Disease relevance of epf

• GLUT-1+/- mice have epileptiform discharges on electroencephalography (EEG), impaired motor activity, incoordination, hypoglycorrhachia, microencephaly, decreased brain glucose uptake as measured by positron emission tomography (PET) scan and decreased brain Glut-1 expression by western blot (66%) [1].
• Because NT-3 expression is reduced after focal seizures, impaired short-term facilitation may represent a protective response that limits the propagation of epileptiform activity from the entorhinal cortex to the hippocampus [2].
• The phenotype of these mice further consists of a late-onset epileptiform hyperexcitability, behavioral modifications in a radial maze and in an open field, female nurturing defect, and male infertility [3].
• Intra-hippocampal kainate injection induces an epileptiform activity termed status epilepticus [4].
• Forty days after intracerebral inoculation with scrapie isolate Sc237, we recorded prolonged, epileptiform discharges in cortex and hippocampus [5].

Psychiatry related information on epf

• This impaired synaptic inhibition may be involved in the epileptiform activity seen in Creutzfeldt-Jakob disease and we argue that loss of function of PrPC may contribute to the early synaptic loss and neuronal degeneration seen in these diseases [6].
• METHODS: In vivo (minimal electroshock delivered transcorneally) and in vitro techniques (field-potential recordings in neocortical and hippocampal brain slice preparations exposed to bicuculline methiodide) were used to determine whether the susceptibility to epileptiform activity is enhanced in reeler homozygous mice relative to controls [7].

High impact information on epf

• We report here that, in hippocampal slices, selective antagonists of GLU(K5)-containing kainate receptors prevented development of epileptiform activity--evoked by the muscarinic agonist, pilocarpine--and inhibited the activity when it was pre-established [8].
• The presence of the transgene leads to a complex deregulation of endogenous Shaker genes in the adult central nervous system as well as an increase in network excitability that includes spontaneous cortical spike and wave discharges and a lower threshold for epileptiform bursting in isolated hippocampal slices [9].
• Neuronal degeneration and Lafora inclusion bodies predate the onset of impaired behavioral responses, ataxia, spontaneous myoclonic seizures and EEG epileptiform activity [10].
• Our findings demonstrate that interictal discharges of hippocampal origin control the expression of ictal epileptiform activity in the entorhinal cortex [11].
• Both treatments induce epileptiform activity in hippocampus lasting several hours [12].

Chemical compound and disease context of epf

• The latency of the appearance of spontaneous epileptiform activity from CA1 region of hippocampal slices was long (> 2 min) after NMDA perfusion and short (< 1 min) after L-glutamate, high K+ and hypoxia [13].
• Single MPTP injections (30 mg/kg i.p.) produced limbic and/or generalized seizures in older (6 mo) and frank epileptiform interictal hippocampal spikes in younger (6-8 wks) mice [14].
• PURPOSE: Recently the Ca(v)2.3 (E/R-type) voltage-gated calcium channel (VGCC) has turned out to be not only a potential target for different antiepileptic drugs (e.g., lamotrigine, topiramate) but also a crucial component in the pathogenesis of absence epilepsy, human juvenile myoclonic epilepsy (JME), and epileptiform activity in CA1 neurons [15].
• Comparison of the effects of losigamone and its isomers on maximal electroshock induced convulsions in mice and on three different patterns of low magnesium induced epileptiform activity in slices of the rat temporal cortex [16].
• Experiments were carried out in mice to assess the protection provided by thiopentone (Intraval, May and Baker) and propofol (Diprivan, I.C.I.) against epileptiform seizures induced by electroshock and pentylenetetrazol [17].

Biological context of epf

• In vitro studies suggest a role for Y2 receptors in modulating excitatory hippocampal synaptic transmission and epileptiform discharge [18].
• Next we investigated the consequences of depotentiation on SLEs themselves by applying low-frequency stimulation after onset of low-Mg(2+)-induced epileptiform activity [19].
• These changes at the receptor level explain the previously observed hyperexcitability with the appearance of epileptiform field potentials and the long duration of excitatory postsynaptic potentials four weeks after ischemia [20].
• Calcium oscillations in neocortical astrocytes under epileptiform conditions [21].
• An epileptiform syndrome was induced in rats by injection of tetanus toxin (approximately 10 mouse LD50) unilaterally into the hippocampus [22].

