Electrophysiology of mammalian thalamic neurones in vitro

Llinás, Rodolfó R.; Jahnsen, Henrik

doi:10.1038/297406a0

Cited by 682 publications

(364 citation statements)

References 11 publications

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“…T-type channel activation depolarizes the postsynaptic membrane potential (Vm), opening L-type HVA Ca 2C channels (1). The resulting increase in intracellular Ca 2C concentration triggers NO production that diffuses retrogradely to the presynaptic element (2) and induces pre-synaptic LTP through guanylate cyclase activation. A different mechanism, independent of HVA channel activation, requires Ca 2C ions specifically entering in the post-synaptic dendrite through the T-type channels to activate the phosphatase calcineurin and trigger LTD (3).…”

Section: Sleep-associated Synaptic Plasticitymentioning

confidence: 99%

“…A. Excitatory synapses. Activation of postsynaptic T-type calcium channels induces a post-synaptic Ca 2C increase either directly (1) and/or as a consequence of the membrane potential (Vm) depolarization that can in turn either trigger the opening of the HVA Ca 2C channel (2) and/or relieve the Mg 2C block of NMDA receptors (2 0 ). In addition to T channels activation, various types of metabotropic receptors can be recruited (3) further enhancing intracellular Ca 2C concentration by mobilizing the Ca 2C stores.…”

Section: Sleep-associated Synaptic Plasticitymentioning

confidence: 99%

“…At that time, the group of R. Llinas identified a Ca 2C -mediated rebound depolarization, the so-called lowthreshold spike (LTS), that follows a transient hyperpolarization of inferior olive and thalamic neurons. [1][2][3][4] Functionally, the Ca 2C current responsible for this depolarization was rapidly recognized as one of the key conductances underlying the characteristic rhythmic high-frequency burst firing activity of thalamic neurons during various NREM sleep stages. 5,6 In parallel, studies mainly performed in primary sensory neurons [7][8][9][10] demonstrated that this low-threshold Ca 2C current, named T-type current, is activated around ¡60 mV and fully inactivated after a few tens of milliseconds.…”

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T-type calcium channels in synaptic plasticity

Leresche

Lambert

2016

Channels

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The role of T-type calcium currents is rarely considered in the extensive literature covering the mechanisms of long-term synaptic plasticity. This situation reflects the lack of suitable T-type channel antagonists that till recently has hampered investigations of the functional roles of these channels. However, with the development of new pharmacological and genetic tools, a clear involvement of T-type channels in synaptic plasticity is starting to emerge. Here, we review a number of studies showing that T-type channels participate to numerous homo-and heterosynaptic plasticity mechanisms that involve different molecular partners and both pre-and postsynaptic modifications. The existence of T-channel dependent and independent plasticity at the same synapse strongly suggests a subcellular localization of these channels and their partners that allows specific interactions. Moreover, we illustrate the functional importance of T-channel dependent synaptic plasticity in neocortex and thalamus.

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Section: Sleep-associated Synaptic Plasticitymentioning

confidence: 99%

Section: Sleep-associated Synaptic Plasticitymentioning

confidence: 99%

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confidence: 99%

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T-type calcium channels in synaptic plasticity

Leresche

Lambert

2016

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“…Thalamic neurons can also re bursts of action potentials, which consist of a slow calcium-mediated spike, crowned by high-frequency action potentials. This 'burst' mode of ring is a consequence of an intrinsic voltage-dependent current, the low-threshold (T-type) calcium current (Llinás & Jahnsen 1982).…”

Section: Introductionmentioning

confidence: 99%

The initiation of bursts in thalamic neurons and the cortical control of thalamic sensitivity

Destexhe

Sejnowski

2002

Phil. Trans. R. Soc. Lond. B

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Thalamic neurons generate high-frequency bursts of action potentials when a low-threshold (T-type) calcium current, located in soma and dendrites, becomes activated. Computational models were used to investigate the bursting properties of thalamic relay and reticular neurons. These two types of thalamic cells differ fundamentally in their ability to generate bursts following either excitatory or inhibitory events. Bursts generated with excitatory inputs in relay cells required a high degree of convergence from excitatory inputs, whereas moderate excitation drove burst discharges in reticular neurons from hyperpolarized levels. The opposite holds for inhibitory rebound bursts, which are more dif cult to evoke in reticular neurons than in relay cells. The differences between the reticular neurons and thalamocortical neurons were due to different kinetics of the T-current, different electrotonic properties and different distribution patterns of the T-current in the two cell types. These properties enable the cortex to control the sensitivity of the thalamus to inputs and are also important for understanding states such as absence seizures.

