{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T15:19:13Z","timestamp":1791299953654,"version":"4.1.0"},"reference-count":57,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[2005,11]]},"abstract":"<jats:p> The fast transient potassium or A current ( I<jats:sub>A<\/jats:sub>) plays an important role in determining the activity of central pattern generator neurons. We have previously shown that the shal K<jats:sup>+<\/jats:sup> channel gene encodes I<jats:sub>A<\/jats:sub> in neurons of the pyloric network in the spiny lobster. To further study how I<jats:sub>A<\/jats:sub> shapes pyloric neuron and network activity, we microinjected RNA for a shal-GFP fusion protein into four identified pyloric neuron types. Neurons expressing shal-GFP had a constant increase in I<jats:sub>A<\/jats:sub> amplitude, regardless of cell type. This increase in I<jats:sub>A<\/jats:sub> was paralleled by a concomitant increase in the hyperpolarization-activated cation current I<jats:sub>h<\/jats:sub> in all pyloric neurons. Despite significant increases in these currents, only modest changes in cell firing properties were observed. We used models to test two hypotheses to explain this failure to change firing properties. First, this may reflect the mislocalization of the expressed shal protein solely to the somata and initial neurites of injected neurons, rendering it electrically remote from the integrating region in the neuropil. To test this hypothesis, we generated a multicompartment model where increases in I<jats:sub>A<\/jats:sub> could be localized to the soma, initial neurite, or neuropil\/axon compartments. Although spike activity was somewhat more sensitive to increases in neuropil\/axon versus somatic\/primary neurite I<jats:sub>A<\/jats:sub>, increases in I<jats:sub>A<\/jats:sub> limited to the soma and primary neurite still evoked much more dramatic changes than were seen in the shal-GFP\u2013injected neurons. Second, the effect of the increased I<jats:sub>A<\/jats:sub> could be compensated by the endogenous increase in I<jats:sub>h<\/jats:sub>. To test this, we modeled the compensatory increases of I<jats:sub>A<\/jats:sub> and I<jats:sub>h<\/jats:sub> with a cycling two-cell model. We found that the increase in I<jats:sub>h<\/jats:sub> was sufficient to compensate the effects of increased I<jats:sub>A<\/jats:sub>, provided that they increase in a constant ratio, as we observed experimentally in both shal-injected and noninjected neurons. Thus an activity-independent homeostatic mechanism maintains constant neuronal activity in the face of dramatic increases in I<jats:sub>A<\/jats:sub>. <\/jats:p>","DOI":"10.1152\/jn.00281.2005","type":"journal-article","created":{"date-parts":[[2005,7,28]],"date-time":"2005-07-28T00:34:01Z","timestamp":1122510841000},"page":"3601-3617","source":"Crossref","is-referenced-by-count":125,"title":["Activity-Independent Coregulation of <i>I<\/i><sub>A<\/sub> and <i>I<\/i><sub>h<\/sub> in Rhythmically Active Neurons"],"prefix":"10.1152","volume":"94","author":[{"given":"Jason N.","family":"MacLean","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ying","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marie L.","family":"Goeritz","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard","family":"Casey","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ricardo","family":"Oliva","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John","family":"Guckenheimer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ronald M.","family":"Harris-Warrick","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1038\/35000592"},{"key":"R1A","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.09-08-02846.1989"},{"key":"R2","unstructured":"Back A, Guckenheimer J, Meyers M, Wicklin F, and Worfolk P. 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