role of adenosine A1 receptor activity of piriform cortex neurons on amygdala kindled seizures in rats

Considering the anticonvulsant effects of A1 Adenosine Receptors and the anatomical connections between piriform Cortex and Amygdala, in this study, the role of A1 adenosine receptors activity of piriform cortex neurons on amygdala kindled seizures was investigated in rats. The rats were fully kindled by daily electrical stimulation of amygdala. N6-cyclohexyleadenosine [CHA; 1,10 and 100 mM], as a selective A1 agonist and 1,3-dimethyl-8-cyclohexylexantine [CPT; 20 and 10 mM], as a selective A1 antagonist were microinjected [0.5ml, 0.25 ml/min] into the piriform cortex. Animals were stimulated at 5, 15 or 90 min after drug microinjection and seizure parameters were measured. Intra-piriform CHA [10 or 100 mM] reduced afterdischarge duration and stage 5 seizure duration and prolonged stage 4 latency significantly. Pretreatment with CPT [10 mM] 5 min before CHA [100 mM] eliminated the effects of CHA. These observations suggest that A1 adenosine receptors activity in piriform cortex reduced the seizure severity and attenuated the distribution of seizure activity to other brain regions

Adenosine Al receptors of amygdala has not anticonvulsant effects on piriform cortex kindled seizures in rats

Adenosine is an endogenous anticonvulsant which exerts its anticonvulsant effects through adenosine Al receptors. As the piriform/amygdala is a critical circuit for limbic seizure propagation, in this study the role of amygdala Al receptors on piriform cortex kindled seizures was investigated. Rats were kindled by daily electrical stimulation of piriform cortex. In the first experiment fully kindled animals received intra-amygdala N6-cyclohexyladenosine [CHA; 10-500 micro M, a selective Al receptor] or 2% lidocaine [for reversal neuronal inhibition] bilaterally. 5 min later, animals were stimulated and seizure parameters were measured. In the second experiment, the effect of daily microinjection of CHA [100 microM] into the amygdala on piriform cortex kindling rate was investigated. Different doses of CHA had no effect on kindled seizure parameters. On the other hand, intra-amygdala 2% lidocaine reduced the kindled seizures severity. There were significant increase in stage 4 latency and decrease in stage 5 duration. Also, daily intra-amygdala CHA had no significant effect on kindling rate. The amygdala neuronal activity has a role in propagation of epileptic seizures from piriform cortex. Elimination of this activity by lidocaine decreases the severity of piriform cortex kindled seizures. However, the amygdala Al receptors have no role in this regard