Models of the cellular mechanism underlying propagation of epileptiform activity in the CA2-CA3 region of the hippocampal slice

Traub, Roger D.; Knowles, W. Douglas; Miles, Richard; Wong, Robert K. S.

doi:10.1016/0306-4522(87)90135-7

Cited by 79 publications

(39 citation statements)

References 45 publications

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“…Excitatory waves in brain tissue have been examined extensively (Albowitz and Kuhnt 1995;Chervin et al 1988;Demir et al 1998;Fleidervish et al 1998;Golomb and Amitai 1997;Grinvald et al 1984;Miyakawa et al 2003;Tanifuji et al 1994;Tsau et al 1998;Wu et al 2001). GABAergic inhibition is important for controlling the propagation of excitatory waves (Chagnac-Amitai and Connors 1989;Golomb and Ermentrout 2002;Miles et al 1988;Traub et al 1987;Wadman and Gutnick 1993). When GABA A receptors are blocked with bicuculline, the excitation wave propagates at ϳ0.14 m/s in hippocampal slices (Miles et al 1988) and 0.08 m/s (Chervin et al 1988) to 0.13 m/s (Wu et al 2001) in neocortical slices.…”

Section: Propagating Wavesmentioning

confidence: 99%

Spatiotemporal Patterns of an Evoked Network Oscillation in Neocortical Slices: Coupled Local Oscillators

Bai¹,

Huang²,

Yang³

et al. 2006

Journal of Neurophysiology

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. Spatiotemporal patterns of an evoked network oscillation in neocortical slices: coupled local oscillators. J Neurophysiol 96: 2528 -2538, 2006. First published July 26, 2006 doi:10.1152/jn.00645.2006. We have discovered an evoked network oscillation in rat neocortical slices and have examined its spatiotemporal patterns with voltage-sensitive dye imaging. The slices (visual and auditory cortices) were prepared in a medium of low calcium, high magnesium and with sodium replaced by choline to reduce the excito-toxicity and sodium loading. After slicing, the choline was washed out while normal calcium, magnesium, and sodium concentrations were restored. The oscillation was evoked by a single electrical shock to slices bathed in normal artificial cerebral spinal fluid (ACSF). The oscillation was organized as an all-or-none epoch containing 4 -13 cycles at a central frequency ϳ25 Hz. The activity can be reversibly blocked by 6-cyano-7-nitroquinoxalene-2,3-dione (CNQX). 2-amino-5-phosphonopentanoic acid (APV), and atropine but not by bicuculline, indicating polysynaptic excitatory mechanisms. Voltage-sensitive dye imaging showed high-amplitude oscillation signals in superficial and middle cortical layers. Spatiotemporally, the oscillations were organized as waves, propagating horizontally along cortical laminar. Each oscillation cycle was associated with one wave propagating in space. The waveforms were often different at different locations (e.g., extra cycles), suggesting the co-existence of multiple local oscillators. For different cycles, the waves often initiated at different locations, suggesting that local oscillators are competing to initiate each oscillation cycle. Overall our results suggest that this cortical network oscillation is organized at two levels: locally, oscillating neurons are tightly coupled to form local oscillators, and globally the coupling between local oscillators is weak, allowing abrupt spatial phase lags and propagating waves with multiple initiation sites.

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Section: Propagating Wavesmentioning

confidence: 99%

Spatiotemporal Patterns of an Evoked Network Oscillation in Neocortical Slices: Coupled Local Oscillators

Bai¹,

Huang²,

Yang³

et al. 2006

Journal of Neurophysiology

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“…A model network simulation of hippocampal neuronal bursting demonstrated that bursting can occur, even in the presence of neuronal inhibition, only if connectivity between neurons in the circuit is adequately dense. Low connectivity prevents the development of bursting (Traub et al 1987). In vitro studies in hippocampus and neocortex suggest that the relative paucity of excitatory synaptic connections likely contributes to neonate rodent seizure resistance (Swann and Hablitz 2000).…”

Section: Reduced Magnesium Bursting: Connectivitymentioning

confidence: 99%

“…A model network simulation of hippocampal bursting demonstrated that bursting can occur, even in the presence of neuronal inhibition, only if connectivity between neurons in the circuit is adequately dense. Low connectivity prevents the development of bursting (Traub et al 1984(Traub et al , 1987.…”

Section: Introductionmentioning

confidence: 99%

Factors Underlying Bursting Behavior in a Network of Cultured Hippocampal Neurons Exposed to Zero Magnesium

