Receptorium NMDA

Receptorium NMDA sive abbreviatura internationis NMDAR est unum trium receptoriorum ionotropicorum glutamati postsynapticorum cum effectibus excitatoriis celerrimis in neuronis, ideo est pars actionis raptae neuronalis circum synapsem^[1]. Cum neurotransmissoribus et glutamati et glycini (sive D-serini) ligandis receptorium transgressionem celerissimam ionum calcii (Ca²⁺) permittit.

Cave: notitiae huius paginae nec praescriptiones nec consilia medica sunt.

Anticorpora contra receptoriis NMDA aspectum encephalitidis limbicae efficere possunt^[2].

Structura receptorii NMDA

Receptorium NMDA tetramerus ex duabus vel tribus variis subunitatibus constrictum est (heterotetramerus). Adhuc tria genera subunitatum notae sunt, GluN1 (seu NR1), GluN2 (seu NR2), GluN3 (seu NR3)^[3]. Omnibus subunitatibus quaedam varietates inventae sunt. Functionis rectae semper subunitatem NR1 singularem cum NR2 singulari coniungi oportet.

Subunitas GluN1 (NR1)

Non minus quam octo subunitates descripti sunt. Genum nomine GRIN1 chromosomate 9 (9q34.3) locatum est (OMIM: 138249).

Subunitas GluN2 (NR2)

GluN2 subunitati quattuor subtypi, GluN2A, GluN2B, GluN2C, GluN2D descripti sunt. Subtypi GluN2A et GluN2B imprimis in cortice cerebri et hippocampo locati sunt^[4]. Et GluN2A et GluN2B cum enzymis calcio-calmodulino-pendens proteini kinasis 2 (CaMKII) et PSD-95 coniunctae sunt^[5]. Gena nomine GRIN2A chromosomate 16 (16p13.2) (OMIM: 138253), atque nomine GRIN2B chromosomate 12 (12p13.1) (OMIM: 138253) locata sunt.

Subunitas GluN3 (NR3)

Adhuc subunitati GluN3 (sive NMDAR-L sive chi) subtypi GluN3A et GluN3B noti sunt^[6]. Subunitates GluN3 in cellulis formationis hippocampalis, sed etiam in cellulis granularibus cerebelli^[7] una cum GluN1 et GluN2 constituens reperiuntur. Praeterea constitutio una cum GluN1 tantum inventa est. In neurogenesi GluN3 magis exprimi videtur^[8].

Receptorium NMDA triheteromericum

Receptoria NMDA cum structura triheteromerica numerosa in systemate centrali nervosi videntur^[9]. Ea tetrameri ex tribus subunitatis variis composita. Natura et functionis et structurae eorum ab diheteromericis differunt. Eo super maturationis synapsum et plasticitatis cerebri magnum momentum habent. Nimirum scienta ad substantias fabricandas, quae receptoria triheteromerica inhibere stimulareve queant, spectat. Per exemplum, in cerebelli cellulis granularibus potissmimum receptorium tri-heteromericum cum subunitatibus duabus GluN1, una GluN2A, una GluN2C inveniri videtur. In synaptibus hippocamporum imprimis subunitates GluN1/GluN2A/GluN2B locatae sunt^[10].

Natura physiologica

Receptoria NMDA fluxum imprimis ionum calcii (Ca²⁺) permittunt, sed etiam natrii (Na⁺) et kalii (K⁺)^[4].

Contra NMDA receptoria encephalitis limbica

Encephalitis cum anticorporis contra receptoria NMDA est inflammatio cerebri cum initio repentino apud adulescentes et adultos iuniores^[1]^[11]. Non raro encephalitides limbicae istae cum alio malo oncologico sociatae sunt (teratomis, cancris ovarii, et aliis). Symptomata sunt psychiatrica, impedimentum memoriae.

