Activity-Independent Homeostasis in Rhythmically Active Neurons

MacLean, Jason N.; Zhang, Ying; Johnson, Bruce; Harris-Warrick, Ronald M.

doi:10.1016/s0896-6273(02)01104-2

Cited by 261 publications

(297 citation statements)

References 40 publications

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“…6B). These results parallel studies in lobster that have demonstrated that changes in Shal (Kv4) channel expression levels can result in changes in whole-cell currents because of the up-regulation of other channel types (46). Notably, in both studies up-regulation of compensatory currents depends on the complete absence of a channel protein product, even if the ion conduction pathway of the protein product is blocked.…”

Section: Resultssupporting

confidence: 84%

“…The compensating component may differ radically in its properties from the original component, which was removed (59,60). For example, changes in HCN ion channel expression in response to increased Shal subunit expression have been observed previously in lobster stomatogastric ganglion cells (46,61). In our case, the up-regulation of the SHK-1 current was not observed in either the shl-1 RNAi-treated myocytes nor the dominant negative transgenic line pshl-1::W363F.…”

Section: Discussionsupporting

confidence: 48%

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Mutant Analysis of the Shal (Kv4) Voltage-gated Fast Transient K+ Channel in Caenorhabditis elegans

Fawcett

Santi

Butler

et al. 2006

Journal of Biological Chemistry

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. We show that Shal channels also play a role as the predominant transient outward current in Caenorhabditis elegans muscle. Green fluorescent protein promoter experiments also revealed SHL-1 expression in a subset of neurons as well as in C. elegans body wall muscle and in male-specific diagonal muscles. The shl-1 (ok1168) null mutant removed all fast transient outward current from muscle cells. SHL-1 currents strongly resembled Shal currents in other species except that they were active in a more depolarized voltage range. We also determined that the remaining delayed-rectifier current in cultured myocytes was carried by the Shaker ortholog SHK-1. In shl-1 (ok1168) mutants there was a significant compensatory increase in the SHK-1 current. Male shl-1 (ok1168) animals exhibited reduced mating efficiency resulting from an apparent difficulty in locating the hermaphrodite vulva. SHL-1 channels are apparently important in fine-tuning complex behaviors, such as mating, that play a crucial role in the survival and propagation of the species.2 channels are key regulators of membrane excitability. Based on their inactivation kinetics, Kv currents can loosely be divided into two categories as follows: noninactivating or slowly inactivating K ϩ currents, and rapidly inactivating transient currents also known as "A-type" currents. A-type currents were first described in molluscan neurons by Hagiwara et al. (3) and later by Connor and Stevens (4), Neher (5), and Thompson (6). Classical A-type currents (I A ) are voltage-dependent, Ca 2ϩ -independent K ϩ currents that undergo rapid activation and inactivation. The classical A-type currents activate at subthreshold voltages and recover from inactivation quickly compared with other Kv currents. They are also characterized by strong steady-state voltagedependent inactivation. Repolarization to potentials negative to Ϫ50 mV is typically required to restore channel availability. A-type currents have a widespread distribution and are abundantly expressed in neurons and cardiac and smooth muscle cells, where they are thought to play many important physiological roles (2, 7-11).Connor and Stevens (12) proposed that the I A may determine the interspike interval in repetitively firing neurons. Studies in cerebellar granule cells demonstrated a role for I A in determining the latency to first spike (13). I A has also been demonstrated to limit the back propagation of action potentials into the dendritic arbor (14), to impact long term potentiation in CA1 hippocampal neurons (15), to affect neuronal excitability in the visual cortex (16), and to modulate compartmentalization of membrane excitability in distal dendritic spines (17). Fast transient K ϩ currents in cardiac muscles contribute both to myocyte excitability (18) and to the fast repolarization phase of the cardiac action potential (2,8,19,20). Finally, the pharmacological block of channels that carry fast transient currents in gastrointestinal smooth muscle in mice supports the conclusion that the window currents carried by ...

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Section: Resultssupporting

confidence: 84%

Section: Discussionsupporting

confidence: 48%

Mutant Analysis of the Shal (Kv4) Voltage-gated Fast Transient K+ Channel in Caenorhabditis elegans

Fawcett

Santi

Butler

et al. 2006

Journal of Biological Chemistry

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“…In all species studied, acute removal of the influence of these descending inputs always results in a decrease in pyloric rhythm frequency and often results in a complete cessation of the pyloric rhythm. Complete stomatogastric nervous systems consisting of the STG, OG, and CoG and their intact connecting nerves, however, remain rhythmic for several days after dissection when kept sterile (MacLean et al 2003). In our hands, intact C. borealis preparations remain stably rhythmic for several days (2-6 days; n ϭ 10, data not shown).…”

Section: Pyloric Rhythm Ceases When Modulatory Inputs Are Removed Butmentioning

confidence: 51%

“…Episodic bouts of activity accompany recovery of rhythmic output by a neuromodulator-and activity-deprived adult neural network. J Neurophysiol 90: 2720 -2730, 2003. First published July 2, 2003 10.1152/jn.00370.2003.…”

mentioning

confidence: 99%

Episodic Bouts of Activity Accompany Recovery of Rhythmic Output By a Neuromodulator- and Activity-Deprived Adult Neural Network

