In December I submitted my first year dissertation, and last week I faced a viva on this dissertation. Opinions from colleagues and supervisors varied as to whether or not this was really an exam, and how much I should relax about it. Naturally (me being me) I did not relax about it. One feature I knew that this viva (exam or not) shared with real exams was that failure was a possibility, and that failure had consequences.
So this mattered.
I was lucky enough to be able to invite two scientists I like and get on with to examine me. But still - people can show a whole new side of their personality in this kind of role. And I hate the idea of making a fool of myself in front of people I respect. So I was tense for at least a week beforehand, and preparing diligently.
In the event, the whole thing was very amiable - enjoyable even. Defending my dissertation was a pretty minor part of it. Most of our time was spent chewing over the implications of different technical choices as I go forward with my project. Chemical LTP or glutamate uncaging? Organotypic or acute slices?
And I passed. And got some pretty nice feedback. So I can go on....
Monday 24 January 2011
Tuesday 11 January 2011
Journal club fun
McGuiness et al, "Presynaptic NMDARs in the Hippocampus Facilitate Transmitter Release at Theta Frequency", Neuron 68, 1109–1127, December 22, 2010
I go to two journal clubs, one nice the other nasty. Today was the nasty one, where we looked at the above article. It was the usual pattern - a paper that I thought was quite impressive, turned out to have feet of clay when subjected to the withering scrutiny of the assembled critical intelligences.
In this study, they used Ca-sensitive dyes to image Ca-transients in presynaptic boutons of the CA3-CA1 pathway, in response to action potentials. They claim that the distribution of Ca-transient amplitudes is bimodal. Various drug manipulations, including the use of norketamine to block (internally) only presynaptic NMDARs, demonstrate that the less frequent, large transients are dependent on presynaptic NMDARs. Trouble is, after fig 1 they don’t show us the data – just their opaque Bayesian analysis. And what is worse, they use the same control data in most of their figures.
I go to two journal clubs, one nice the other nasty. Today was the nasty one, where we looked at the above article. It was the usual pattern - a paper that I thought was quite impressive, turned out to have feet of clay when subjected to the withering scrutiny of the assembled critical intelligences.
In this study, they used Ca-sensitive dyes to image Ca-transients in presynaptic boutons of the CA3-CA1 pathway, in response to action potentials. They claim that the distribution of Ca-transient amplitudes is bimodal. Various drug manipulations, including the use of norketamine to block (internally) only presynaptic NMDARs, demonstrate that the less frequent, large transients are dependent on presynaptic NMDARs. Trouble is, after fig 1 they don’t show us the data – just their opaque Bayesian analysis. And what is worse, they use the same control data in most of their figures.
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