Latitude and longitude vertical disparities by Read JCA, Phillipson GP, Glennerster A , ReadPhillipsonGlennerster09.pdf (5.2 MiB) - At around this time I'd been spending a lot of time thinking about vertical disparity, and had been awarded an MRC grant to study it. To begin with, I wasn't even entirely clear what vertical disparity was, and I had difficulty following some of the other papers on it. I realised that a lot of the confusion was occurring because there are actually several different definitions of "vertical disparity" in the literature -- I've identified at least four -- and to make matters worse, different papers aren't always clear about exactly which definition they have in mind. Unsurprisingly, this has caused a lot of confusion about what the properties of vertical disparity actually are. Part of the problem, I think, is that under some circumstances you obtain the same results regardless of whether you define the elevation coordinate as a latitude or a longitude on the retina, and this may have given the impression that it doesn't ever matter -- whereas in fact, under some circumstances, the two definitions give completely different results. So with my PhD student Graeme Phillipson and my old friend and colleague from back in Oxford, Andrew Glennerster, we decided to write a paper really getting into the nitty-gritty of vertical disparity, and laying out clearly what properties follow from different definitions. It may not be the most exciting paper ever, and like many of my papers, it has masses of Appendices filled with equations. But we hoped it would be a useful reference for anyone interested in vertical disparity -- and I did at least try hard to make the pictures pretty.
Extracellular calcium regulates postsynaptic efficacy through group 1 metabotropic glutamate receptors. by Hardingham NR, Bannister NJ, Read JCA, Fox KD, Hardingham GE, Jack JJB , HardinghamEA06.pdf (0.7 MiB) - This project began when I was in my first neuroscience post-doc, doing a Wellcome Training Fellowship in Mathematical Biology with Julian Jack in Oxford. Julian's lab had done a lot of work on synaptic physiology, in particular developing quantal analysis as a tool to examine central synapses. The physiology underlying quantal analysis is the fact that neurons are generally connected by more than one terminal. When the presynaptic neuron fires an action potential, packets - quanta - of neurotransmitter may be released from all, some or none of these terminals. If each packet of neurotransmitter contributes a similar amount to the postsynaptic depolarisation, then a histogram of the effect produced by each presynaptic action potential will have several peaks, corresponding to the release of 0, 1, 2 ... quanta of neurotransmitter. In principle, this histogram can then be analysed to estimate the effect caused by each quantum, and the probability that a quantum will be released from a terminal given an action potential. In practice, this depends critically on things like whether each quantum really does have a very similar postsynaptic effect, whether the release probability is the same at all terminals, whether these quantities are constant over time and so on. Julian's lab had already developed a lot of sophisticated tools for quantal analysis, and I took this further, developing a still more elaborate fitting algorithm to extract the quantal parameters, and also a battery of statistical tests to decide whether the resulting model of the synapse was adequate. There's quite a lot of sceptism as to how far quantal analysis can be trusted in the central nervous system (as opposed to at the neuromuscular junction, where it was originally developed), so these tests were critical in convincing people that our results were reliable. Neil Hardingham, the first author, who was a Ph.D. student and post-doc in Julian's lab when I was there, used these techniques to examine how the quantal parameters change as a function of extracellular calcium. He was able to show that calcium depletion, as well as reducing release probability, also reduces quantal size. Since calcium levels drop as neurons become active, this represents a novel mechanism for regulating information transfer between neurons.
All Pulfrich-like illusions can be explained without joint encoding of motion and disparity. by Read JCA, Cumming BG , ReadCumming05c.pdf (2.8 MiB) - The final step was to build a neuronal model, and show that it experienced the illusion. We modelled a neuronal population constructed of neurons which either encoded motion, or depth (not both), and showed that a very simple way of "reading out" this activity, so as to convert it to a perception of depth, would be subject to the Pulfrich illusion. We also examined other evidence which had been put forward in support of the joint motion/depth idea, such as the illusion of swirling motion which occurs in dynamic noise with an interocular delay. We found that this, too, could be experienced by a brain which encoded motion and depth entirely separately. So, while there certainly are primate neurons which jointly encode motion and depth (notably in MT), there is no reason to suppose that these play a privileged role in supporting the Pulfrich effect and related illusions.
This series of three papers (Read & Cumming 2005abc) has recently attracted some criticism from Ning Qian and Ralph Freeman, in a paper entitled "Pulfrich phenomena are coded effectively by a joint motion-disparity process" (J Vis, 9(5): 1-16). My take on it is that we are all basically in agreement, but the situation is obscured by the lack of a clear agreed definition of "joint" vs "separate" encoding of motion and disparity. For example, we said that to be called a motion detector, a cell not only had to be tuned to speed, it also had to respond differently to opposite directions of motion, whereas Qian & Freeman required only speed tuning. I want to clear up one other point. Qian & Freeman say that our model is "non-causal", apparently because it responds to the disparity between a stimulus in one eye and a stimulus which arrives in the other eye at a later time. At the time that stimulus 1 occurs, stimulus 2 is still in the future. However, at the time the neuron responds to the disparity between the two stimuli, both stimuli have already occurred. Thus, the model is firmly causal. Indeed, our derivation of its properties explicitly sets the temporal kernel to zero for future times.
Stability of power-law discs II. The global spiral modes. by Evans NW, Read JCA, EvansRead97b.pdf (1.1 MiB) - This paper contains the results of our analysis.
