Ionic basis for the electro‐responsiveness and oscillatory properties of guinea‐pig thalamic neurones in vitro.

Jahnsen, Henrik; Llinás, Rodolfó R.

doi:10.1113/jphysiol.1984.sp015154

Cited by 1,006 publications

(460 citation statements)

References 31 publications

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“…Pacemaker neurons have long been known (Jahnsen and Llinas, 1984;Kandel and Spencer, 1961;Leresche et al, 1991;Llinas, 1988), and such properties are important in generating epileptic activity (Traub et al, 1993). Perhaps the most dramatic demonstrations that single neurons can generate oscillations come from freshly dissociated neurons in vitro where synaptic networks are absent (Swensen and Bean, 2003), although structural disruption during dissociation, particularly loss of dendrites, does impact on intrinsic properties (Destexhe et al, 1996).…”

Section: Cellular Oscillatorsmentioning

confidence: 99%

Mechanisms of physiological and epileptic HFO generation

Jefferys

Prida

Wendling

et al. 2012

Progress in Neurobiology

269

238

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High frequency oscillations (HFO) have a variety of characteristics: band-limited or broad-band, transient burst-like phenomenon or steady-state. HFOs may be encountered under physiological or under pathological conditions (pHFO). Here we review the underlying mechanisms of oscillations, at the level of cells and networks, investigated in a variety of experimental in vitro and in vivo models. Diverse mechanisms are described, from intrinsic membrane oscillations to network processes involving different types of synaptic interactions, gap junctions and ephaptic coupling. HFOs with similar frequency ranges can differ considerably in their physiological mechanisms. The fact that in most cases the combination of intrinsic neuronal membrane oscillations and synaptic circuits are necessary to sustain network oscillations is emphasized. Evidence for pathological HFOs, particularly fast ripples, in experimental models of epilepsy and in human epileptic patients is scrutinized. The underlying mechanisms of fast ripples are examined both in the light of animal observations, in vivo and in vitro, and in epileptic patients, with emphasis on single cell dynamics. Experimental observations and computational modeling have led to hypotheses for these mechanisms, several of which are considered here, namely the role of out-ofphase firing in neuronal clusters, the importance of strong excitatory AMPA-synaptic currents and recurrent inhibitory connectivity in combination with the fast time scales of IPSPs, ephaptic coupling and the contribution of interneuronal coupling through gap junctions. The statistical behaviour of fast ripple events can provide useful information on the underlying mechanism and can help to further improve classification of the diverse forms of HFOs.

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Section: Cellular Oscillatorsmentioning

confidence: 99%

Mechanisms of physiological and epileptic HFO generation

Jefferys

Prida

Wendling

et al. 2012

Progress in Neurobiology

269

238

View full text Add to dashboard Cite

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“…Its distinction from the sustained component is based on kinetics. This class contains several types of calcium channels: N-type, 12,16,42,45 Q-type 39 or R-type. 11,38 To what extent each of the candidates is present could not be determined on the basis of voltage-dependent and kinetic properties alone.…”

Section: Current Separationmentioning

confidence: 99%

“…In the model of absence epilepsy (GAERS), 44 the enhanced LVA calcium currents in the thalamus can drive rhythmic activities and underlie rebound activity. 8,16,19 Antiepileptic drugs like ethosuximide, trimethadione 9 and valproic acid 23 have been reported to affect LVA calcium currents.…”

Section: Difference After Kindlingmentioning

confidence: 99%

“…48 An important calcium current with properties well suited to control excitability is the low-voltageactivated (LVA) current. 5,16 Until now, this current could not be detected in dissociated neurons of adult animals. We showed recently 21 that the in situ patchclamp technique in the slice allows the detection of LVA currents.…”

mentioning

confidence: 95%

“…This, either directly by depolarization or indirectly through modulation of second messenger function, will contribute to changes in excitability such as synaptic efficacy, 25,34 firing threshold and firing frequency. 16 Indeed, it has been shown that calcium currents are involved in kindling epileptogenesis in the CA1 area of the rat hippocampus. 46,47 Kindled animals, when compared to untreated animals, showed a marked enhancement in extracellular calcium decreases in the stratum radiatum of the CA1 area, induced by electrical stimulation or iontophoresis of excitatory amino acids.…”

mentioning

confidence: 99%

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Calcium currents in pyramidal CA1 neurons in vitro after kindling epileptogenesis in the hippocampus of the rat

1996

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Calcium currents in pyramidal CA1 neurons in vitro after kindling epileptogenesis in the hippocampus of the rat Faas, G.C.; Vreugdenhil, M.; Wadman, W.J. Disclaimer/Complaints regulationsIf you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: http://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. Abstract--Calcium is an important second messenger which plays a role in the regulation of neuronal excitability and in many forms of synaptic plasticity. In kindling epileptogenesis, a model of focal epilepsy, calcium plays an important role. The in situ patch-clamp technique was used to record calcium currents in slices obtained from kindled rats and controls. We found that low-voltage-activated calcium currents, probably of dendritic origin, were larger after kindling (80%). The transient high-voltage-activated calcium currents were also enhanced after kindling (50% higher). The increase of the current is accompanied by a decrease in the time constant of inactivation. The change was still present six weeks after the kindling stimulations were stopped. These data demonstrate that low-voltage-activated calcium currents are involved in epileptogenesis. Their enhancement in the dendrites will boost synaptic depolarization and result in enhanced calcium influx, which is critically dependent on the specific activation pattern.

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Immunocytochemistry and distribution of parabrachial terminals in the lateral geniculate nucleus of the cat: A comparison with corticogeniculate terminals

et al. 1997

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We used immunohistochemistry in cats to demonstrate the presence of brain nitric oxide synthase (BNOS) in cholinergic fibers within the A-laminae of the lateral geniculate nucleus. We used a double labeling procedure with electron microscopy and found that all terminals labeled for choline acetyltransferase (ChAT) in the geniculate A-laminae were double labeled for BNOS. Also, some interneuron dendrites, identified by labeling for gamma-aminobutyric acid (GABA), contained BNOS, but relay cell dendrites did not. We then compared parabrachial and corticogeniculate terminals, identifying the former by BNOS/ChAT labeling and the latter by orthograde transport of biocytin injected into cortical area 17, 18, or 19. All corticogeniculate terminals and most BNOS- or ChAT-positive brainstem terminals displayed RSD morphology, whereas some brainstem terminals exhibited RLD morphology. However, parabrachial terminals were larger, on average, than corticogeniculate terminals. We also found that parabrachial terminals were located both inside and outside of glomeruli, and they always contacted relay cell dendrites proximally among retinal terminals (the retinal recipient zone). In contrast, the cortical terminals were limited to peripheral dendrites (the cortical recipient zone). Thus, little if any overlap exists in the distribution of parabrachial and corticogeniculate terminals on the dendrites of relay cells.

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Ionic basis for the electro‐responsiveness and oscillatory properties of guinea‐pig thalamic neurones in vitro.

Cited by 1,006 publications

References 31 publications

Mechanisms of physiological and epileptic HFO generation

Mechanisms of physiological and epileptic HFO generation

Calcium currents in pyramidal CA1 neurons in vitro after kindling epileptogenesis in the hippocampus of the rat

Immunocytochemistry and distribution of parabrachial terminals in the lateral geniculate nucleus of the cat: A comparison with corticogeniculate terminals

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