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Learning theories reveal loss of pancreatic electrical connectivity in diabetes as an adaptive response
Cells of almost all solid tissues are connected with gap junctions which
permit the direct transfer of ions and small molecules, integral to regulating
coordinated function in the tissue. The pancreatic islets of Langerhans are
responsible for secreting the hormone insulin in response to glucose
stimulation. Gap junctions are the only electrical contacts between the
beta-cells in the tissue of these excitable islets. It is generally believed
that they are responsible for synchrony of the membrane voltage oscillations
among beta-cells, and thereby pulsatility of insulin secretion. Most attempts
to understand connectivity in islets are often interpreted, bottom-up, in terms
of measurements of gap junctional conductance. This does not, however explain
systematic changes, such as a diminished junctional conductance in type 2
diabetes. We attempt to address this deficit via the model presented here,
which is a learning theory of gap junctional adaptation derived with analogy to
neural systems. Here, gap junctions are modelled as bonds in a beta-cell
network, that are altered according to homeostatic rules of plasticity. Our
analysis reveals that it is nearly impossible to view gap junctions as
homogeneous across a tissue. A modified view that accommodates heterogeneity of
junction strengths in the islet can explain why, for example, a loss of gap
junction conductance in diabetes is necessary for an increase in plasma insulin
levels following hyperglycemia.Comment: 15 pages, 5 figures. To appear in PLoS One (2013
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