Biomedical subjects

Zhouyan Feng

Publications and source records attributed to Zhouyan Feng.

7 recordsLinked to original sources

PubMed2005

Propagation of low calcium non-synaptic induced epileptiform activity to the contralateral hippocampus in vivo.

Recent experiments show that non-synaptic epileptiform activity can be induced by high K+ and low Ca2+ solution in vivo in the hippocampal CA1 region when synaptic transmission is blocked. However, the ability of this type of epileptiform activity to propagate to other brain areas is unknown. Presumably, this epileptiform activity should propagate and project along the axons to remote brain areas. This hypothesis was tested in vivo by inducing non-synaptic seizures in the left hippocampus and by recording spontaneous and evoked field potentials in both left and right hippocampi. The results show that one type of non-synaptic epileptiform activity, late bursts, observed in the left exposed CA1 and CA3 regions could propagate to the contralateral intact CA1 and induce seizures with onsets of high-frequency rhythm. A cut of the commissural fibers near the midline of the brain prevented this propagation. In addition, the measurement of time delays between the exposed left CA3 and contralateral right CA1, as well as between the two recording electrodes in the right CA1, showed that the burst activity propagated through the commissural pathways. Experimental data also showed that these late bursts in the left hippocampus were first generated in the Schaffer collaterals of the CA1 region, traveled to the ipsilateral CA3 region and then propagated through the commissural fibers to the other side. These results suggest that non-synaptic epileptiform activity can propagate along axon projections to intact brain area causing seizure activity. This non-synaptic activity propagating through axonal pathway provides a possible mechanism for the generation of high-frequency low-amplitude onset activity observed commonly in human epileptic EEGs.

Animals↗

PubMed2004

Suppression of excitatory synaptic transmission can facilitate low-calcium epileptiform activity in the hippocampus in vivo.

It has been reported that the inhibitory postsynaptic potential (IPSP) is abolished before the excitatory postsynaptic potential (EPSP) when the extracellular concentration of Ca(2+) ([Ca(2+)](o)) is removed gradually in hippocampal slices. However, the low-Ca(2+) nonsynaptic epileptiform activity does not appear until the [Ca(2+)](o) is decreased to a level sufficient to depress the excitatory synaptic transmission. This suggests the hypothesis that the suppression of excitatory synaptic transmission itself could facilitate the generation of epileptiform activity. In the present study, we tested this hypothesis and developed a new model of nonsynaptic epileptiform activity by gradually raising the neuronal excitability and blocking the synaptic transmission with high K(+), zero Ca(2+) and calcium chelator ethylene glycol-bis (beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) in the CA1 region of hippocampus in vivo. The changes of synaptic transmission and recurrent inhibitory activity during this process were evaluated by measuring the amplitude of the population spikes (PS) in response to paired-pulse orthodromic stimulation. The results show that the epileptiform activity appeared only when the excitatory synaptic transmission was depressed by further lowering [Ca(2+)](o) with EGTA. Similar epileptiform activity could be induced when EGTA was replaced by the excitatory postsynaptic amino acid antagonists D-(-)-2-amino-5-phosphonopentanoic acid (APV) plus 6,7-dinitroquinoxaline-2,3-dione (DNQX) or APV alone but not DNQX alone. The combination application of APV and cadmium enhanced the epileptiform activity. These results suggest that the suppression of excitatory synaptic transmission can facilitate the appearance of epileptiform activity in solution with high K(+) and low Ca(2+) in vivo. These data provide new information to be considered in the development of antiepileptic drugs. They also suggest a possible mechanism to explain the fact that low-frequency electrical stimulation can suppress epileptiform activity.

2-Amino-5-phosphonovalerate↗

PubMed2004

Decrease in synaptic transmission can reverse the propagation direction of epileptiform activity in hippocampus in vivo.

Most types of epileptiform activity with synaptic transmission have been shown to propagate from the CA3 to CA1 region in hippocampus. However, nonsynaptic epileptiform activity induced in vitro is known to propagate slowly from the caudal end of CA1 toward CA2/CA3. Understanding the propagation modes of epileptiform activity, and their causality is important to revealing the underlying mechanisms of epilepsy and developing new treatments. In this paper, the effect of the synaptic transmission suppression on the propagation of epilepsy in vivo was investigated by using multiple-channel recording probes in CA1. Nonsynaptic epileptiform activity was induced by calcium chelator EGTA with varied concentrations of potassium. For comparison, disinhibition synaptic epileptiform activity was induced by picrotoxin (PTX) with or without partial suppression of excitatory synaptic transmission. The propagation velocity was calculated by measuring the time delay between two electrodes separated by a known distance. The results show that in vivo nonsynaptic epileptiform activity propagates with a direction and velocity comparable to those observed in in vitro preparations. The direction of propagation for nonsynaptic activity is reversed from the PTX-induced synaptic activity. A reversal in propagation direction and change in velocity were also observed dynamically during the process of synaptic transmission suppression. Even a partial suppression of synaptic transmission was sufficient to significantly change the propagation direction and velocity of epileptiform activity. These results suggest the possibility that the measurement of propagation can provide important information about the synaptic mechanism underlying epileptic activity.