Mangan

2004

Journal of Neurophysiology

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Mangan, Patrick S. and Jaideep Kapur. Factors underlying bursting behavior in a network of cultured hippocampal neurons exposed to zero magnesium. J Neurophysiol 91: 946 -957, 2004. First published October 8, 2003 10.1152/jn.00547.2003. Factors contributing to reduced magnesium-induced neuronal action potential bursting were investigated in primary hippocampal cell culture at high and low culture density. In nominally zero external magnesium medium, pyramidal neurons from high-density cultures produced recurrent spontaneous action potential bursts superimposed on prolonged depolarizations. These bursts were partially attenuated by the NMDA receptor antagonist D-APV. Pharmacological analysis of miniature excitatory postsynaptic currents (EPSCs) revealed 2 components: one sensitive to D-APV and another to the AMPA receptor antagonist DNQX. The components were kinetically distinct. Participation of NMDA receptors in reduced magnesium-induced synaptic events was supported by the localization of the NR1 subunit of the NMDA receptor with the presynaptic vesicular protein synaptophysin. Presynaptically, zero magnesium induced a significant increase in EPSC frequency likely attributable to increased neuronal hyperexcitability induced by reduced membrane surface charge screening. Mean quantal content was significantly increased in zero magnesium. Cells from low-density cultures did not exhibit action potential bursting in zero magnesium but did show increased EPSC frequency. Low-density neurons had less synaptophysin immunofluorescence and fewer active synapses as determined by FM1-43 analysis. These results demonstrate that multiple factors are involved in network bursting. Increased probability of transmitter release presynaptically, enhanced NMDA receptor-mediated excitability postsynaptically, and extent of neuronal interconnectivity contribute to initiation and maintenance of elevated network excitability.

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“…This possibility receives some support from the reliable presence of monosynaptic IPSPs in the secondary focus when EPSPs were blocked. However, CA3 pyramidal cell synapses could not have been extensively blocked, or we would not then have been able to record EPSPs nor indeed to recruit epileptic discharges (Wong et al 1986;Traub, Knowles, Miles & Wong, 1987). Furthermore we found no differences between the groups in estimated EPSP conductances.…”

Section: Inhibition In a Secondary Epileptic Focusmentioning

confidence: 99%

Synaptic inhibition in primary and secondary chronic epileptic foci induced by intrahippocampal tetanus toxin in the rat.

Empson

Jefferys

1993

The Journal of Physiology

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SUMMARY1. Injecting twelve mouse minimum lethal doses of tetanus toxin into one hippocampus of a rat leads to the development of chronic epileptic foci in both hippocampi. These generate intermittent epileptic discharges for 6-8 weeks. Here we compare GABAergic inhibition, 10-18 days after injection, in slices prepared from the injected and contralateral hippocampi (respectively the primary and the secondary or 'mirror' foci), using both neurochemical and electrophysiological methods.2. Epileptic activity was recorded from slices of both hippocampi from all tetanus toxin-injected rats. Evoked epileptic discharges were similar on the two sides, but spontaneous epileptic discharges were more common contralaterally.3. Ca2"-dependent, K+-stimulated (synaptic) release of radiolabelled GABA was depressed in slices from the injected hippocampus, compared with vehicle-injected controls. In contrast, slices from the contralateral hippocampus had normal levels of Ca2"-dependent, K+-stimulated GABA release, even though adjacent slices were epileptogenic.4. Intracellular recordings revealed that both fast and slow stimulus-evoked inhibitory postsynaptic potentials (IPSPs) were abolished in CA3 pyramidal cells in the primary focus. In the secondary focus, however, fast IPSPs were seen in seven of twenty-five cells, and slow IPSPs were seen in all cells if the stimulus was strong enough.5. Monosynaptic IPSPs were isolated pharmacologically by blocking glutamatergic excitatory postsynaptic potentials (EPSPs) with 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and D(-)-2-amino-5-phosphopentanoic acid . No monosynaptic IPSPs were uncovered in cells from the primary focus at any stimulus strength. Monosynaptic IPSPs were evoked in all cells from both the secondary focus and control slices. The estimated conductances of monosynaptic fast IPSPs were similar in cells from the secondary focus and from the controls, although the former required twice the stimulus strength.6. Slow IPSPs were found in the secondary focus and in controls, but not in the primary focus. They were sensitive to 3-amino-2-(4-chlorophenyl)-2-hydroxypropylsulphonic acid (2-OH saclofen). The estimated conductances of slow IPSPs M1S 1729 R. MI. E2JPSON AND J. G. R. JEFFERYS evoked by weak stimuli in the secondary focus were much smaller than in the controls. However, stimuli that could trigger epileptic discharges in the secondary focus, evoked 2-OH saclofen-sensitive slow IPSPs with estimated conductances approaching the controls. This marked increase in the slow IPSP did not occur when EPSPs, and epileptic bursts, were blocked with CNQX and AP-5, suggesting that a strong barrage of excitation is needed to generate full-sized slow IPSPs in the secondary focus. 7. The chronic epileptic foci induced by tetanus toxin in the injected and contralateral hippocampi have distinct mechanisms. The ipsilateral focus behaved as expected from the acute actions of tetanus toxin; the synaptic release of GABA was disrupted and IPSPs were abolished, providing a probable mechanism f...

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Models of the cellular mechanism underlying propagation of epileptiform activity in the CA2-CA3 region of the hippocampal slice

Cited by 79 publications

References 45 publications

Spatiotemporal Patterns of an Evoked Network Oscillation in Neocortical Slices: Coupled Local Oscillators

Spatiotemporal Patterns of an Evoked Network Oscillation in Neocortical Slices: Coupled Local Oscillators

Factors Underlying Bursting Behavior in a Network of Cultured Hippocampal Neurons Exposed to Zero Magnesium

Synaptic inhibition in primary and secondary chronic epileptic foci induced by intrahippocampal tetanus toxin in the rat.

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