PLT Test Blog

Today’s post is really for the regular readers of this blog who are interested in the GABA switch and Bumetanide. It is not light reading.  We see how advanced some Taiwanese researchers are in their understanding of GABA A dysfunctions in Huntington’s Disease. Taipei 101, briefly the world’s tallest building It is an excellent paper and much of it is applicable to autism. There are some omissions, but you will struggle to find a more complete paper. They even go into the detail of altered the sub-unit expression of GABA A receptors that occurs as the disease progresses. I think that correcting sub-unit miss-expression has great potential in treating some autism. Huntington’s is an inherited brain disorder that first manifests itself around the age of 40 and then progresses for the next 15 to 20 years. Much autism is present prior to birth but there is a progression that occurs as the brain develops in early childhood. Some people do seem to be entirely typical at birth and only...

Japan, home to today’s complicated research Today’s post hopes to give a more complete picture of the various processes involved in shifting the immature neurons often found in autism towards the mature neurons, found in most people.   This stalled process is complex and may only apply to around half of all autism. The post assumes prior knowledge from previous posts about the GABA switch and the KCC2 and NKCC1 chloride cotransporters. The best graphic I found is below and includes almost everything. The paper itself is very thorough and I recommend the scientists among you read the paper rather than my post. What we want to understand is why neurons did not switch from immature to mature, in the process I am calling the “GABA switch”.   We know a great deal about what happens before and after the switch and many processes that can be   involved, but the exact switch itself remains undefined. In a previous post I highlighted that neuroligin 2 (NL2)/RORa may be the GABA sw...