebral Cortex / Q000503:physiopathology; D004558:Electric Stimulation; D006624:Hippocampus / Q000187:drug effects* / Q000503:physiopathology; D007696:Kindling, Neurologic; D008297:Male; D010627:Phenethylamines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D043682:Receptor, Adenosine A1 / Q000502:physiology*; D043705:Receptor, Adenosine A2A / Q000502:physiology*; D018048:Receptors, Purinergic P2; D012640:Seizures / Q000503:physiopathology*; D014227:Triazines / Q000494:pharmacology; D014230:Triazoles / Q000494:pharmacology; D014970:Xanthines / Q000494:pharmacology
C112774:1,3-dimethyl-8-cyclopentylxanthine; D058907:Adenosine A1 Receptor Agonists; D058916:Adenosine A1 Receptor Antagonists; D058908:Adenosine A2 Receptor Agonists; D058917:Adenosine A2 Receptor Antagonists; D010627:Phenethylamines; D043682:Receptor, Adenosine A1; D043705:Receptor, Adenosine A2A; D018048:Receptors, Purinergic P2; D014227:Triazines; D014230:Triazoles; D014970:Xanthines; C097270:ZM 241385; C061282:2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine; C027513:N(6)-cyclohexyladenosine; D000241:Adenosine