Julianna Kardos

TL;DR: It is suggested that copper may play a role in regulating neuronal excitability by monitoring GABA-activated influx of the radiotracer 36Cl- ion and the effect of Cu2+ was concentration dependent and occurred with saturating as well as low GABA concentrations.

TL;DR: In this paper, the authors studied changes in field potentials (fp) together with measurements of extracellular, intracellular, and intramitochondrial calcium concentration ([Ca(2+)]e, [Ca( 2+)]i, and [Ca[2+]m, respectively), mitochondrial membrane potential (deltapsi), NAD(P)H auto-fluorescence, and dihydroethidium (HEt) fluorescence in hippocampal slice cultures by means of simultaneous electrophysiological and microfluorimetric measurements.

TL;DR: Evidence is presented that glutamate uptake-induced release of GABA from astrocytes has a direct impact on the excitability of pyramidal neurons in the hippocampus, suggesting the existence of a novel molecular mechanism by which astroCytes transform glutamatergic excitation into GABAergic inhibition providing an adjustable, in situ negative feedback on theexcitability of neurons.

TL;DR: It is found that removal of Glu by astrocytic transporters triggers an elevation in the extracellular level of GABA, which represents a direct link between inhibitory and excitatory neurotransmission and may function as a negative feedback combating intense excitation in pathological conditions such as epilepsy or ischemia.

TL;DR: A deeper understanding of of the regulatory effects of copper on neuro-glia coupling via polyamine metabolism may reveal novel copper signalling functions and new directions for therapeutic intervention in brain disorders associated with aberrant copper metabolism.