| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Physiology, Ben-Gurion University, Be'er-Sheva, Israel
2 Physiology, Hebrew University, Jerusalem, Israel
* To whom correspondence should be addressed. E-mail: golomb{at}bgu.ac.il.
The intrinsic firing modes of adult CA1 pyramidal cells vary along a continuum of 'burstiness' from regular firing to rhythmic bursting, depending on the ionic composition of the extracellular milieu. Burstiness is low in neurons exposed to a normal extracellular Ca2+ concentration (Ca2+]o), but is markedly enhanced by lowering [Ca2+]o, though not by blocking Ca2+ and Ca2+-activated K+ currents. We show experimentally using intracellular recordings that burstiness in low [Ca2+]o persists even after truncating the apical dendrites, suggesting that bursts are generated by an interplay of membrane currents at or near the soma. To study the mechanisms of bursting, we have constructed a conductance-based, one-compartment model of CA1 pyramidal neurons. In this neuron model, reduced [Ca2+]o is simulated by negatively shifting the activation curve of the persistent Na+ current (INaP), as indicated by recent experimental results. The neuron model accounts, with different parameter sets, for the diversity of firing patterns observed experimentally in both zero and normal [Ca2+]o. Increasing INaP in the neuron model induces bursting and increases the number of spikes within a burst, but is neither necessary nor sufficient for bursting. We show, using fast-slow analysis and bifurcation theory, that the M-type K+ current (IM) allows bursting by shifting neuronal behavior between a silent and a tonically-active state, provided the kinetics of the spike generating currents are sufficiently, though not extremely, fast. We suggest that bursting in CA1 pyramidal cells can be explained by a single compartment "square bursting" mechanism with one slow variable, the activation of IM.
This article has been cited by other articles:
|
|
 |
|
  S. Maljevic, T. V. Wuttke, and H. Lerche Nervous system KV7 disorders: breakdown of a subthreshold brake J. Physiol., April 1, 2008; 586(7): 1791 - 1801. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Chen and Y. Yaari Spike Ca2+ influx upmodulates the spike afterdepolarization and bursting via intracellular inhibition of KV7/M channels J. Physiol., March 1, 2008; 586(5): 1351 - 1363. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. V. Wuttke, J. Penzien, M. Fauler, G. Seebohm, F. Lehmann-Horn, H. Lerche, and K. Jurkat-Rott Neutralization of a negative charge in the S1 S2 region of the KV7.2 (KCNQ2) channel affects voltage-dependent activation in neonatal epilepsy J. Physiol., January 15, 2008; 586(2): 545 - 555. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. E. Metz, N. Spruston, and M. Martina Dendritic D-type potassium currents inhibit the spike afterdepolarization in rat hippocampal CA1 pyramidal neurons J. Physiol., May 15, 2007; 581(1): 175 - 187. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Yaari, C. Yue, and H. Su Recruitment of apical dendritic T-type Ca2+ channels by backpropagating spikes underlies de novo intrinsic bursting in hippocampal epileptogenesis J. Physiol., April 15, 2007; 580(2): 435 - 450. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
