Many have attributed the unconscious processing of sensory events to the cerebellum (Bosco and Poppele 2001; Eccles et al.1967; Gelfan and Carter 1967; Doty 1969; Tononi et al. 2008ab). For a visual signal to arrive at the cerebellum it takes over 30 ms. During this time, an entire saccadic eye movement can be completed (Schiller and Tehovnik 2015). So that the cerebellum affects a saccadic eye movement in mid-flight, a feedback signal must arrive at well under 30 ms. The fastest sense on record for this is the proprioceptive sense (Fadiga and Pupilli 1964; Fuchs and Kornhuber 1969; Schubert and Minor 2004; Snider, Stowell 1944; but the vestibular latency is comparable, Shinoda and Yoshima 1975). It has been found that neurons in vermal lobules V-VII, the oculomotor lobule (Noda and Fujikado 1987ab, see Fig. 1), respond to a stretch of an ocular muscle at latencies as short as 4 ms (in cats which have a nervous system as fast as the primate nervous system, Fuchs and Kornhuber 1969), with similar latencies for neurons situated about the fastigial nucleus. The response was abolished by cutting the sensory nerve, whose proprioceptors innervate the trigeminal nucleus (Sivanandasigham 1978). Electrical stimulation of the visual cortex or the frontal eye fields of a monkey evoke neural responses in the oculomotor lobule (Snider and Eldred 1952). And if one electrically stimulates the cerebellum (at the fastigial nucleus) or stimulates the ocular proprioceptors that the eyes during a memory or visually-guided saccades, respectively, never acquire the target (Chen 2019; Noda et al. 1991), suggesting that both the cerebellum and ocular proprioceptors are within the feedback loop for altering the efference-copy code (Chen 2019; Noda et al. 1991; Chen Roll and Roll 1987; Roll et al. 1991; Valey et al. 1994, 1995, 1997).
Thus, the cerebellum is centrally involved in modifying the efference-copy code for oculomotor as well as skeletomotor control (Bell et al. 1997; De Zeeuw 2021; Loyola et al. 2019; Shadmehr 2020; Tehovnik et al. 2021; Wang et al. 2023), even though many 'efference-copy' studies have excluded the role of the cerebellum in this regard(e.g., Duhamel et al. 1992; Goldberg and Bruce 1990; Rao et al. 2016; Sommer and Wurtz 2004, 2006). Indeed, it was proposed as early as 1980 by Fred Miles that the cerebellum receives an efference-copy signal when volitional commands are issued from the neocortex (Miles et al. 1980b), which is then compared to the sensory feedback record for any efference-copy updates.
Figure 1: Locations in the cerebellar vermis of the cat within which short latency responses could be evoked by activation of the ocular proprioceptors of the cat. From figure 2 of Fuchs and Kornhuber (1969).
What was the question? I am not sure what you are trying to suggest. Are you merely making a statement or are you asking a question?
Are you saying the cerebellum is unlikely involved in the feedback in VOR? Or is it not involved in sending the efferent copy?
If not, what are you proposing? What is your alternate hypothesis that proves them wrong?
It seems you are addressing the negative findings as evidence but what are the positive findings?
If you are making a statement, what are you asking then?
What is an alternative to the original hypothesis if they are wrong? What is right about the cerebellum?
All these experimental conclusions are based on isolated stimulation (or ablation) of a specific pathway. But that doesn't even address the other pathways that may be involved and/or addressing the network properties rather than the isolated single neuron's contribution.
The operation of any part of the brain does not depend on the properties of a single neuron or a single pathway, rather it is the network that contributes to the processing.
Anyway, it does not contribute to the understanding of the processing function of a subgroup of neurons by looking at the isolated responses from stimulation (or ablation), those are artificial stimuli for the convenience of the experimenters, not necessarily how the neural network operates in its natural state for processing signals.
Essentially, the question is out of context for the neurons when they are stimulated using artificial signals.
Simply put, the network is processing a spike train of signals from inputs to outputs. It is the sequence of spike timing patterns that encodes the signals. When you stimulate them artificially with bursts, the bursts are meaningless and out of context because they encode nothing.
When you use latency timing by stimulating them, you are stimulating not just one neuron, all neurons in the surroundings, may or may not be involved in the processing of the signals downstream. More specifically, it could also stimulate the inhibitory neurons, which would result in suppressing the signals, rather than activating the signals downstream, especially when there is a surround-inhibition.
