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Cell Communication in Nervous and Immune System by Eckart D. Gundelfinger, Constanze Seidenbecher, Burkhart

By Eckart D. Gundelfinger, Constanze Seidenbecher, Burkhart Schraven

At first look, the frightened and immune platforms look very assorted. although, either structures have constructed mechanisms for reminiscence formation – although of relatively diversified caliber and value for the organism. One extraordinary instance is that either platforms shape and converse through synapses armed with related units of proteins. This number of studies, contributed via across the world well-known immunologists and molecular and mobile neurobiologists, places facet via aspect mobile communique units and signaling mechanisms within the immune and apprehensive structures and discusses mechanisms of interplay among the 2 platforms, the importance of which has only in the near past been totally appreciated.

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Staining of α5, on the other hand, was found to be diffuse in all hippocampal cells and never co-localized with gephyrin clusters (Brunig et al. 2002). Pharmacological studies have revealed the importance of receptor composition in defining the biophysical properties of GABAA receptors (reviewed in Farrant and Nusser 2005). The type of α subunit, for example, plays an important role in defining the sensitivity of the receptor to GABA and the deactivation rate of the receptor (Lavoie et al. 1997; Bohme et al.

2004; Levinson and El-Husseini 2005). Neuroligins are postsynaptic transmembrane proteins encoded by four different genes. All four neuroligins (NL 1–4) have been shown to bind the presynaptic transmembrane protein β-neurexin but not its splice isoform αneurexin in vitro and in vivo (Ichtchenko et al. 1996; Dean et al. 2003). An elegant study by Scheiffele et al. demonstrated that the interaction between neuroligins and β-neurexin played an important role in triggering excitatory synaptogenesis in non-neuronal cells (Scheiffele et al.

2005). Interestingly, expression of NL1 together with PSD-95 results in the formation of new excitatory but not inhibitory synapses (Prange et al. 2004). Furthermore overexpression of PSD-95 causes a redistribution of NL2 to excitatory synapses, presumably by an interaction between PSD-95 and the PDZ domain in NL2 (Levinson et al. 2005). Overall these data suggest that the neurolign–neurexin complex plays an important role in excitatory and inhibitory synaptogenesis, although it appears that, in addition, postsynaptic scaffolding proteins may be required for con- Molecular Organization and Assembly of the Central Inhibitory Postsynapse 31 trolling the balance between excitatory and inhibitory synapses (Levinson and El-Husseini 2005).

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