Meridian Watters Posted September 19, 2014 Share Posted September 19, 2014 Dear Associates,The webinar today will be from 10:00am -12:00 pm CDT for Queretaro, Mexico (11:00am-1:00pm EDT for Washington, DC). Remember to plan accordingly based on your time zone. You can access the webinar here and click on Neurobiologia LATP.If you have any questions you would like the organizer to address during the webinar, please reply to this post (click on "Reply to eGroup" on the right hand side) and Gina will choose a few to answer at the end. If we do not get to a question you asked during the webinar, NeurOnLine is the perfect place to start a new thread and see what your peers and other faculty members can contribute to your thought or question. Please email me (mwatters@sfn.org) during the webinar with any issues that may arise.Best, Meridian Link to comment Share on other sites More sharing options...
acarvajalg Posted September 19, 2014 Share Posted September 19, 2014 Hi very interesting paper. I do have a few questions? -Could any of the effects of epinephrine in memory due to the increase in the oxygen concentrations after the increase in cardiac output? -Is there any evidence that individuals with intolerance to glucose who had moderate increased levels of glucose have a better cognitive performance? -What happens if you inject an enhancing dose of glucose to rats but previously you have blocked the acetylcholine receptors? Many thanks Link to comment Share on other sites More sharing options...
Meridian Watters Posted September 19, 2014 Author Share Posted September 19, 2014 Hi Alexander, Thank you for submitting your questions. Are you watching the webinar live now? http://132.248.212.20/videos/video/434/?live=true There is a chat function available on the webinar for you to post your questions to Dr. Quirartes. If not, I will send your question to her. Meridian Link to comment Share on other sites More sharing options...
nanakutsi Posted September 19, 2014 Share Posted September 19, 2014 Hi Gina, I have a question If the astrocytes have a rol on the glucose uptake and the enhancement of memory, there IS a difference in the population of the astrocytes of the hippocampus or something different at the cellular level?? Link to comment Share on other sites More sharing options...
Mikal Nunez Posted September 19, 2014 Share Posted September 19, 2014 Hello, I have and question: What about the consumption of the artificial sweeteners effects on this dopaminergyc system involved on memory, the leptin has an important role because the homology with the insulin receptor? Link to comment Share on other sites More sharing options...
mbcanto Posted September 19, 2014 Share Posted September 19, 2014 Some of the questions of the webinar that I would like to further discussion are: If glucose enhance memory, what molecular factors are involved in the impairment of memory when the concentration of glucose is high? The contribution of Dopamine on the memory. In traumatic stress we have and increase response in adrenaline and noradrenaline, that could be related with traumatic memory in Postraumatic stress disorders?If the astrocytes have a rol on the glucose uptake and the enhancement of memory, there Is a difference in the population of the astrocytes of the hippocampus or something different at the cellular level?? Link to comment Share on other sites More sharing options...
eperez4 Posted October 18, 2014 Share Posted October 18, 2014 Hi. Thanks to the article reviewed in the second webinar I came to understand that signals from autonomous nervous system are important for the formation and consolidation of memory, especially those signals associated with the vagus verve. Unfortunately experiences can leave a trace so strong that approximately 30% of people who have a traumatic event develop posttraumatic stress disorder (PTSD) (Nemeroff et al., 2006). I see that is important to understand how to attenuate fearful responses through learning.Recently, Peña and col., published an article where they show that the extinction of conditioned fear is enhanced by pairing vagus nerve stimulation with a conditioned stimuli (CS) -a tone- that was previously associated with an unconditioned stimuli (UCS) -a footshock-. New learning about the context is taking place and the fearful behavior is diminished. They were able to quantify a reduction in the freezing time not only when the CS was presented, but also in the time between tones. An important question was about the neural substrate of this behavior and how it changes. Patients suffering from PTSD show reduced ventromedial prefrontal cortex activation and increased amygdala activation (Hayes et al 2012; Stevens et al 2013). This makes sense given that the prefrontal cortex is a brain area important for rational thinking and the amygdala is part of the limbic system associated with emotions. Therefore it seems that there is a loose of control over our emotional state.So Peña and col., perform in vivo stimulation of the infralimbic medial prefrontal cortex and recording of field potentials at the basolateral amygdala to study the interaction of these areas. The group that received vagus nerve stimulation displayed long-term potentiation in this pathway, unlike the other groups that did not received vagus nerve stimulation that showed long-term depression or not changes in plasticity at all. Thus, the changes in fearful behavior are associated with plasticity in the infralimbic-amygdala pathway.The authors propose that a synergistic action of several neuromodulators like acetylcholine, serotonin and norepinephrine are important in the mechanism by which the vagus nerve modifies the plasticity in the above mentioned pathway. My view is that although changes in glucose levels are not proposed as a piece of this plastic picture, it is a variable to take into account, as changes in glucose levels are important for brain functioning. Another issue to be addressed is the identification of cellular types and brain nucleus that mediate the actions of vagus nerve in plasticity. Peña DF, Childs JE, Willett S, Vital A, McIntyre CK, Kroener S. Vagus nerve stimulation enhances extinction of conditioned fear and modulates plasticity in the pathway from the ventromedial prefrontal cortex to the amygdala. Front Behav Neurosci. 2014 Sep 18;8:327. PMID: 25278857http://journal.frontiersin.org/Journal/10.3389/fnbeh.2014.00327/abstract Hayes, J. P., Hayes, S. M., and Mikedis, A. M. (2012). Quantitative meta-analysis of neural activity in posttraumatic stress disorder. Biol. Mood Anxiety Disord. 2:9. doi: 10.1186/2045-5380-2-9Nemeroff, C. B., Bremner, J. D., Foa, E. B., Mayberg, H. S., North, C. S., and Stein, M. B. (2006). Posttraumatic stress disorder: a state-of-the-science review. J. Psychiatr. Res. 40, 1-21. doi: 10.1016/j.jpsychires.2005.07.005Stevens, J. S., Jovanovic, T., Fani, N., Ely, T. D., Glover, E. M., Bradley, B., et al. (2013). Disrupted amygdala-prefrontal functional connectivity in civilian women with posttraumatic stress disorder. J. Psychiatr. Res. 47, 1469-1478. doi: 10.1016/j.jpsychires.2013.05.031 Link to comment Share on other sites More sharing options...
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