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Review
. 2006 Oct 11;26(41):10362-7.
doi: 10.1523/JNEUROSCI.3194-06.2006.

Cellular excitability and the regulation of functional neuronal identity: from gene expression to neuromodulation

David J Schulz  1 , Richard A Baines, Chris M Hempel, Lingjun Li, Birgit Liss, Hiroaki Misonou
Affiliations
Review

Cellular excitability and the regulation of functional neuronal identity: from gene expression to neuromodulation

David J Schulz et al. J Neurosci. .
No abstract available

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Figures

Figure 1.
Figure 1.
Exposure to synaptic excitation regulates INa and membrane excitability in Drosophila motoneurons. A, The amplitude of the voltage-gated INa recorded in Drosophila motoneurons is inversely related to the synaptic excitation that these neurons receive. B, The abundance of para mRNA in isolated CNS is significantly greater in the loss-of-function pumbem allele. By comparison, overexpression of UAS (upstream activating sequence)–pum in all of the neurons of the CNS (1407 GAL4) is sufficient to significantly reduce para mRNA. C, Membrane excitability, measured as action potential firing, shows a significant increase in Pumiliobem (loss-of-function) and a significant decrease after overexpression of UAS-pumilio (gain-of-function), respectively. The action potential firing rate was determined by injection of constant current (1–10 pA/500 ms) from a holding potential of −60 mV. A is reprinted from Baines and Pym (2006). B and C are reprinted from Mee et al. (2004).
Figure 2.
Figure 2.
Mice in which subpopulations of neurons are genetically labeled are used for electrophysiological recordings and cell type-specific microarray analysis to obtain a correlated profile of firing properties and gene expression.
Figure 3.
Figure 3.
K-ATP channel activity triggers selective degeneration of SN DA neurons. A, A schematic overview of analyzing electrophysiological function and gene expression of individual dopaminergic neurons (mouse/human) combining brain slice patch clamping (inset, typical spontaneous activity of DA neurons) or laser microdissection with gene expression profiling (reverse transcription-PCR/microarrays). Scale bars, 15 μm. B, Dopaminergic neurons in SN and VTA [ marked by tyrosine hydroxylase (TH) immunostain] display differential vulnerability in the chronic mouse MPTP-model of PD. Differential mRNA levels of K-ATP channel subunits and UCP2 are indicated. C, Results of quantitative stereology indicated complete rescue of highly vulnerable SN DA neurons in the chronic MPTP PD model in a K-ATP channel knock-out mouse (Kir6.2 −/−; left). In contrast, MPTP-induced moderate loss of VTA DA neurons was independent from the presence (+ /+) or absence (−/−) of K-ATP channels (right).
Figure 4.
Figure 4.
A, Dephosphorylation of Kv2.1 induced by seizures and ischemia. Rats were subjected to either kainate-induced continuous seizures (Kainate) or CO2-induced brain ischemia (Ischemia). Total brain membrane was prepared, and a fraction was treated in vitro with alkaline phosphatase (AP) to completely dephosphorylate Kv2.1. The arrow indicates the highly phosphorylated Kv2.1, and arrowhead indicates fully dephosphorylated Kv2.1. Numbers on the left denote the molecular weight standards. B, Dispersion of Kv2.1 clusters in brain by ischemia. Brain sections from control and ischemic rats were stained with a specific anti-Kv2.1 antibody. Images show pyramidal neurons in the cerebral cortex. It should be noted that kainate-induced seizures also resulted in dispersion of Kv2.1 clusters. Scale bar, 10 μm. C, Changes in the biophysical properties of IK/Kv2.1 by glutamate stimulation and ischemia in cultured neurons. IK currents were recorded in a cultured hippocampal neuron under whole-cell voltage clamp. The half-maximal activation membrane potential (G1/2) and the slope of the activation curve are shown (means ± SEM). The values are from Misonou et al. (2004, .
Figure 5.
Figure 5.
Development of a mass spectrometry-based peptidomic approach for understanding functional consequence of neuropeptide multiplicity. A, An overview of mass spectrometry-based strategy for neuropeptide discovery and characterization. B, Differential degradation of three FLRFamide (Phe-Leu-Arg-Phe-NH2) peptides by peptidase located in the pericardial organ monitored by matrix-assisted laser desorption/ionization Fourier transform mass spectrometry. A is reprinted from DeKeyser and Li (2006). B is adapted from Cruz-Bermudez et al. (2006). MS, Mass spectrometry; MALDI, matrix-assisted laser desorption/ionization; ESI, electrospray ionization; RT, reverse transcription; CM PO, Cancer magister pericardial organ.
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References

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