SearcharxivSearch

arXiv subjects

Saeed Aljaberi

Publications and source records attributed to Saeed Aljaberi.

3 recordsLinked to original sources

Global and local synaptic regulation determine the stability of homeostatic plasticity

Neurons regulate the distribution of signaling components across an extended tree-like cellular structure using both local and global feedback control. This is hypothesized to allow homeostatic control of the electrical activity of a neuron and at the same time enable normalization of distribution of inputs received from other cells. The performance and robustness of these mechanisms are poorly understood, and are subject to nonlinearities, making their analysis difficult. Firstly, we formally show that global homeostasis of electrical activity and local activity-dependent degradation can coexist under sufficient timescale separation. The interplay of the two feedback mechanisms is also analyzed through simulations, which reveal a bidirectional effect (stabilizing and destabilizing) of activity-dependent degradation on the overall neuron performance.

nlin.AO

Dendritic trafficking: synaptic scaling and structural plasticity

Neuronal circuits internally regulate electrical signaling via a host of homeostatic mechanisms. Two prominent mechanisms, synaptic scaling and structural plasticity, are believed to maintain average activity within an operating range by modifying the strength and spatial extent of network connectivity using negative feedback. However, both mechanisms operate on relatively slow timescales and thus face fundamental limits due to delays. We show that these mechanisms fulfill complementary roles in maintaining stability in a large network. In particular, even relatively, slow growth dynamics improves performance significantly beyond synaptic scaling alone.

q-bio.NC

Qualitative behavior and robustness of dendritic trafficking

The paper studies homeostatic ion channel trafficking in neurons. We derive a nonlinear closed-loop model that captures active transport with degradation, channel insertion, average membrane potential activity, and integral control. We study the model via dominance theory and differential dissipativity to show when steady regulation gives way to pathological oscillations. We provide quantitative results on the robustness of the closed loop behavior to static and dynamic uncertainties, which allows us to understand how cell growth interacts with ion channel regulation.

q-bio.SC