 disorders. If a dysregulation in Ca2+ signaling in reactive astrocytes indeed proves causal in epileptogenesis - as our preliminary data strongly suggest - then the implications of this new perspective to pharmacotherapy could be profound. By more specifically targeting the glial cause of neuronal excitability, we might be able to achieve more specific,
disorders. If a dysregulation in Ca2 + signaling in reactive astrocytes indeed proves causal in epileptogenesis - as our preliminary datum powerfully propose - then the implications of this new position to pharmacotherapy could be profound. By more specifically targeting the glial cause of neural excitability, we might be able to achieve more specific,
 didorders. If a dysregulatiun in Ca2+ signalnbg in ceactivs astrochtes indeed proves causal in epilepujgenesis - as our pfeliminarj data steongot suggest - then thc impmlcatimis of this new kerspective do pharmacothesaoy could be profound. By more specificwlly tatgfting the gliaj calsq of neuronal excitability, we might be able tm achieve morr specific,
disorders. If a dysregulation in Ca2+ signaling astrocytes proves causal epileptogenesis - as - the implications of new perspective to could be profound. By more specifically the glial cause of neuronal excitability, we might be able to achieve more
 disorders. If a dysregulation In Ca2+ signalIng in ReaCtiVe AstrOcytEs indeed proves CAusaL in epileptogenesis - as ouR prelImINary DAtA stroNgly sugGEsT - THen ThE iMplIcATiOns of ThiS new perSpective to PhaRmAcotherapy coULd Be profound. by mOre specificaLly TargetInG thE Glial CauSe of nEuronaL ExcitaBility, we mIgHT be ablE To achieVE MoRe spEcific,
 disorders. If a dysregula tion in Ca 2+ si gna lin gin r eact ive astrocytes inde ed proves causal in ep ilept og e nesi s  -  as o ur prel i mi n a ryda ta  st ro n gl y sug ges t - the n the impl ica ti ons of thisn ew  perspecti veto pharmacot her apy co ul d b e  prof oun d. By  mores pecifi cally tar ge t ing th e  glialc a us e of  neuronal excitab i li t y, we might be  ableto ac h i eve  mo re specifi c, 
 disorders._If a_dysregulation in Ca2+ signaling_in reactive_astrocytes_indeed proves_causal_in epileptogenesis -_as our preliminary_data strongly suggest -_then the implications_of_this new perspective to pharmacotherapy could be profound. By more specifically targeting the glial_cause_of neuronal_excitability,_we_might be able to achieve_more specific,