That's funny. Eyelid conditioning is a well-known example of classical conditioning which is supposed to rely on the cerebellum. But the cerebellum isn't an associative learning machine-- it is an error learning machine! And yet classical conditioning is supposedly associative. This is confusing.

Ants moving by stepping a given number of times, each step in a given direction. An accumulator neuron could keep track of the number of steps taken and estimate the displacement of the ant. Perhaps this same line of thinking could also account for direction but I can't see how at the moment. Accumulator neurons have a memory of events, but are not necessarily associative.

4 cameras, 3 computer solution

If purkinje cells project directly to the LC, then they could signal errors to the LC. Perhaps these PN error signals oppose reward signals in the LC.

This would be one way to sort cell types by metabolic cost, if a balance sheet of ATP made and spent were available. The cell that spends the most ATP is the most metabolically costly.

If ChR2 learning is a process of dumb error correction, what kind of error is it correcting? Naively, it would be a movement in the direction opposite of the ChR2-evoked movement. So that the learned movement would counteract the cued, ChR2-evoked destabilization.

Could motor cortex remap over this time?

Where is the motor cortex?

Anybody else reading this?

Since purkinje cells use so much ATP, they could be particularly sensitive to the health of their mitochondria. So Purkinje Neurons might be particularly susceptible to mitochondrial disease.

The behavioral measure for mice and rabbits was a conditioned suppression task where a tone of a given frequency was paired with a shock that was incompatible with water-drinking. Once the animal associated shock with a given frequency, the loudness threshold for that frequency was determined through trial and error.

I had to find other references for this phenomenon. The wikipedia page on Einstein's equivalency principle was helpful. As was this pdf with merfeld and zupan Until there is information from other sensory systems, fluid movement in otolith organs cannot disambiguate between a head tilt or a head acceleration.

Do rates for spontaneous blinking change with classical eyelid conditioning? For example, Mauk's studies of rabbit eyeblink require a 250 msec blink-free period before a conditioned stimulus presentation. Are these blink-free periods more abundant with training, less abundant, or about the same? As noted by Chettih, studies using airpuff as the unconditioned stimulus involve a mixture of classical/operant conditioning. Both spontaneous blinking and eyelid closure prevents the airpuff from impinging the cornea, albeit at different time scales. Given that the animal learns to use the CS to block the airpuff, it may also learn to increase its rate of spontaneous blinking to prevent trial onset.

This is similar to a proposed mechanism for extinction of classically conditioned eyelid responses: inhibitory inputs to the inferior olive encode an expectation of the unconditioned stimulus.

This LC sub-population could project downward to spinal cord.

Could this non-specific labeling account for the putative Purkinje neuron inputs?