Animals↗

PubMed2004

[Using the histogram analysis method to assess the time-frequency features of rat EEG under different vigilance states].

To investigate the non-stationary time-frequency features in rat Electroencephalogram (EEG) under different vigilance states, the methods of multi-resolution wavelet transform (WT) and statistical histogram analysis were used. EEGs of the freely moving rats were recorded with implanted electrodes under the vigilance states of waking, slow wave sleep (SWS) and rapid eye movement sleep (REM). The EEGs were firstly decomposed into four frequency components of delta, theta, alpha and beta by using multi-resolution wavelet transform. Then, the parameters of mean value, standard deviation, skewness and kurtosis of the logarithm power histograms and the power percentage histograms of each of the frequency components were calculated. The results showed that the distributions of the logarithm power histograms were not quite different from the normal distribution. However, most of the power percentage histograms were significantly different from the normal distribution. The results of one-way ANOVA indicated that there were significant differences in the parameter values of the histograms both among different states and among different frequency components. Moreover, Skewness and kurtosis of the logarithm power histograms of some characteristic waves in EEG, such as delta wave during SWS and theta wave during waking and REM, obtained high values. Thus, the histogram parameters of EEG WT components might become as quantitative measures to describe the dynamic time-frequency features of EEG.

Animals↗

PubMed2003

Low-calcium epileptiform activity in the hippocampus in vivo.

It has been clearly established that nonsynaptic interactions are sufficient for generating epileptiform activity in brain slices. However, it is not known whether this type of epilepsy model can be generated in vivo. In this paper we investigate low-calcium nonsynaptic epileptiform activity in an intact hippocampus. The calcium chelator EGTA was used to lower [Ca2+]o in the hippocampus of urethane anesthetized rats. Spontaneous and evoked field potentials in CA1 pyramidal stratum and in CA1 stratum radiatum were recorded using four-channel silicon recording probes. Three different types of epileptic activity were observed while synaptic transmission was gradually blocked by a decline in hippocampal [Ca2+]o. A short latency burst, named early-burst, occurred during the early period of EGTA application. Periodic slow-waves and a long latency high-frequency burst, named late-burst, were seen after synaptic transmission was mostly blocked. Therefore these activities appear to be associated with nonsynaptic mechanisms. Moreover, the slow-waves were similar in appearance to the depolarization potential shifts in vitro with low calcium. In addition, excitatory postsynaptic amino acid antagonists could not eliminate the development of slow-waves and late-bursts. The slow-waves and late-bursts were morphologically similar to electrographic seizure activity seen in patients with temporal lobe epilepsy. These results clearly show that epileptic activity can be generated in vivo in the absence of synaptic transmission. This type of low-calcium nonsynaptic epilepsy model in an intact hippocampus could play an important role in revealing additional mechanisms of epilepsy disorders and in developing novel anti-convulsant drugs.

Animals↗

PubMed2002

The inhibitory effects of jujuboside A on rat hippocampus in vivo and in vitro.

Jujuboside A (JuA) is a glycoside extracted from the seed of Ziziphus jujuba Mill var. spinosa (Bunge) Hu ex H F Chou, a Chinese herbal medicine, which has long been known as a sedative-hypnotic drug. The present study used the method of intracerebroventricular (i.c.v.) JuA in vivo to detect the effect of JuA on paired-pulse responses of dentate gyrus granule cells in urethane-anaesthetized rats, and the method of hippocampal slice bathing in JuA in vitro to detect the effects of JuA on the responses of CA1 pyramidal cells. The results showed that JuA significantly decreased the slopes of excitatory postsynaptic potential (EPSP) and the amplitudes of population spike (PS) in the first responses of granule cells and significantly decreased EPSP and PS in the responses of CA1 pyramidal cells. The good quantitative correspondence between in vitro and in vivo results indicates that studies using hippocampal formation allow research on the inhibitory effects of JuA in the rat central nervous system (CNS). In conclusion, our study accessed the inhibitory effects of JuA on hippocampal formation in vivo and in vitro, which contributed to the further research on the mechanism of its effects on CNS.

Animals↗

PubMed2002

[Effects of sampling parameter variation on the complexity analysis of EEG].

The algorithmic complexity and the approximate entropy of EEG were calculated and analyzed with different data points, different sample frequencies and different sample time duration. The results showed that under fixed sample frequency, the longer the data was, the more stable the complexity values were. With fixed sample time duration or fixed data point, lower sample frequency would be better both for EEG distinguishing and for computing time saving.

Algorithms↗