||Acetyl-L-carnitine is known to improve many aspects of the neural activity even if its exact role in neurotransmission is
still unknown. This study investigates the effects of acetyl-L-carnitine in T segmental sensory neurons of the leech Hirudo
medicinalis. These neurons are involved in some forms of neural plasticity associated with learning processes.
Their physiological firing is accompanied by a large afterhyperpolarization that is mainly due to the Na+/K+ ATPase
activity and partially to a Ca2+-dependent K+ current. A clear-cut hyperpolarization and a significant increase of the
afterhyperpolarization have been recorded in T neurons of leeches injected with 2 mM acetyl-L-carnitine some days
before. Acute treatments of 50 mM acetyl-L-carnitine induced similar effects in T cells of naive animals.
Moreover, in these cells, widely arborized, the afterhyperpolarization seems to play an important role in determining
the action potential transmission at neuritic bifurcations.
A computational model of a T cell has been previously developed considering detailed data for geometry and the
modulation of the pump current. Herein, we showed that to a larger afterhyperpolarization, due to the
acetyl-L-carnitine-induced effects, corresponds a decrement in the number of action potentials
reaching synaptic terminals.
||Bursts of spikes in leech T cells produce an AHP, which results from activation of a Na+/K+ pump and
a Ca2+-dependent K+ current. Activity-dependent increases in the AHP are believed to induce conduction
block of spikes in several regions of the neuron, which in turn, may decrease presynaptic invasion of spikes and
thereby decrease transmitter release. To explore this possibility, we used the neurosimulator SNNAP to develop
a multi-compartmental model of the T cell. Each compartment was modeled as an equivalent electrical circuit,
in which some currents were regulated by intracellular Ca2+ and Na+. The membrane model consisted of
a membrane capacitance (Cm), for which we used the value 1 uF/cm2, in parallel with
two inward currents (Na+ and Ca2+), two K+ currents, a leak current and pump current.
The model incorporated empirical data that describe the geometry of the cell and activity-dependent changes of the
AHP (see paper for details).
Simulations indicated that at some branching points, activity-dependent increases of the AHP reduced the number
of spikes transmitted from the minor receptive field to the soma and beyond.
These results suggest that the AHP can regulate spike conduction within the presynaptic arborizations of the cell and
could in principle contribute to the synaptic depression that is correlated with increases in the AHP.