{'fraction_non_alphanumeric': 0.019319227230910764, 'fraction_numerical': 0.0027598896044158236, 'mean_word_length': 5.217142857142857, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Rapid reversal of impaired inhibitory and excitatory transmission but not spine dysgenesis in a mouse model of mental retardation

Non‐technical summary  Intellectual disability has long been attributed at the cellular level to abnormalities in the structures that receive incoming connections to the major classes of neurons in the brain. These misshaped ‘dendrites’ and especially misshaped ‘dendritic spines’ have been found in many types of intellectual disability. We have used a mouse model of one of the human intellectual disability mutations on a gene on the X‐chromosome called Ophn‐1. We show that, in addition to the misshaped dendritic spines, these mice have abnormal physiology in the inability of both excitatory and inhibitory inputs (‘synapses’) to operate repetitively as they need to in many aspects of normal brain function. A drug known as a Rho‐GAP inhibitor was able to reverse the physiological impairment within 20 min, without changing the structure of dendrites or dendritic spines. This class of drug may have a role in limiting disability in this condition.