Exploring the pathways of manganese (Mn(2+)) transport in the nervous system becomes of interest as many recent studies use Mn(2+) as a neural tract tracer in mammals. In this study, we performed manganese enhanced MRI (MEMRI) at 17.2 T on the buccal ganglia of Aplysia californica. The main advantage of this model over mammalian systems is that it contains networks of large identified neurons. Using Mn(2+) retrograde transport along selected nerves, we first validated the mapping of motor neurons' axonal projections into peripheral nerves, previously obtained from optical imaging (Morton et al., 1991). This protocol was found not to alter the functional properties of the neuronal network. Second, we compared the Mn(2+) dynamics inside the ganglia in the presence or absence of chemical stimulation. We found that 2h of stimulation with the modulatory transmitter dopamine increased the extent of areas of intermediate signal enhancement caused by manganese accumulation. In the absence of dopamine, an overall decrease of the enhanced areas in favor of non-enhanced areas was found, as a result of natural Mn(2+) washout. This supports the hypothesis that, upon activation, Mn(2+) is released from labeled neurons and captured by other, initially unlabeled, neurons. However, the latter could not be clearly identified due to lack of sensitivity and multiplicity of possible pathways starting from labeled cells. Nonetheless, the Aplysia buccal ganglia remain a well-suited model for attempting to visualize Mn(2+) transport from neuron to neuron upon activation, as well as for studying dopaminergic modulation in a motor network.
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