Bursting Activity in Weakly Electric Fish - Computational Neuroscience: A Comprehensive Approach - page 230

ent and feedback input may also shape the bursts and contribute to their termination.
Furthermore, the basilar dendrites of E-units warrant closer investigation since they
have been shown to be equipped with Na + channels as well as Apt Kv3.3 K + chan-
nels, and might thus also support backpropagation and bursting in a way similar to
the apical dendrite [96, 97, 125] (see also [100] for similar conclusions in neocortical
pyramidal neurons).

8.5.2 Multicompartmental model of pyramidal cell bursts

Based on the detailed spatial reconstruction of a dye-filled E-type pyramidal cell
[17], Doiron et al. [33, 34] developed a multicompartmental model that successfully
reproduces burst firing as it is observed in vitro ( Figure 8.9 ). The main goal of these
studies was to identify the components of the burst mechanism that underlie dendritic
spike broadening and somatic DAP potentiation since those are responsible for the
progressive decrease in ISI duration and eventual burst termination. A key feature of
the model was the presence of fast Na + and K + currents in both somatic and dendritic
compartments, to account for Na + action potential generation and backpropagation
( Figure 8.10a ). In order to achieve the narrow somatic and broader dendritic spike
shapes (see 5.5.1), the time constants of the active conductances in the dendrite had
to be increased relative to the soma. This also yielded a relatively longer refractory
period for the dendritic spike compared to the somatic one.
While the core model outlined above reproduced key features of the somatic and
dendritic response, it failed to generate spike bursts. Doiron et al. [33] were able to
exclude a number of potential burst mechanisms described for other systems: Ca 2 + -
or voltage-dependent slowly activating K + channels, slow inactivation of the den-
dritic Na + channel, and slow activation of the persistent Na + current. Finally, modi-
fication of the dendritic delayed rectifier channel yielded burst properties correspond-
ing to the in vitro findings: A low-threshold slow inactivation of the K + conductance
led to dendritic spike broadening in the course of a burst and to a corresponding
increase in the DAP amplitude, which eventually triggered a doublet, leading to den-
dritic spike failure and burst termination due to the AHP. Whereas slow activation of
the persistent Na + current proved insufficient to elicit proper bursting, it was recently
shown to be an important component of the DAP potentiation [34]. It is activated by
the broadening of dendritic spikes and boosts the sub-threshold depolarization of the
somatic membrane. Thereby it largely determines the time it takes to reach threshold
for doublet firing. Since the doublet terminates the burst, the persistent Na + current
thus controls burst duration. With the interburst period being largely fixed by the
duration of the AHP, the persistent Na + current also determines burst oscillation pe-
riod [34]. Since it can be activated by descending feedback to the apical dendrites
[15, 17], this provides a potential mechanism for controlling burst firing depending
on behavioral context.
To summarize, the key features of the pyramidal cell burst mechanism are i) a
dendritic Na + conductance that supports active backpropagation of spikes into the
dendrite and that feeds the somatic DAP, ii) a slow cumulative inactivation of a de-
layed rectifier current which leads to dendritic spike broadening in the course of a