It is like whacking the brain with a baseball bat to see a response to prove how it works. That is out of context and proves nothing. That is not how the neural circuitries work. That is not how to figure out what the network processes unless it is processing the natural signals (in context).
In sum, most of the outdated experimental approaches were electrically stimulating or lesioning a brain structure to deduce its physiological functions. However, these approaches have significant issues and caveats in their conclusions for several reasons:
(1) The electrical stimulation is not confined to activating the target structure but all other neural pathways surrounding it.
(2) The stimulation was too often assumed to activate excitatory neurons but failed to acknowledge it can activate inhibitory neurons which can suppress the pathway instead of activating the pathway.
(3) The use of timing latency of stimulation as a measure of signal conduction speed from point A to point B cannot be used as the absolute timing of natural signals from A to B if the electrical stimulation activated inhibitory pathways that suppress the signal from A to B or slow them down.
(4) Since the stimulation can activate other neural pathways than the intended one, the conclusion would be erroneously attributing to the intended pathways.
(5) If the electrical stimulation activates other neural pathways, they may contribute feedback to alter the signals of the original pathways, leading to erroneous conclusions.
(6) The electrical stimuli are usually large electrical current pulses that are unnatural (i.e., non-physiological action potentials or spike trains) signals that disrupt the natural physiological processing of signals downstream, i.e., it cannot be assumed that is how natural action potentials are processed or propagated downstream for processing.
(7) It cannot even be used to assume that the time delay of arrival is the conduction velocity of the axon being stimulated when it crosses multiple synapses. Each of these synaptic connections can also be altered by the firing of neighboring neurons when the original electrical stimulus is never confined to stimulate a single neuron.
(8) It is the cooperative network processing that provides the physiological function (such as efferent copy), it is never encoded by a single neuron to assume that is what the circuitry does, therefore, the timing latency of the electrical stimulation means nothing to the encoding of the signal by the network.
(9) The ablation (lesioning) experimental approach is well-known in neuroscience to produce erroneous and inclusive results using double-negative does not imply positive results because removing a component of a system does not imply that component is necessary for the operation.
(10) Using the example of a car, when you remove the fuel pump, the car won't go, so one may conclude that it is the fuel pump that drives the car. But the fact is it is the engine that drives the car, and, of course, when you remove the fuel pump, the engine won't work. Worse yet, when there are parallel circuits that do the work, removing one does not abort the function because there is another parallel circuitry that can compensate for it.
(11) The well-known age-old failed chronic pain treatment therapy by lesioning the pain pathway in the spinal cord is an example. After lesioning the pain pathway, the pain is gone, but after a while, the pain comes back because it finds an alternate pathway to transmit pain to the higher center. So what is the conclusion?
That's why nowadays no one does these stimulation or ablation experiments anymore because they prove nothing. Unless you record the natural signals used by the neurons (i.e., the spike trains during normal physiological operation) in a relevant cognitive or behavioral task to determine the functional operation of the circuit, none of those archaic experimental approaches will produce any meaningful results. Neural functions are never produced by a single neuron or a single spike response to stimulation in a snapshot at one instance in time. They are produced by the pattern of spike train firings in a group of neurons over time in relation to the firing of other groups of neurons. They are never done in isolation (or out of context).
I don't think you understand the encoder and decoder concept to understand how the brain works.
The signals generated by the encoder have to match with the decoder for it to work or communicate property. They are never done in isolation.
There is a simpler answer: "Electricity" IS (stands for) some thin/kin/g "moving in time" - whereas "grey brain substance" IS (stands for) some thin/kin/g "material" - that is "stable in time".
You need witch-craft to "solve - or dis-solute" this problem.
The neural encoding problem can be identified with any of the modern-day recording techniques (from using micro-electrode arrays to brain imaging) to record ongoing neural firing patterns over time in multiple brain structures simultaneously during an ongoing cognitive or behavioral task in animals and humans. That is the right way to prove how signals are processed in the brain naturally during physiologically appropriate conditions.
Otherwise, electrical stimulation is in many ways analogous to zapping the brain into a seizure and measuring the conduction latency time as proof of the function of the neural circuitry (in your case, proof of the efferent copy). That is absurd.
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