Exploring the principles that govern activity-dependent changes in excitability is an essential step to understand the function of the nervous system, because they act as a general postsynaptic control mechanism that modulates the flow of synaptic signals. We show an activity-dependent potentiation
Role of cell-cell interactions in the developmental regulation of Ca2+-activated K+ currents in vertebrate neurons
β Scribed by Dryer, Stuart E.
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 195 KB
- Volume
- 37
- Category
- Article
- ISSN
- 0022-3034
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β¦ Synopsis
The functional expression of the quired by CG neurons. In addition to target tissue Ca 2/ -activated K / current (I K[Ca] ) is dependent on interactions, an intact preganglionic innervation is recell-cell interactions in developing chick autonomic neurons. In chick ciliary ganglion (CG) neurons, exquired for the normal in vivo development of I K[Ca] in pression of macroscopic I K[Ca] coincides with the forchick CG neurons. The trophic effects of the afferent mation of synapses with target tissues. CG neurons innervation do not require synaptic activation of the that develop in vivo in the absence of normal target CG neurons, indicating secretion of a trophic factor, tissues fail to express functional I K[Ca] , although voltpossibly an isoform of b-neuregulin. The results are age-activated Ca 2/ currents and most other ionic curconsistent with the hypothesis that target-and nerve rents are expressed at normal amplitudes and densiterminal-derived trophic factors interact at a postties. CG neurons placed in cell culture prior to formatranslational level in the regulation of a functional tion of synapses with target tissues also fail to express I K[Ca] . Together, this body of data demonstrates an macroscopic I K[Ca] . However, CG neurons cultured in essential role for cell-cell interactions in the differenthe presence of a heat-and trypsin-sensitive extract of tiation of neuronal excitability. α§ 1998 John Wiley & Sons, target tissues express I K[Ca] at normal levels. Similarly,
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