Adenosine A1 Receptors Participate in Excitability Changes after Cortical Epileptic Afterdischarges in Immature Rats.

: Postictal refractoriness, i.e., the inability to elicit a new epileptic seizure immediately after the first one, is present in mature animals.

Electrographic seizures induced by activation of ET and ET receptors following intrahippocampal infusion of endothelin-1 in immature rats occur by different mechanisms.

We have demonstrated previously that activation of either the ET or ET receptor can induce acute electrographic seizures following the intrahippocampal infusion of endothelin-1 (ET-1) in immature (P12) rats. We also demonstrated that activation of the ET receptor is associated with marked focal ischemia, while activation of the ET receptor is not. Exploring the mechanisms underlying seizures induced by these two ET-1 receptor interactions can potentially provide insight into how focal ischemia in immature animals produces seizures and whether ischemiarelated seizures differ from seizures not associated with ischemia.

Adenosine A1 Receptor Agonist 2-chloro-N6-cyclopentyladenosine and Hippocampal Excitability During Brain Development in Rats.

The adenosinergic system may influence excitability in the brain. Endogenous and exogenous adenosine has anticonvulsant activity presumably by activating A1 receptors. Adenosine A1 receptor agonist 2-chloro-N6-cyclopentyladenosine (CCPA) may thus bolster anticonvulsant effects, but its action and the number of A1 receptors at different developmental stages are not known.

Activation of either the ETA or the ETB receptors is involved in the development of electrographic seizures following intrahippocampal infusion of the endothelin-1 in immature rats.

The period around birth is a risky time for stroke in infants, which is associated with two major acute and subacute processes: anatomical damage and seizures. It is unclear as to what extent each of these processes independently contributes to poor outcome. Furthermore, it is unclear whether there is an interaction between the two processes - does seizure activity cause additional brain damage beyond that produced by ischemia and/or does brain damage foster seizures? The model of focal cerebral ischemia induced by the intrahippocampal infusion of endothelin-1 (ET-1) in 12-day-old rat was used to examine the role of the endothelin receptors in the development of focal ischemia, symptomatic acute seizures and neurodegeneration.

Effects of cadmium chloride inhalation on airflow limitation to histamine, carbachol and adenosine 5'-monophosphate assessed by barometric whole body plethysmography in healthy dogs.

The effects of pharmacological bronchoprovocation on airflow patterns and surrogate respiratory parameters assessed by barometric whole body plethysmography (BWBP) were investigated in healthy dogs, previously exposed to cadmium chloride inhalation. BWBP-derived respiratory variables were calculated (1) at baseline and (2) following nebulisation of increasing concentrations of histamine, carbachol and adenosine 5'-monophosphate (AMP) until enhanced pause (PENH) increased to 300% of baseline (PCPENH300). Bronchoalveolar lavage fluid (BALF) cytology before (BCC) and after (ACC) cadmium chloride inhalation revealed cadmium-induced airway inflammation.