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Physiological role of dendrotoxin sensitive k channels in the rat cerebellar Purkinje neurons
H. Haghdoust, M. Janahmadi, G. Behzadi
Jazyk angličtina Země Česko
NLK
Directory of Open Access Journals
od 1991
Free Medical Journals
od 1998
ProQuest Central
od 2005-01-01
Medline Complete (EBSCOhost)
od 2006-01-01
Nursing & Allied Health Database (ProQuest)
od 2005-01-01
Health & Medicine (ProQuest)
od 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
od 1998
- MeSH
- draslíkové kanály izolace a purifikace metabolismus MeSH
- elektrofyziologie metody přístrojové vybavení MeSH
- financování organizované využití MeSH
- kůra mozečku fyziologie metabolismus MeSH
- peptidy fyziologie metabolismus MeSH
- potkani Sprague-Dawley fyziologie metabolismus MeSH
- Purkyňova vlákna fyziologie metabolismus MeSH
To understand the contribution of potassium (K+) channels, particularly ?-dendrotoxin (D-type)-sensitive K+ channels (Kv.1, Kv1.2 or Kv1.6 subunits), to the generation of neuronal spike output we must have detailed information of the functional role of these channels in the neuronal membrane. Conventional intracellular recording methods in current clamp mode were used to identify the role of ?-dendrotoxin (?-DTX)-sensitive K+ channel currents in shaping the spike output and modulation of neuronal properties of cerebellar Purkinje neurons (PCs) in slices. Addition of ?-DTX revealed that D-type K+ channels play an important role in the shaping of Purkinje neuronal firing behavior. Repetitive firing capability of PCs was increased following exposure to artificial cerebrospinal fluid (aCSF) containing ?-DTX, so that in response to the injection of 0.6 nA depolarizing current pulse of 600 ms, the number of action potentials insignificantly increased from 15 in the presence of 4-AP to 29 action potentials per second after application of DTX following pretreatment with 4-AP. These results indicate that D-type K+ channels (Kv.1, Kv1.2 or Kv1.6 subunits) may contribute to the spike frequency adaptation in PCs. Our findings suggest that the activation of voltage-dependent K+ channels (D and A types) markedly affect the firing pattern of PCs.
Lit.: 40
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- $a To understand the contribution of potassium (K+) channels, particularly ?-dendrotoxin (D-type)-sensitive K+ channels (Kv.1, Kv1.2 or Kv1.6 subunits), to the generation of neuronal spike output we must have detailed information of the functional role of these channels in the neuronal membrane. Conventional intracellular recording methods in current clamp mode were used to identify the role of ?-dendrotoxin (?-DTX)-sensitive K+ channel currents in shaping the spike output and modulation of neuronal properties of cerebellar Purkinje neurons (PCs) in slices. Addition of ?-DTX revealed that D-type K+ channels play an important role in the shaping of Purkinje neuronal firing behavior. Repetitive firing capability of PCs was increased following exposure to artificial cerebrospinal fluid (aCSF) containing ?-DTX, so that in response to the injection of 0.6 nA depolarizing current pulse of 600 ms, the number of action potentials insignificantly increased from 15 in the presence of 4-AP to 29 action potentials per second after application of DTX following pretreatment with 4-AP. These results indicate that D-type K+ channels (Kv.1, Kv1.2 or Kv1.6 subunits) may contribute to the spike frequency adaptation in PCs. Our findings suggest that the activation of voltage-dependent K+ channels (D and A types) markedly affect the firing pattern of PCs.
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