Table 2.
Effect of MEF2C genetic manipulations on neuronal and behavioral features.
| Neuronal Effect | Behavioral Effect | References | |
|---|---|---|---|
| Conditional knock-out of MEF2C in Calcium/calmodulin-dependent protein kinase II (CaMKII)- Cre93 line after birth. | Increased quantity of spines in the mice hippocampus. | No changes in learning and memory ability, LTP or social conduct. | [160] |
| Removal of MEF2C in mice forebrain at late embryonic day. Overexpression of MEF2C in transgenic mice (NSE-MEF2C-VP16 mice). |
Increased quantity of spinous processes and excitatory synapses. Intensified basal and induces synaptic transmission. Decrease in glutamatergic synapse density of hippocampal pyramidal neurons. |
Dependent on hippocampus learning and memory diminished ability. | [9] |
| Silencing of MEF2C. | Condensation of branches and spines on dendrites of Purkinje cells and impaired localization of synaptic proteins. | [116,117] | |
| Conditional knock-out of MEF2C in the progenitor/stem cells. | Neurons from cortical plate with atypical cell body size and density. | Strong changes in behavior and electrophysiological features typical for immature neurons and severe behavioral deficits reminiscent of Rett syndrome, an autism-related disorder. | [116] |
| Knockdown of MEF2C in vivo and in vitro. | Suppression of nicotine-mediated modifications of dendritic complexity. | Diminished nicotine-dependent changes in passive avoidance behavior. | [161] |
| Knockdown of MEF2C in excitatory neurons of embryonic mice cortex and hippocampus (EmxCre × MEF2C flox/flox). |
Reduction of cortical network activity due to increase in inhibitory and decrease in excitatory synaptic transmission. MEF2C regulates inhibitory/excitatory (E/I) synapse density. |
Deficiency in fear learning, memory, various social conduct, socially-motivated ultrasonic vocalizations and reward-related behaviors, features reminiscent of autism, intellectual disability and schizophrenia. | [62] |
| Silencing of MEF2C by HSV-Cre-GFP virus in MEF2C fox/fox mice at postnatal day 2 (P2) or at postnatal day 14–15 (P14–15). Overexpression of MEF2C by electroporation of pcBIG-MEF2C-VP16 plasmids at E12.5 in wild-type embryos. |
Amplified number of dendritic spines in striatal projector neurons (SPNs) at P8. Reduced number of dendritic spines in SPNs at P14. |
Malfunctioning neonatal isolation-induced USVs (form of vocal communication in neonatal rodents). | [162] |
| Knockdown of postnatal MEF2C AAV-Cre-GFP neocortical cultures. |
Reduction of pyramidal neurons excitatory synapses. Decreased spine density on normal branching dendrites in neurons. |
[163] | |
| Exon 2-deleted allele of MEF2C. | Lower neurons number and axon length. Impaired dendritic connections. Elevated E/I ratio hippocampus. |
Autism-like symptoms, intellectual disability, speech deficiency, seizures or motor impairments. | [135] |
| MEF2C overexpression in mature prefrontal cortex (PFC) by AAV-MEF2C virus. | Reduced mushroom spines ratio in layer III of PFC and no alteration in total spine quantity. | Congenital improvement. | [122] |