Fragile X Syndrome is the most common form of heritable cognitive disability. It is caused by a genetic mutation that leads to a lack of protein from the FMR1 gene. This protein (FMRP) is used to regulate the translation of many other proteins, thereby leading to a wide range of effects. Because the origin of this disease is based on the lack of a single protein, an animal model with construct validity can be used to investigate the potential effects leading to the symptoms of the disease.
Many studies have investigated the synaptic plasticity differences of CA1 pyramidal neurons between a mouse model of fragile X syndrome (KO) and a wild type mouse (WT). This study investigates the differences in firing properties of a CA1 pyramidal neuron between the KO and WT. Specifically, contributions of two ion channels are investigated: the Ca2+ and voltage activated potassium channel (BK) and the potassium channel (M) inhibited by the muscarinic acetylcholine receptor.
This study finds some differences that warrant further investigation, including differences in spike timing, spike width and the initial rate of rise of an action potential. However, several areas of investigation yield subtle or confounding results, which may indicate that the CA1 pyramidal neurons affected by the lack of FMRP may make up more than one population. / text
| Identifer | oai:union.ndltd.org:UTEXAS/oai:repositories.lib.utexas.edu:2152/20036 |
| Date | 26 April 2013 |
| Creators | Dickson, Andrea Haessly |
| Source Sets | University of Texas |
| Language | en_US |
| Detected Language | English |
| Format | application/pdf |
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