Epilepsia del lóbulo temporal y las neuronas hipocampales de las áreas CA1 y CA3 / Temporal lobe epilepsy and hippocampal neurons from areas CA1 and CA3

La epilepsia del lóbulo temporal es la forma más común de epilepsia que padece el ser humano. El sustrato fisiopatológico que la caracteriza es la esclerosis del hipocampo, que se distingue por pérdida neuronal, gliosis y disminución del volumen del hipocampo y áreas vecinas como la amígdala, el giro parahipocámpico y la corteza entorrinal. Lo anterior ocasiona atrofia y esclerosis del hilus del giro dentado y de las áreas CA1 y CA3 del hipocampo. Además se establece cierta reorganización de las vías neuronales que favorecen la neoespinogénesis, la morfogénesis, la neosinaptogénesis y la neurogénesis, con desarrollo aberrante de células y fibras, que contribuyen a la formación de un foco cuyo componente neuronal muestra un significativo aumento en la excitabilidad. El interés por entender el proceso de la epileptogénesis ha motivado al diseño de modelos de este tipo de epilepsia en animales de experimentación. La epileptogénesis evoluciona en el tiempo y muestra que la reorganización dinámica de las vías neuronales establece una red neuronal con cambios funcionales y anatómicos muy significativos. En este trabajo se realiza una revisión de la información obtenida por estudios electrofisiológicos que combinan el marcaje celular mediante el registro intra o extracelular en el hipocampo y en particular de las áreas CA1 y CA3 involucradas estrechamente con la epileptogénesis.

Temporal Lobe Epilepsy is the most common form of human epilepsy. Hippocampal sclerosis, neuronal loss, gliosis and hippocampal volume reduction are the representative changes of this pathology. Also some other near areas like amygdala, gyrus parahipocampal and entorrinal cortex are affected. Furthermore the neural circuits undergo activity-dependent reorganization during epileptogenesis. This brain circuits remodeling include neuronal loss (acute and delayed), neurogenesis, gliosis, plasticity (axonal and dendritic), inflammation and molecular reorganization. Two significant changes are evident, aberrant sprouting of granule cell axons in the dentate gyrus and hilar ectopic granular cells. Because temporal lobe epilepsy commonly develops after brain injury, most experimental animal models involve use of this factor. The pilocarpine-induced status epilepticus rat model may be the most widely used model of temporal lobe epilepsy. In the present work, we review the experimental support for seizure-induced plasticity in neural circuits, and then turn to evidence that seizure-induced plasticity occurs in human temporal-lobe.

The inhibitory effects of PNS oncardiac hypertrophy and its nervous mechanism / 中国药理学通报

Aim To investigate the antagonistic action o f total saponins of panaxnotoginseng(PNS) on cardiac hypertrophy and its nervous mechanism.Methods (1)cardiac hypertrophy of rats due to pressure overload was induced by constricting of abdominal aorta. There were five groups in the experiments. The rats in Group A(control group)were sham operated . Group B was aorta-constricted group.The rats in Group C,D,E were given ip PNS 50,100,150 mg?kg?d -1 for three weeks respectively. Three weeks later, We measured the heart-weight(HW),left ventricular weight(LVW), the ratio of HW/BW,LVW/BW (LVI) and the cardiomyocyte diameters(MD) after dyeing by HE color.(2)The effects of PNS on the fast excitatory postsynaptic potential(f-EPSP),membrane depolarization induced by application of acetylcholine (ACh),membrane potential and membrane resistance of the isolated Stellate ganglion(SG)of the rats were investigated by means of intracellular recording techniques. Results (1)HW/BW, LVI and MD of Group E were significantly lower than that of Group B(P0.05).(2)At the concentration of 0.10 ～0.16 g?L -1, PNS reversibly depressed the amplitude of f-EPSP, but the ACh depolarization,membrane potential and membrane resistance were not significantly altered by PNS. Conclusion PNS can prevent cardiac hypertrophy due to pressure overload in rats and this action may underline its inhibitory action on presyn aptic effect of regulating calcium influx.