Anatomical context of epf

• These data indicate that epileptiform physiological activity differentially affects the regulation of 3 neuroactive peptides contained within the hippocampal mossy fiber system and suggest a mechanism through which seizurelike episodes can have a lasting influence on the operation of specific hippocampal circuitries [12].
• Both effects contribute to depolarising CA3 pyramidal cells and the latter has been implicated in eliciting prolonged epileptiform population bursts [23].
• In some slices, zero-magnesium cerebrospinal fluid (CSF) was used to evoke spontaneous epileptiform discharges [18].
• Our data demonstrate that the absence of functional GABA(B) receptors causes epileptiform activity through a mechanism that crucially involves dentate gyrus granule cells, and that this pathological activity is accompanied by adaptive changes [24].
• In vitro intracellular recordings from three major forebrain regions, neocortex, hippocampus and olfactory (piriform) cortex (OC) showed that only the OC exhibits abnormal enhanced synaptic excitability and spontaneous epileptiform discharges [25].

Associations of epf with chemical compounds

• When the muscimol dose was increased (4-6 mg/kg), the D2R-/- mice exhibited seizure-like behavior, and the electroencephalographic (EEG) recordings during these behaviors showed a high amplitude rhythmic epileptiform activity in these mice [26].
• Moreover, epileptiform discharges elicited by 4-aminopyridine were attenuated in slices from Cx36 -/- mice [27].
• The L-type Ca2+ blocker, nifedipine, enhanced epileptiform activity [28].
• However, 27a also inhibited spontaneous epileptiform discharges in the cortical wedge (reversed by glycine), while 1 was ineffective [29].
• The AMPA antagonist, CNQX, blocked all epileptiform activity, whereas the NMDA antagonist, APV, did not [28].

Regulatory relationships of epf

• The results suggest that mGluR1 and mGluR5 are activated synaptically during prolonged epileptiform discharges induced by bicuculline and 4-AP [30].
• Ablation of GluR5 leads to a higher susceptibility of the network to the oscillogenic and epileptogenic effects of kainate, whereas lack of GluR6 prevents kainate-induced gamma oscillations or epileptiform bursts [31].
• Neuropeptide Y inhibits in vitro epileptiform activity in the entorhinal cortex of mice [32].

Other interactions of epf

• The effects of these antagonists were additive when applied together, suggesting that mGluR1 and mGluR5 exert independent actions on the epileptiform bursts [30].
• In addition, the data indicate that the synaptic effects of the group I mGluRs on the duration of epileptiform discharges were mediated by a PLCbeta1-independent mechanism [30].
• Extracellular signal-regulated kinase 1/2 is required for the induction of group I metabotropic glutamate receptor-mediated epileptiform discharges [33].
• PD98059 or another MEK inhibitor, 1,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio]butadiene (10 microm), also prevented the induction of the prolonged epileptiform discharges by DHPG [33].
• With the low-Mg(2+)-model of epilepsy, this study investigated the effect of electrical LTD, chemical LTD, and depotentiation on the susceptibility of the entorhinal cortex to epileptiform activity [19].

Analytical, diagnostic and therapeutic context of epf

• GLU(K5) antagonism also prevented epileptiform activity induced by electrical stimulation, both in vitro and in vivo [8].
• The steroids also were examined for activity against extracellularly recorded epileptiform discharges in the CA3 region of the rat hippocampal slice induced by perfusion with 55 microM 4-aminopyridine (4-AP) [34].
• The mechanisms involved in the genesis and elaboration of electrical epileptiform activity in animal models are examined in relation to known processes involved in the physiology of sleep, and compared with data derived from long-term studies of the time distribution of epileptic events in humans [35].
• We combined fast calcium imaging of network activity with whole-cell recordings to examine epileptiform propagation in mouse neocortical slices [36].
• We studied the effect of active immunization with glutamate-bovine serum albumin conjugate on acute generalized epileptiform activity evoked by single administration of corazol [37].

References