NLGN1

NLGN1

A gene on chromosome 3q26.31 that encodes neuroligin 1, a neuronal cell surface protein involved in cell–cell interactions, which forms intercellular junctions by binding to beta-neurexins. NLLGN1 may play role in forming or maintaining synaptic junctions; it may be involved in specification of excitatory synapses.
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C57BL/ 6J mice, a strain commonly used in addiction studies due to their high levels of self-administration of most drugs of abuse, have lower levels of Nrxn2[beta] and Nlgn3 expression in the substantia nigra and increased expression of Nlgn1 in the subthalamic nucleus compared to non-drug-preferring mice [115].
A complete consideration of this topic is beyond the scope of this review, but it has been noted that many of the cell adhesion molecules discussed here are located in portions of corticostriatal circuitry involved in addiction on dopaminergic or glutamatergic neurons including CDH13, PTPRD, NLGN1, and NRXN3 [9].
Cell adhesion molecule Abbreviation Neural cell adhesion molecule NCAM Polysialated neural cell adhesion molecule PSA-NCAM Neuronal cell adhesion molecule NRCAM Immunoglobulin super family IGSF Synaptic cell adhesion molecule SYNCAM Intercellular adhesion molecule 5 ICAM5 Cadherin 13 CDH13 Neurexin 3 NRXN3 Neurexin 2[beta] NRXN2[beta] Neuroligin 3 NLGN3 Neuroligan 1 NLGN1 Neurexin 3[beta] NRXN3[beta] Protein tyrosine phosphatase receptor D PTPRD Protein tyrosine phosphatase receptor B PTPRB CUB and Sushi multiple domains 1 CSMD1 Protein tyrosine phosphatase receptor Z 1 PTPRZ1 Table 2: Gene expression changes after repeated cocaine treatment.
The protein - Neuroligin-1 (NLGN1) - is known to be involved in memory formation; this is the first time it's been linked to amyloid-associated memory loss.
Using animal models, Cleveland Clinic researchers discovered that during this neuroinflammatory process, the epigenetic modification of NLGN1 disrupts the synaptic network in the brain, which is responsible for developing and maintaining memories.
So extending the assumption of X chromosome evolution from autosome we can assume that paralog of X-linked genes must be on autosome and should be involved in the same disorder; like ARHGEF6 (X chromosome) has its paralog ARHGEF3 and ARHGEF4 on autosome; similarly NLGN3, NLGN4 on X -chromosome has paralog NLGN1 and NLGN2 on autosome.
Genes involved in neuronal cell adhesion (including NRXN1, CNTN4, NLGN1, ASTN2) were enriched with copy number variation in ASD cases, compared with controls, as were genes involved in ubiquitin degradation (including UBE3A, PARK2, RFWD2, and FBXO40).
Transcripts belonging to this category that are of particular interest include neurexins 1 and 3 (NRXN1 and NRXN3, resp.) and neuroligin 1 (NLGN1), whose mutations are found to associate with various neurological diseases, including autism spectrum disorders [56].
This genome-wide ChIP-on-chip analysis of target genes of RORA, as well as additional methods of validation, confirmed that RORA transcriptionally regulates the genes A2BP1, CYP19A1, HSD17B10, ITPR1, NLGN1, and NTRK2, such that when RORA levels are cut in half, all six genes also go down in their expression.
NLGN1 and NLGN3 have increased surface membrane levels upon chemically induced LTP and decreased levels after LTD as a result of being dynamically exchanged at the postsynaptic membrane through active cytoskeleton transport [32].
In the case of the postsynaptic adhesion molecule NLGN1, shedding destabilizes the presynaptic partner neurexin 1[beta] at synapses and decreases the presynaptic release probability of synaptic vesicles, thereby depressing synaptic transmission [48, 50].
For example, NLGN1 can induce synapse formation in young primary hippocampal cultures, but SynCAMl cannot [59].