Topic: intrahippocampal kainic acid

Medial temporal lobe epilepsy (MTLE) is a common cause of treatment-resistant seizures where excessive and hyper-synchronized neuronal activity is associated with reactive astrogliosis. Emerging evidence has indicated a role for neuron-astrocyte interactions in seizure activity. Previous studies have found increased astrocyte Ca2+ signals in mouse models for MTLE, but it has been difficult to disentangle how these drive or mitigate seizure activity in chronic epilepsy. We used an AAV8-GFAP-hM3Dq-mCherry vector to manipulate reactive astrocytes in the chronic phase of the mouse intrahippocampal

The adenosine A1 receptor (A1R) is a promising therapeutic target in epilepsy by mediating neuronal inhibition. In this study, we investigated whether A1R signaling is still functional in the intrahippocampal kainic acid (IHKA) mouse model for temporal lobe epilepsy (TLE). Moreover, we evaluated the feasibility of spatial selective inhibition of specific hippocampal subregions through photopharmacology. Electrically evoked field postsynaptic potentials (fPSPs) were recorded in the CA1 and DG of acute hippocampal slices. The effect of adding 40 nM of the A1R agonist N6cyclopentyladenosine (CPA)