Luther

Robie

Yarotsky

et al. 2003

Journal of Neurophysiology

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. Episodic bouts of activity accompany recovery of rhythmic output by a neuromodulator-and activity-deprived adult neural network. J Neurophysiol 90: 2720 -2730, 2003. First published July 2, 2003 10.1152/jn.00370.2003. The pyloric rhythm of the stomatogastric ganglion of the crab, Cancer borealis, slows or stops when descending modulatory inputs are acutely removed. However, the rhythm spontaneously resumes after one or more days in the absence of neuromodulatory input. We recorded continuously for days to characterize quantitatively this recovery process. Activity bouts lasting 40 -900 s began several hours after removal of neuromodulatory input and were followed by stable rhythm recovery after 1-4 days. Bout duration was not related to the intervals (0.3-800 min) between bouts. During an individual bout, the frequency rapidly increased and then decreased more slowly. Photoablation of back-filled neuromodulatory terminals in the stomatogastric ganglion (STG) neuropil had no effect on activity bouts or recovery, suggesting that these processes are intrinsic to the STG neuronal network. After removal of neuromodulatory input, the phase relationships of the components of the triphasic pyloric rhythm were altered, and then over time the phase relationships moved toward their control values. Although at low pyloric rhythm frequency the phase relationships among pyloric network neurons depended on frequency, the changes in frequency during recovery did not completely account for the change in phase seen after rhythm recovery. We suggest that activity bouts represent underlying mechanisms controlling the restructuring of the pyloric network to allow resumption of an appropriate output after removal of neuromodulatory input.

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“…It is now well recognized that embryonic gene deletion or mutation can lead to unintended increases in the expression of untargeted proteins that may be compensatory to mask a phenotype (20,21,22) or secondary changes that may produce phenotypes not directly related to the targeted or mutant protein (23,24,25). Acute administration and rapid clearance of T-588 in the normal brain allows LTD to be transiently prevented without the consequences of an embryonic mutation.…”

Section: Discussionmentioning

confidence: 99%

Normal motor learning during pharmacological prevention of Purkinje cell long-term depression

Welsh

Yamaguchi

Zeng

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

128

104

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Systemic delivery of (1R-1-benzo thiophen-5-yl-2[2-diethylamino)-ethoxy] ethanol hydrochloride (T-588) prevented long-term depression (LTD) of the parallel fiber (PF)-Purkinje cell (PC) synapse induced by conjunctive climbing fiber and PF stimulation in vivo.However, similar concentrations of T-588 in the brains of behaving mice and rats affected neither motor learning in the rotorod test nor the learning of motor timing during classical conditioning of the eyeblink reflex. Rats given doses of T-588 that prevented PF-PC LTD were as proficient as controls in learning to adapt the timing of their conditioned eyeblink response to a 150-or 350-ms change in the timing of the paradigm. The experiment indicates that PF-PC LTD under control of the climbing fibers is not required for general motor adaptation or the learning of response timing in two common models of motor learning for which the cerebellum has been implicated. Alternative mechanisms for motor timing and possible functions for LTD in protection from excitotoxicity are discussed.cerebellum ͉ eyeblink ͉ field potentials ͉ rotorod A longstanding hypothesis concerning cerebellar function has been the proposal that it serves as the repository for new motor skills through plasticity of the parallel fiber (PF)-Purkinje cell (PC) synapse (1, 2). In the prevailing hypothesis of ''cerebellar learning,'' the acquisition of new skills is controlled by climbing fibers (CFs), which function to depress the strength of the PF-PC synapse when the two afferents are conjointly active. The cerebellar learning hypothesis has inspired much research since the demonstration, in vivo, that near-synchronous activation of CFs and PFs by direct electrical stimulation depressed the strength of the excitatory potentials triggered by PFs in PCs (3). Because the depression required repeated pairings of CF and PF synaptic input and was retained for many hours, the phenomenon has been termed cerebellar long-term depression (LTD) and has been invoked to explain the acquisition and lifetime retention of many motor skills, including learned motor timing, reflex adaptation, and procedural and implicit learning (4).A substantial body of evidence has established the necessary intracellular events that produce PC LTD in vitro, and these events have been assumed to relate to motor learning in vivo. Moreover, a recent experiment showed that mouse PCs genetically modified to lack protein kinase C (PKC) function could not undergo LTD (5, 6); when such transgenic mice were tested in classical eyeblink conditioning, they were unable to learn the appropriate motor timing of conditioned eyeblinks [conditioned response (CR)] (7). That finding, complemented by the finding that cerebellar decortication also impaired the learned motor timing of CRs (8), has sustained the hypothesis that PF-PC LTD is required for motor learning. However, it is also evident that, up to this time, it has not been determined whether LTD occurs in awake animals as they acquire and retain new motor skills. Thus, it has been diffic...

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Activity-Independent Homeostasis in Rhythmically Active Neurons

Cited by 261 publications

References 40 publications

Mutant Analysis of the Shal (Kv4) Voltage-gated Fast Transient K+ Channel in Caenorhabditis elegans

Mutant Analysis of the Shal (Kv4) Voltage-gated Fast Transient K+ Channel in Caenorhabditis elegans

Episodic Bouts of Activity Accompany Recovery of Rhythmic Output By a Neuromodulator- and Activity-Deprived Adult Neural Network

Normal motor learning during pharmacological prevention of Purkinje cell long-term depression

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