Topic: epileptiform activity

Epileptiform activity (EA) comprises abnormal excessive neuronal discharges (spikes and sharp waves) detectable by electroencephalogram. The term EA originates from epilepsy research, where interictal EA appears in EEG between seizures. Importantly, EA occurs not only in epilepsy but also in various pathologies, possibly contributing to cognitive impairment. EA has been observed in neurodegenerative disorders like Alzheimer's and Parkinson's diseases. However, a direct causal link between EA and cognitive impairment remains elusive. A significant issue is the lack of a pure EA model for invest

Neuropeptide S is a 20 amino acid neuromodulator and it is the physiological ligand of Neuropeptide S receptor, NPSR. NPSR activates intracellular pathways that control long-term gene expression as well as PLC-Calcium pathway. The expression of the NPS receptor in olfactory regions like piriform cortex, suggests that there may be a functional relationship between NPS and epileptic activity.The aim of this study was to investigate the effects of suppression of the NPS receptor pathway on epileptiform activity in piriform cortex. Acute brain slices were obtained from 6-8 weeks old C57BL/6 mice.

Long-term changes of the morphology and function of astrocytes are well known to occur in epilepsy and are thought to play an important role in the development and manifestation of the disease. However, the initial astrocytic processes triggered at the onset of status epilepticus or epileptiform activity are less clear. For instance, it remains to be established how quickly epileptic activity induces changes of astrocyte morphology and what the associated molecular cascades is.We used two-photon excitation fluorescence imaging to monitor changes in astrocyte morphology concurrently with the in

In recent years, the interaction between glioma and brain cells has emerged as one important regulator of tumor progression. In order to investigate the molecular and physiologic alterations of the peritumoral neurons induced by glioma growth, we used two well-established glioma syngeneic cell lines: GL261 and CT-2A. We performed in vivo electrophysiological recordings of visual evoked potentials (VEPs) to longitudinally monitor the neural dysfunctions along with tumor progression. With respect to controls, glioma-bearing (GBM) mice showed a decay of visual responses that started from day 14 a