One paper a day for a month. My plan is to post a summary of each paper, as well as any context I can provide, and any things I was confused about in the paper. Most importantly, I am going to list all the questions I thought of while reading the paper that WEREN'T addressed.
Summary: C. elegans neurons are mostly thought to lack action potentials due to a lack of voltage gated sodium channels, but some studies have found evidence of all-or-nothing signaling via calcium plateau potentials. Most previous electrophysiological papers have reported on a single neuron, including sensory neurons or interneurons, but none have studies motor neurons. Do C. elegans motor neurons communicate with muscles in digital or analog?
For cholinergic motor neurons (and I have no idea which neurons in particular they did this with, its probably in the methods but isnt clear in the main text) they show that the ratio of motorneuron inward current (driven by light stimulation in channelrhodopsin-expressing cholinergic motoneurons) to muscle inward current is constant. They are proportional. This is characteristic of graded transmission, but in the case of a spiking or nonlinear motor neuron, they would not be. This seemingly was only tested in cholinergic neurons and not GABAergic motoneurons.
They also surmise that there is nonzero synaptic transmission at the motoneuron's resting potential, and use halorhodopsin to hyperpolarize a cholinergic motoneuron. This reduces the apparent mini EJP (EPP? EPSP?) frequency in the muscle, suggesting there is tonic synaptic vesicle release, and that the tonic release rate is proportional to the membrane potential. This seemingly was only tested in acetylcholinergic neurons, again.
They next delved into plasticity at the neuromuscular junction. This is complicated by the fact that channelrhodopsin has its own dynamics, and rapidly but briefly inactivates when in light. After attempting to correct for channelrhodopsins own apparent depression, they find that cholinergic NMJs rapidly depress under high-frequency stimulation, whereas GABAergic neurons are first facilitated for less than half a second, then depressed. To determine the origin of the cholinergic depression, they start with looking at acetylcholine receptors. Worms have two types (nicotinic and levamisole), and mutants expressing only the levamisole type didn't
What I didn't understand:
I'm not clear why 5+ Hz muscle stimulation is relevant since the motor neurons don't seem to spike. From their experiments, I'm also still not clear whether and when DC (tonic) muscle stimulation would yield synaptic facilitation or depression.
Questions I should look into further:
As I understand it, GABA is inhibitory and acetylcholine is excitatory in C. elegans NMJs. Why do both drive positive current into the cell? Is this because the muscle was voltage clamped at a hyperpolarized state more negative than the reversal potential of the GABA-gated channel?