| 18189 | Q9CS84 | NRX1A_MOUSE | Neurexin-1 (Neurexin I-alpha) (Neurexin-1-alpha) | DISRUPTION PHENOTYPE | No visible phenotype, but mice display subtle behavorial deficits. Females show deficits in nest building and taking care of pups. Mice lacking the alpha-type isoforms of NRXN1, NRXN2 and NRXN3 are born at the expected Mendelian rate, but die during the first day after birth, probably due to neurological defects in the brainstem that impair normal breathing. These mice express normal levels of the beta-type isoforms of NRXN1, NRXN2 and NRXN3. Mice show reduced density of synapses in the brainstem, especially a reduction in the numbers of GABA-releasing synapses. Their brains display a reduced frequency of spontaneous neurotransmitter release, and decreased neurotransmitter release in response to an action potential. Likewise, the activity of voltage-gated calcium channels is strongly decreased. A small proportion (5-10%) of mice lacking the alpha-type isoforms of both NRXN1 and NRXN2 survive to adulthood; these mice do not show any gross anatomical defects in their brains or changes in the distribution of synaptic proteins, but they have fewer synapses in the neocortex and show defects in neurotransmitter release at neuromuscular junctions. {ECO:0000269|PubMed:12827191, ECO:0000269|PubMed:14983056, ECO:0000269|PubMed:16406382, ECO:0000269|PubMed:17035546, ECO:0000269|PubMed:17347997, ECO:0000269|PubMed:19822762, ECO:0000269|PubMed:9430716}. |