ArticleThe Journal of physiology2002
Control of the propagation of dendritic low-threshold Ca(2+) spikes in Purkinje cells from rat cerebellar slice cultures.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 47 citations in OpenAlex.
- BK Channel Regulation of Afterpotentials and Burst Firing in Cerebellar Purkinje Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- The Impact of BK Channels on Cellular Excitability Depends on their Subcellular Location.Frontiers in cellular neuroscience · 2016Article
- Article
- Contributions of T-type voltage-gated calcium channels to postsynaptic calcium signaling within Purkinje neurons.Cerebellum (London, England) · 2012Review
- Current treatment of vestibular, ocular motor disorders and nystagmus.Therapeutic advances in neurological disorders · 2009Article
- Large-conductance calcium-dependent potassium channels prevent dendritic excitability in neocortical pyramidal neurons.Pflugers Archiv : European journal of physiology · 2009Article
- Kv1 channels selectively prevent dendritic hyperexcitability in rat Purkinje cells.The Journal of physiology · 2005Article
- Physiological and morphological development of the rat cerebellar Purkinje cell.The Journal of physiology · 2005Article
- Robustness of burst firing in dissociated purkinje neurons with acute or long-term reductions in sodium conductance.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Low threshold calcium currents in rat cerebellar Purkinje cell dendritic spines are mediated by T-type calcium channels.The Journal of physiology · 2005Article
- Role of the alpha1G T-type calcium channel in spontaneous absence seizures in mutant mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Dendritic control of spontaneous bursting in cerebellar Purkinje cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Low-voltage-activated ("T-Type") calcium channels in review.Journal of bioenergetics and biomembranes · 2003Review
- Ionic mechanisms of burst firing in dissociated Purkinje neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Properties and functional role of voltage-dependent potassium channels in dendrites of rat cerebellar Purkinje neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Somatic and dendritic small-conductance calcium-activated potassium channels regulate the output of cerebellar Purkinje neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Dendritic low-threshold Ca2+ channels in rat cerebellar Purkinje cells: possible physiological implications.Cerebellum (London, England) · 2003Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To investigate the ionic mechanisms controlling the dendrosomatic propagation of low-threshold Ca(2+) spikes (LTS) in Purkinje cells (PCs), somatically evoked discharges of action potentials (APs) were recorded under current-clamp conditions. The whole-cell configuration of the patch-clamp method was used in PCs from rat cerebellar slice cultures. Full blockade of the P/Q-type Ca(2+) current revealed slow but transient depolarizations associated with bursts of fast Na(+) APs. These can occur as a single isolated event at the onset of current injection, or repetitively (i.e. a slow complex burst). The initial transient depolarization was identified as an LTS Blockade of P/Q-type Ca(2+) channels increased the likelihood of recording Ca(2+) spikes at the soma by promoting dendrosomatic propagation. Slow rhythmic depolarizations shared several properties with the LTS (kinetics, activation/inactivation, calcium dependency and dendritic origin), suggesting that they correspond to repetitively activated dendritic LTS, which reach the soma when P/Q channels are blocked. Somatic LTS and slow complex burst activity were also induced by K(+) channel blockers such as TEA (2.5 x 10(-4) M) charybdotoxin (CTX, 10(-5) M), rIberiotoxin (10(-7) M), and 4-aminopyridine (4-AP, 10(-3) M), but not by apamin (10(-4) M). In the presence of 4-AP, slow complex burst activity occurred even at hyperpolarized potentials (-80 mV). In conclusion, we suggest that the propagation of dendritic LTS is controlled directly by 4-AP-sensitive K(+) channels, and indirectly modulated by activation of calcium-activated K(+) (BK) channels via P/Q-mediated Ca(2+) entry. The slow complex burst resembles strikingly the complex spike elicited by climbing fibre stimulation, and we therefore propose, as a hypothesis, that dendrosomatic propagation of the LTS could underlie the complex spike.
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