Power spectral analysis of electroencephalographic activity in kindled rats

Summary:Purpose: Amygdala kindling is an epilepsy model involving long-term network plasticity in the nervous system. In this model, repeated weak stimulation of the amygdala eventually leads to severe motor seizures. The mechanisms for worsening behavioral seizures, and the possible role of enhanced connectivity between the amygdala and other structures have not been thoroughly investigated.Methods: We performed simultaneous field potential recordings from the amygdala, frontal cortex, and medial thalamus during kindling in rats. Seizures were analyzed for signal power compared with baseline and for correlation between recording sites. Interictal signals were analyzed for changes in coherence between electrode contacts in kindled animals compared with sham kindled controls.Results: We found that increased behavioral severity of seizures was related to increased seizure duration and to increased signal power in the frontal cortex and medial thalamus. Kindling was associated with increased connectivity between the amygdala and frontal cortex, based on increased amygdalafrontal signal correlation during seizures. In addition, during the interictal period, increased coherence was noted between amygdala and frontal contacts in kindled animals compared with controls.Conclusions: We found evidence for increased connectivity between the amygdala and frontal cortex both during seizures and in the interictal period, as a result of kindling. Enhanced connections between limbic and neocortical circuits may be important for the development of epilepsy, as well as for normal long-range network plasticity in the nervous system.

Section: Discussionmentioning

confidence: 99%

Neocortical and Thalamic Spread of Amygdala Kindled Seizures

Blumenfeld

Rivera²,

Vásquez³

et al. 2007

“…The DGKε −/− mice demonstrated unchanged power spectral activity during the kindling procedure; the spectral analysis of the kindled mice revealed an increment of power in the 4‐ to 15‐Hz band (Fig. 3B and C), as we expected (18).…”

Section: Resultsmentioning

confidence: 99%

Diacylglycerol Kinase Epsilon Modulates Rapid Kindling Epileptogenesis

Musto

Bazán

2006

Summary:Purpose: Diacylglycerol kinase epsilon (DGK ) regulates seizure susceptibility and long-term potentiation through arachidonoyl-inositol lipid signaling. We studied the significance of arachidonoyl-diacylglycerol (20:4 DAG) in epileptogenesis in DGK -deficient mice undergoing rapid kindling epileptogenesis.Methods: Tripolar electrode units were implanted in right dorsal hippocampi of male DGK +/+ and DGK −/− mice. Ten days after surgery, kindling was achieved by stimulating 6 times daily for 4 days with a subconvulsive electrical stimulation (10-s train of 50-Hz biphasic pulses, 75-200 μA amplitude) at 30-min intervals. After 1 week, mice were rekindled. EEGs were recorded and analyzed to characterize epileptogenic events as spikes, sharp waves, or abnormal amplitudes and rhythms. Right hippocampi were analyzed by histology [Timm's staining, neuropeptide Y (NPY) and glial fibrillary acidic protein immunoreactivity], and for DNA fragmentation (TUNEL).Results: DGK −/− mice had significantly fewer motor seizure and epileptic events compared with DGK +/+ mice from the second day of stimulation. These differences were maintained during rekindling. DGK −/− mice also exhibited lowamplitude spike-wave complexes, short spreading depression, and predominant lower-frequency (1-4 Hz) bands throughout stimulation, whereas DGK +/+ mice exhibited increased highfrequency bands (4-8 Hz; 8-15 Hz) from the second day of stimulation, as determined by power spectral analysis. DGK −/− mice displayed no sprouting in the supragranular area or NPY inmunoreactivity in the hilus and had weak astrocyte reactivation in all hippocampal areas. No TUNEL-positive cells were detected in any group of mice.Conclusions: DGK modulates kindling epileptogenesis through inositol lipid signaling. Because arachidonatecontaining diacylglycerol phosphorylation to phosphatidic acid is selectively blocked in DGK −/− mice, we postulate that the shortage of arachidonoyl-moiety inositol lipids and/or the messengers derived thereof is a key signaling event in epileptogenesis. Key Words: Diacylglycerol kinase-Kindling epileptogenesis-Inositol lipid signaling-Hippocampus.Partial complex seizure with secondary generalized seizure is one of the semiologic characteristics of mesial temporal lobe epilepsy (MTLE). In most cases, MTLE progresses with severe recurrence of seizures, becomes refractory to antiepileptic drugs (AEDs), and is related to certain mental and learning disabilities and psychosocial problems (1).Abnormal electrophysiologic responses through different mechanisms (abnormal excitation, enhanced synchronization, less frequency adaptation, diminutions of feedforward inhibition, abnormal burst, and paroxysmal firing) were found in hippocampal regions from patients who had MTLE (2). Excitatory glutamatergic signaling is one of the mechanisms proposed to trigger paroxysm shift depolarization (PSD), characterized as spikes that correlate with Accepted August 18, 2005. Address correspondence and reprint requests to Dr. N. G. Bazan at LSU Neuroscience ...

“…The latter is reflected in the longer interval between onset responses and rebound responses in kindled cats. The rebound response interval is typically related to the dominant EEG frequency, and kindling has been shown to alter persistently the power spectra of the interictal EEG (26). Generally a high correlation exists between the frequency of spontaneous EEG sleep spindles and the best modulation frequency (21).…”

Section: Discussionmentioning

confidence: 99%

Kindling Limits the Interictal Neuronal Temporal Response Properties in Cat Primary Auditory Cortex

Valentine¹,

Teskey²,

Eggermont

2005

Summary:Purpose: The present study examined the effect of electrical kindling on the interictal temporal response properties of single units recorded from primary auditory cortex (AI) of the adult cat.Methods: Cats were permanently implanted with electrodes in AI, kindled twice daily for 40 sessions, and the contralateral AI was subsequently mapped. Kindling stimulation consisted of 1-s trains of biphasic square-wave pulses applied at a frequency of 60 Hz, 100 µA above the afterdischarge (AD) threshold. The EEG activity was recorded during each kindling session, and the behavioral manifestation was scored. Subsequent to kindling, multiple single-unit responses were recorded under ketamine anesthesia in response to 1-s-long periodic click trains, with click rates between 2 and 64 Hz. Neuronal responses were characterized according to their ability to respond in time-locked fashion to the clicks.Results: Kindling stimulation resulted in progression of the AD characteristics and seizure behavior, with six of 10 kindled cats reaching a fully generalized state. In the fully kindled cats, the best modulation frequencies and limiting following rates for the single-unit responses were significantly lower compared with those of naive and sham controls.Conclusions: Repeated epileptiform activity interferes with temporal processing in cat auditory cortex in the interictal state. This may have implications for people with epileptic foci in auditory-related areas.