Characteristic intracellular response to lidocaine and MK-801 of hippocampal neurons: An in vivo intracellular neuron recording study

This study used in vivo intracellular recording in rat hippocampus to evaluate the effect of lidocaine and MK-801 on the membrane properties and the synaptic responses of individual neurons to electrical stimulation of the commissural pathway. Cells in control group typically fired in a tonic discharge mode with an average firing frequency of 2.4+/-0.9 Hz. Neuron in MK-801 treated group (0.2 mg/kg, i.p.) had an average input resistance of 32.8 +/- 5.7 Mg and a membrane time constant of 7.4 +/- 1. 8 ms. These neurons exhibited 2.4 +/- 0.2 ms spike durations, which were similar to the average spike duration recorded in the neurons of the control group. Slightly less than half of these neurons were firing spontaneously with an average discharge rate of 2.4 +/- 1.1 Hz. The average peak amplitude of the ABP following the spikes in these groups was 7.4+/-0.6 mV with respect to the resting membrane potentiaL Cells in MK-801 and lidocaine treated group (5 mg/kg, i.c.v.) had an average input resistance of 34.5+/-6.0 Mg and an average time constant of 8.0+/-1.4 ms. The cells were firing spontaneously at an average discharge rate of 0.6+/-0.4 Hz. Upon depolarization of the membrane by 0.8 nA for 400 ms, all of the tested cells exhibited accommodation of spike discharge. The most common synaptic response contained an EPSP followed by early-IPSP and late-IPSP. Analysis of the voltage dependence revealed that the early-IPSP and late-IPSP were putative Cl-and K+-dependent, respectively. Systemic injection of the NMDA receptor blocker, MK-801, did not block synaptic responses to the stimulation of the commissural pathway. No significant modifications of EPSP, early-IPSP, or late-IPSP components were detected in the MK-801 and/or lidocaine treated group. These results suggest that MK-801 and lidocaine manifest their CNS effects through firing pattern of hippocampal pyramidal cells and neural network pattern by changing the synaptic efficacy and cellular membrane properties.

Preferential Suppression of the On Pathway by r-Aminobutyric Acid in the Catfish Retina

The effects of r-aminobutyric acid(GABA) agonsits and antagonists were explored by the intracellular recording method to discern the preferential suppression of the ON component by GABA on the ON-OFF transient cell in the catfish (Ictalurus punctatus) retina. Experiments were performed in the superfused eyecup preparation. The animals were decapitated and pited before the eye, and the surrounding tissue was removed from the skull. The retina was exposed by excising the cornea, iris, and vitreous. This preparation rested on a wad of Ringer`s soaked cotton in contact with an Ag/Agcl reference electrode. Solutions were delivered through a manifold system that was connected to a pipette located near the absorbent wick. Electro-physiological recordings were made using standard intracellular electrodes filled with 2 M potassium acetate. The electrical signal was recorded with an amplifierand a penwriter, viewed on an oscilloscope, and stored on a data recorder. The light sources were red light-emitting-diode (LED) and the stimuli were full field illumination covering the cntire retina. GABA preferentially reduced ON light responses in ON-OFF transient cell. and GABA hyperpolarized bipolar cells, but the effects on ON bipolar cells were more sensitive than OFF bipolar cells. CACA and TACA, GABAc receptor agonist, did not act on bipolar cells. CACA and TACA, GABAc receptor agonists, hyperpolarized bipolar cells but the sensitivity deferences between ON and OFF bipolar cell were not observed. These results suggest that the preferential suppression of the ON component of the ON-OFF transient cell by GABA was resulted from the presynaptic mechanism that reduced bipolar cell input.

Effects of Extracellular Chloride Ions on the Catfish Retinal Neurons

The catfish (Ictalurus punctatus) retinal neurons were investigated by using the intracellular recording techniques to analyze the function of the chloride ions in the light responses and the ionic mechanisms of the depolarizing actions by GABA. Experiments were performed in the superfused retina-eyecup preparation. The retina was exposed by exicising the cornea, iris, and vitreous. A piece of absorbent tissue with a hole large enough to expose the retina was centered over the eyecup to serve as a wick to draw off the superfusate. Diffuse light stimuli were generated by light-emitting diode positioned above the eyecup. The recordings were made with the use of borosilicate glass micropipettes fashioned from' omega dot' capillary tubing filled with 2 M potassium acetate. Voltage recordings were obtained using an amplifier and amplified signals were recorded on a storage oscillocope, penwriter, and a data recorder. In the catfish retina, the dark membrane potentials were depolarized and the light evoked responses were enhanced in the chloride"-free medium on the catfish horizontal cells. The amplitude of the light evoked potentials were increased by chloride free Ringer's solution on the ON- and OFF-bipolar cells. But the dark membrane potentials were hyperpolarized on the ON-bipolar cell and depolarized on the OFF-bipolar cells in the chloride free medium. The chloride free Ringer's solution changed the light response from ON-sustained to OFF-sustained without any change in amplitude on the ON-sustained cell. The depolarizing actions by GABA on the horizontal cells were maintained in chloride-free environment. But GABA did not abolished the light evoked potentials of the horizontal cell and the ON-sustained cell under the chloride free environment. The results suggest that chloride ion has important roles on the signal transmission of the dark periods in the catfish retina and the depolarizing actions by GABA on the neurons in the catfish retina might be chloride dependent.