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“…Thalamic burst firing, which is generated by a major contribution from Ca V 3.1-mediated LTS, is known to be involved in the generation of low-frequency oscillations (8,19). It is well known that hyperpolarization, generated by NMDA receptor block, is sufficient to deinactivate T-type Ca 2+ channels, resulting in rhythmic thalamic bursting (20).…”

Section: Discussionmentioning

confidence: 99%

Altered thalamocortical rhythmicity and connectivity in mice lacking Ca _V 3.1 T-type Ca ²⁺ channels in unconsciousness

Choi

Lee

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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In unconscious status (e.g., deep sleep and anesthetic unconsciousness) where cognitive functions are not generated there is still a significant level of brain activity present. Indeed, the electrophysiology of the unconscious brain is characterized by well-defined thalamocortical rhythmicity. Here we address the ionic basis for such thalamocortical rhythms during unconsciousness. In particular, we address the role of Ca V 3.1 T-type Ca 2+ channels, which are richly expressed in thalamic neurons. Toward this aim, we examined the electrophysiological and behavioral phenotypes of mice lacking Ca V 3.1 channels (Ca V 3.1 knockout) during unconsciousness induced by ketamine or ethanol administration. Our findings indicate that Ca V 3.1 KO mice displayed attenuated low-frequency oscillations in thalamocortical loops, especially in the 1-to 4-Hz delta band, compared with control mice (Ca V 3.1 WT). Intriguingly, we also found that Ca V 3.1 KO mice exhibited augmented highfrequency oscillations during unconsciousness. In a behavioral measure of unconsciousness dynamics, Ca V 3.1 KO mice took longer to fall into the unconscious state than controls. In addition, such unconscious events had a shorter duration than those of control mice. The thalamocortical interaction level between mediodorsal thalamus and frontal cortex in Ca V 3.1 KO mice was significantly lower, especially for delta band oscillations, compared with that of Ca V 3.1 WT mice, during unconsciousness. These results suggest that the Ca V 3.1 channel is required for the generation of a given set of thalamocortical rhythms during unconsciousness. Further, that thalamocortical resonant neuronal activity supported by this channel is important for the control of vigilance states.electroencephalogram | local field potential | mediodorsal thalamus | coherence T halamocortical interactive rhythmic activities are well-defined physiological correlates of both conscious and unconscious conditions (1, 2). From a functional perspective, abnormal slow cortical rhythms and their synchronized network dynamics are omnipresent correlates of unconscious states, such as coma and general anesthesia (3, 4). Moreover, a dynamic alteration of coherence as well as coupling/uncoupling in thalamocortical circuits also can be characterized as likely correlates of unconsciousness (3-5).Since the discovery of low threshold, T-type Ca 2+ channels (6, 7) and the subsequent studies of intrinsic electrophysiological properties in the thalamic neurons (8, 9), T-type Ca 2+ channels have been implicated in many physiological and pathological brain states (for a review, see ref. 10). The ionic conductances they support have been shown to generate synchronized oscillatory activity in thalamocortical circuits through calcium-dependent low-threshold spikes (LTSs). Indeed, these LTSs, generated by "deinactivation" of T-type Ca 2+ channels, underlie thalamic burst firing. This activity is reflected as high-amplitude low-frequency oscillations in electroencephalography, and its presence is recognized...

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Electrophysiology of mammalian thalamic neurones in vitro

Cited by 682 publications

References 11 publications

T-type calcium channels in synaptic plasticity

T-type calcium channels in synaptic plasticity

The initiation of bursts in thalamic neurons and the cortical control of thalamic sensitivity

Altered thalamocortical rhythmicity and connectivity in mice lacking Ca _V 3.1 T-type Ca ²⁺ channels in unconsciousness

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Electrophysiology of mammalian thalamic neurones in vitro

Cited by 682 publications

References 11 publications

T-type calcium channels in synaptic plasticity

T-type calcium channels in synaptic plasticity

The initiation of bursts in thalamic neurons and the cortical control of thalamic sensitivity

Altered thalamocortical rhythmicity and connectivity in mice lacking Ca V 3.1 T-type Ca 2+ channels in unconsciousness

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Altered thalamocortical rhythmicity and connectivity in mice lacking Ca _V 3.1 T-type Ca ²⁺ channels in unconsciousness