I have noticed an increased in the asymmetrical synaptic excitatory junctions to be increased in the diabetic brain but could not find any discussion of this in the literature at present. If you have any information or publications regarding this question please share with me when you have the time.
My hypothesis is that in younger diabetic brains this increase in asymmetrical synaptic excitatory junctions may result in an overuse phenomenon and result in a later or older models in their attentuation and or loss as in accelerated aging in the diabetic brain. Thank you for your time and consideration.
Sincerely,
M.R. (Pete) Hayden, MD
Dear Melvin, I hope that the article on the mechanisms of action of glucose in the brain will help you understand the problem of asymmetrical synaptic excitatory junctions.
Is this Streptozotocin induced diabetes? There are a number of papers discussing the effects of insulin and STZ on excitatory synaptic transmission and synapses, particularly in the hippocampus (and some in the cortex). One example is Martinez-Tellez et al (2005) Alteration in dendritic morphology of cortical neurons in rats with diabetes mellitus induced by streptozotocin. Brain research v 1048 p108. But there are a number of others as well.
Hi Melvin, we have a study on how high fat food influences synaptic plasticity in the VTA (see Liu S et al, 2016, PNAS, PMID: 26884159). In the last figure (fig 7 E), we have shown that STZ treated mice have increased excitatory transmission on to VTA DA neurons after high fat food treatment.
Yes, my current observations were in a Streptozotocin induced diabetic model (location in the mid brain were affected as compared to the cerebellum, which was not) but was relatively young when sacrificed. So I am considering these observations as possible early changes and possibly adaptive in nature. I wish to thank both Aaron G Roseberry and Shuai Liu for their kind answers and their references and I may have more questions for each of them after reading their suggestions and papers in Brain Research and PNAS Journals. This will be really helpful for me to better understand these early observational findings so that we may be able to better study these results in future experiments and papers and even possibly go back and look at this specific model in the coming months as I thing these observations may turn out to be important.
M.R. Hayden
Dr. S. Liu,
Your answer was very much appreciated and I have learned a great deal due to your paper in PNAS. I am going to be studying the db/db K strain model in the coming months, while I will be focusing my TEM studies of this model primarily on the neurovascular unit I will also be evaluating the dysmorphic myelin white matter and due to the better understancing of you PNAS paper I will be keeping a close observation regarding the assymettrical excitatory snapses as well. You paper really helped and I am so thankful for your earlier response to my questions regarding an observation of increased excitatory synapses in the type 1 model and now will be alert to observe similar changes in the obese T2DM of obesity insulin resistance hyperinsulinemia and persisitent elevation of glucose levels well above the diabetic range for mice - approximately 300-400 ranges.
Sincerely ,
M.R.(Pete) Hayden MD
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