Notae

↑ ^1.0 ^1.1 Karakas E, Furukawa H (2014). "Crystal structure of a heterotetrameric NMDA receptor ion channel". Science 344 (6187): 992-7
↑ Zubair UB, Majid H (2018). "Anti-NMDA Receptor Encephalitis in a Young Girl with Altered Behaviour and Abnormal Movements". J Coll Physicians Surg Pak 28 (8): 643-4
↑ Kehoe LA, Bernardinelli Y, Muller D (2013). "GluN3A: an NMDA receptor subunit with exquisite properties and functions". Neural Plast 2013: 145387
↑ ^4.0 ^4.1 Sanz-Clemente A, Nicoll RA, Roche KW (2013). "Diversity in NMDA receptor composition: many regulators, many consequences". Neuroscientist 19 (1): 62-75
↑ Gardoni F., Polli F., Cattabeni F., Di Luca M. (2006). "Calcium-calmodulin-dependent protein kinase II phosphorylation modulates PSD-95 binding to NMDA receptors". Eur J Neurosci 24 (10): 2694-704
↑ Skrenkova K., Lee S., Lichnerova K., Kaniakova M., Hansikova H., Zapotocky M., Suh Y. H., Horak M. (2018). "N-Glycosylation Regulates the Trafficking and Surface Mobility of GluN3A-Containing NMDA Receptors". Front Mol Neurosci 11: 188
↑ Bhattacharya S., Khatri A., Swanger S. A., DiRaddo J. O., Yi F., Hansen K. B., Yuan H., Traynelis S. F. (2018). "Triheteromeric GluN1/GluN2A/GluN2C NMDARs with Unique Single-Channel Properties Are the Dominant Receptor Population in Cerebellar Granule Cells". Neuron 99 (2): 315-28
↑ Wong H. K., Liu X. B., Matos M. F., Chan S. F., Pérez-Otaño I., Boysen M., Cui J., Nakanishi N., Trimmer J. S., Jones E. G., Lipton S. A., Sucher N. J. (2002). "Temporal and regional expression of NMDA receptor subunit NR3A in the mammalian brain". J Comp Neurol 450 (4): 303-17
↑ Stroebel D., Casado M., Paoletti P. (2018). "Triheteromeric NMDA receptors: from structure to synaptic physiology". Curr Opin Physiol 2: 1-12
↑ Rauner C., Köhr G. (2011). "Triheteromeric NR1/NR2A/NR2B receptors constitute the major N-methyl-D-aspartate receptor population in adult hippocampal synapses". J Biol Chem 286 (9): 7558-66
↑ Shimoyama Y, Umegaki O, Agui T, Kadono N, Minami T (2016). "Anti-NMDA receptor encephalitis presenting as an acute psychotic episode misdiagnosed as dissociative disorder: a case report". JA Clin Rep 2 (1): 22

Nexus interni

Nexus externi

Pagina interretialis Universitatis Bristoliensis de structura receptorii NMDA. (Anglice)

[SCI_STR-1] 1.0 ^1.1 Karakas E, Furukawa H (2014). "Crystal structure of a heterotetrameric NMDA receptor ion channel". Science 344 (6187): 992-7

[2] Zubair UB, Majid H (2018). "Anti-NMDA Receptor Encephalitis in a Young Girl with Altered Behaviour and Abnormal Movements". J Coll Physicians Surg Pak 28 (8): 643-4

[3] Kehoe LA, Bernardinelli Y, Muller D (2013). "GluN3A: an NMDA receptor subunit with exquisite properties and functions". Neural Plast 2013: 145387

[SANZ_13-4] 4.0 ^4.1 Sanz-Clemente A, Nicoll RA, Roche KW (2013). "Diversity in NMDA receptor composition: many regulators, many consequences". Neuroscientist 19 (1): 62-75

[5] Gardoni F., Polli F., Cattabeni F., Di Luca M. (2006). "Calcium-calmodulin-dependent protein kinase II phosphorylation modulates PSD-95 binding to NMDA receptors". Eur J Neurosci 24 (10): 2694-704

[6] Skrenkova K., Lee S., Lichnerova K., Kaniakova M., Hansikova H., Zapotocky M., Suh Y. H., Horak M. (2018). "N-Glycosylation Regulates the Trafficking and Surface Mobility of GluN3A-Containing NMDA Receptors". Front Mol Neurosci 11: 188

[7] Bhattacharya S., Khatri A., Swanger S. A., DiRaddo J. O., Yi F., Hansen K. B., Yuan H., Traynelis S. F. (2018). "Triheteromeric GluN1/GluN2A/GluN2C NMDARs with Unique Single-Channel Properties Are the Dominant Receptor Population in Cerebellar Granule Cells". Neuron 99 (2): 315-28

[8] Wong H. K., Liu X. B., Matos M. F., Chan S. F., Pérez-Otaño I., Boysen M., Cui J., Nakanishi N., Trimmer J. S., Jones E. G., Lipton S. A., Sucher N. J. (2002). "Temporal and regional expression of NMDA receptor subunit NR3A in the mammalian brain". J Comp Neurol 450 (4): 303-17

[9] Stroebel D., Casado M., Paoletti P. (2018). "Triheteromeric NMDA receptors: from structure to synaptic physiology". Curr Opin Physiol 2: 1-12

[10] Rauner C., Köhr G. (2011). "Triheteromeric NR1/NR2A/NR2B receptors constitute the major N-methyl-D-aspartate receptor population in adult hippocampal synapses". J Biol Chem 286 (9): 7558-66

[11] Shimoyama Y, Umegaki O, Agui T, Kadono N, Minami T (2016). "Anti-NMDA receptor encephalitis presenting as an acute psychotic episode misdiagnosed as dissociative disorder: a case report". JA Clin Rep 2 (1): 22

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