The Role Of NMDA Receptor NR2B Subunit In Long-term Potentiation Induced In C57BL/6 Mice During Postnatal Development

Since Long-term Potentiation was discovered, it has been thought to be highly relevant to learning and memeory because its cooperation, input-specificity, association. It was reported that the earliest time to induce LTP in young rats' cortex is consistent to critical period of neural structral plasticity. For example, LTP can be induced in visual cortex slices in 2-5 weeks old rats, which is basically consistent to its critical period of structral plasticity; while LTP can not be induced in rats older than 5 weeks. All these experiments indicate that LTP is greatly important for developmental plasticity.NMDA receptor acts as a significant role in LTP mechanism.Because NMDA receptor is both ligand-dependent and voltage-dependent, it is opened only if depolarization is reached to a certain degree and ligands are released. NMDA receptor has a Mg +-combination location, which blocks the channel. In general synaptic transmission, NMDA receptor can not be opened because of the low degree of depolarization. But when post-synaptic depolarization reached a certain degree, Mg2+ was driven out of channel, Ca2+ can flow into the cell through the channel, which aroused a series of reaction inside a cell. NMDA receptor is made up of subunits NR1 and NR2. NR1 is indispensable to NMDA receptor; NR2 includes NR2A, NR2B, NR2C and NR2D, different NR2 subunits and NR1 subunit compose hereceptor embodies its special properties as well as their common properties. NMDA receptorsthat include NR2 subunits have special phsiological and pharmacological properties: the duration of EPSCs they transmit is long, such receptors are much susceptive to Mg2+, Glu, Gly, which makes such NMD A receptors much more easy to be influenced by ambience, therefor trigger all kinds of structral and functional reactions in development.Previous studies indicate that NR2B subunit expression changes are related to development plasticity changes in animals. Tsien discovered in gene-knocked mouses that when NR2A, NR2C or NR2D was knocked, mouses can survive, and their development was normal, but NR1 -knocked mouses died after born a few days, while NR2B-knocking led to neural death, and that relevant neural mechanisms can not develop.This experiment uses ELVAX technique, in little mouses' one side of auditory cortex released NR2B subunit specific antagon ifenprodil, hypothesize that blocking the expression of NR2B subunit in critical period may influence formation of special synapses, or weaken the strength of synaptic connection. Rudoh found that LTP recorded in auditory cortex was much bigger than LTP in visual cortex, for the density of horizental synapses in auditory cortex was twice bigger than in visual cortex. So we examine the LTP in NR2B-blocked mouses, providing the evidence for the mechanism of NMD A in developmental plasticity.This paper includes two parts: (1) the basic characteristics of LTP in auditory cortex. We ascertain primary auditory cortex by recording the sound-induced reaction, then we stimulate white matter with electrode current, inducing and recording LTP in layer II /III. And we observe the changes of LTP in different stimulation conditions. (2) after mouses are born 13-15 days, we use Elvax technique to bury NR2B subunit specific antagon ifenprodil in one side of primary auditory cortex, and check the expression of LTP when they are grown up.