***Disclaimer: None of the science here is mine and credit is given where due. These summaries are my understanding of what I listened to.
I made dense plans yesterday – visit all the posters in my sub-theme of interest: Basal Ganglia physiology, attend the Presidential lecture and a networking session. I would say that I thought having a more organized itinerary compared to last year would leave me less exhausted. I couldn’t have been more wrong. I was not overwhelmed which was a big progress from last year, however, after almost 2.5 hours of talking science and listening to science, I think I had reached my standing-absorption ceiling (your limit to absorb new material while standing – yes, I just invented a term and gave it a definition). Overall, I would say it was a great first day – brilliant science, motivated scientists and schmoozing networkers. I loved it.
My favorite poster of the day had to be:
Excitatory input onto midbrain dopaminergic neurons: nucleus-specific influence on long-term synaptic change.
J.L. Bland, C.A. Paladini; Department of Biology, UTSA, San Antonio, Texas, U.S.A.
The author investigated the influence of excitatory inputs on the dopaminergic neurons of the substantia nigra compacta by using both traditional electrical stimulation and optogenetic stimulation. The two major nuclei that give excitatory inputs into the Compacta are the subthalamic nucleus (STN) and the Pedunclopontine nucleus (PPN). Being that they both provide excitatory input, it is expected that their stimulation would elicit burst firing either individually or together. Interestingly, she found that using either of the methods, stimulation either via the STN or PPN alone, did not elicit burst firing in the compacta neurons, but dual stimulation did. Using an LTP protocol, she found that the AMPA currents from the PPN were consistently low compared to the NMDA currents, which was not the case in the STN. There were large AMPA currents (calcium-permeable) from the stimulation of the STN, and these were GluR2 lacking. She proved this by the use of a blocker and a voltage step I-V curve that showed an inward rectification of the current. In addition to that, synaptic facilitation was observed from the STN, whereas depression was observed from the PPN. From this work so far, she has shown that despite the co-stimulation of these two structures causing burst firing in the compacta neurons, there are different mechanisms that underlie their of action.
In sum, I saw this work through the lenses of “different means lead to the same end”. On the one hand, while stimulation of either set of afferents doesn’t led to bursting in the compacta, co-stimulation does. One would think that they would use the same mechanistic method to elicit the end result. The novelty of her work is that this isn’t the case.
It was my favorite because I had to give her props for the finding, not only is it novel and unexpected, but it involves the PPN, a structure with which there is a slight relative deficit in knowledge of it’s excitability properties compared to say the compacta and reticulata neurons of the substantia nigra. In addition to that, in my opinion, I think that the large influx of calcium into the compacta that occurs via the STN sheds more light on the possible routes of mechanistic failure that can occur leading up to the death of compacta neurons in Parkinson’s disease. A large influx of calcium is believed to be the culprit in this case. While L-type gated calcium channels are implicated in the just mentioned case, it is possible other sources of calcium could contribute just as well.
Overall, I definitely got some synapses potentiated. Great presentation skills from the author too!
And now I am off to schmooze some more with fellow neuroscientists and attend the best mini-symposium ever – 🙂
Come back later for Day 2’s favorite of the day!