{'fraction_non_alphanumeric': 0.02238388360380526, 'fraction_numerical': 0.013989927252378288, 'mean_word_length': 6.209677419354839, '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}}
Whisker experience‐dependent mGluR signaling maintains synaptic strength in the mouse adolescent cortex

Sensory experience‐dependent plasticity in the somatosensory cortex is a fundamental mechanism of adaptation to the changing environment not only early in the development but also in adolescence and adulthood. Although the mechanisms underlying experience‐dependent plasticity during early development have been well documented, the corresponding understanding in the mature cortex is less complete. Here, we investigated the mechanism underlying whisker deprivation‐induced synaptic plasticity in the barrel cortex in adolescent mice. Layer 4 (L4) to L2/3 excitatory synapses play a crucial role for whisker experience‐dependent plasticity in rodent barrel cortex and whisker deprivation is known to depress synaptic strength at L4–L2/3 synapses in adolescent and adult animals. We found that whisker deprivation for 5 days or longer decreased the presynaptic glutamate release probability at L4–L2/3 synapses in the barrel cortex in adolescent mice. This whisker deprivation‐induced depression was restored by daily administration of a positive allosteric modulator of the type 5 metabotropic glutamate receptor (mGluR5). On the other hand, the administration of mGluR5 antagonists reproduced the effect of whisker deprivation in whisker‐intact mice. Furthermore, chronic and selective suppression of inositol 1,4,5‐trisphosphate (IP3) signaling in postsynaptic L2/3 neurons decreased the presynaptic release probability at L4–L2/3 synapses. These findings represent a previously unidentified mechanism of cortical plasticity, namely that whisker experience‐dependent mGluR5‐IP3 signaling in the postsynaptic neurons maintains presynaptic function in the adolescent barrel cortex.