PMID- 11600618
OWN - NLM
STAT- MEDLINE
DCOM- 20011204
LR  - 20171213
IS  - 0022-3077 (Print)
IS  - 0022-3077 (Linking)
VI  - 86
IP  - 4
DP  - 2001 Oct
TI  - Model of gamma frequency burst discharge generated by conditional 
      backpropagation.
PG  - 1523-45
AB  - Pyramidal cells of the electrosensory lateral line lobe (ELL) of the weakly 
      electric fish Apteronotus leptorhynchus have been shown to produce oscillatory 
      burst discharge in the gamma-frequency range (20-80 Hz) in response to constant 
      depolarizing stimuli. Previous in vitro studies have shown that these bursts 
      arise through a recurring spike backpropagation from soma to apical dendrites 
      that is conditional on the frequency of action potential discharge ("conditional 
      backpropagation"). Spike bursts are characterized by a progressive decrease in 
      inter-spike intervals (ISIs), and an increase of dendritic spike duration and the 
      amplitude of a somatic depolarizing afterpotential (DAP). The bursts are 
      terminated when a high-frequency somatic spike doublet exceeds the dendritic 
      spike refractory period, preventing spike backpropagation. We present a detailed 
      multi-compartmental model of an ELL basilar pyramidal cell to simulate somatic 
      and dendritic spike discharge and test the conditions necessary to produce a 
      burst output. The model ionic channels are described by modified Hodgkin-Huxley 
      equations and distributed over both soma and dendrites under the constraint of 
      available immunocytochemical and electrophysiological data. The currents modeled 
      are somatic and dendritic sodium and potassium involved in action potential 
      generation, somatic and proximal apical dendritic persistent sodium, and K(V)3.3 
      and fast transient A-like potassium channels distributed over the entire model 
      cell. The core model produces realistic somatic and dendritic spikes, 
      differential spike refractory periods, and a somatic DAP. However, the core model 
      does not produce oscillatory spike bursts with constant depolarizing stimuli. We 
      find that a cumulative inactivation of potassium channels underlying dendritic 
      spike repolarization is a necessary condition for the model to produce a 
      sustained gamma-frequency burst pattern matching experimental results. This 
      cumulative inactivation accounts for a frequency-dependent broadening of 
      dendritic spikes and results in a conditional failure of backpropagation when the 
      intraburst ISI exceeds dendritic spike refractory period, terminating the burst. 
      These findings implicate ion channels involved in repolarizing dendritic spikes 
      as being central to the process of conditional backpropagation and oscillatory 
      burst discharge in this principal sensory output neuron of the ELL.
FAU - Doiron, B
AU  - Doiron B
AD  - Physics Department, University of Ottawa, Ottawa, Ontario K1N 6N5, Canada. 
      bdoiron@science.uottawa.ca
FAU - Longtin, A
AU  - Longtin A
FAU - Turner, R W
AU  - Turner RW
FAU - Maler, L
AU  - Maler L
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurophysiol
JT  - Journal of neurophysiology
JID - 0375404
RN  - 0 (Potassium Channels, Voltage-Gated)
RN  - 0 (Sodium Channels)
RN  - 9NEZ333N27 (Sodium)
RN  - RWP5GA015D (Potassium)
SB  - IM
MH  - Action Potentials/physiology
MH  - Animals
MH  - Dendrites/physiology
MH  - Electric Fish
MH  - Excitatory Postsynaptic Potentials/physiology
MH  - Ion Channel Gating/physiology
MH  - Mechanoreceptors/cytology/*physiology
MH  - *Models, Neurological
MH  - Neurons, Afferent/physiology/ultrastructure
MH  - *Periodicity
MH  - Potassium/metabolism
MH  - Potassium Channels, Voltage-Gated/physiology
MH  - Pyramidal Cells/*physiology/ultrastructure
MH  - Reaction Time/physiology
MH  - Sodium/metabolism
MH  - Sodium Channels/physiology
EDAT- 2001/10/16 10:00
MHDA- 2002/01/05 10:01
CRDT- 2001/10/16 10:00
PHST- 2001/10/16 10:00 [pubmed]
PHST- 2002/01/05 10:01 [medline]
PHST- 2001/10/16 10:00 [entrez]
AID - 10.1152/jn.2001.86.4.1523 [doi]
PST - ppublish
SO  - J Neurophysiol. 2001 Oct;86(4):1523-45. doi: 10.1152/jn.2001.86.4.1523.