Muscarinic receptors modulate the afterhyperpolarizing potential in neostriatal neurons

Pineda, Juan Carlos; Bargas, José; Flores‐Hernández, Jorge; Galarraga, Elvira

doi:10.1016/0014-2999(95)00263-k

Cited by 33 publications

(35 citation statements)

References 29 publications

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“…The postburst AHP is affected by activation of PKC (Malenka et al, 1986;Agopyan and Agopyan, 1991;Pineda et al, 1995;Seroussi et al, 2002), protein kinase A (PKA) (Pedarzani and Storm, 1993;Pedarzani et al, 1998;Haug and Storm, 2000;Seroussi et al, 2002), and Ca 2ϩ -calmodulin kinase II (Sah, 1996). Although the effects of ERK on the postburst AHP and neuronal adaptation after learning imply that its primary role after learning is to maintain the reduced conductance of the sI AHP , other potential effects on basic membranal properties such as input resistance or the duration of the single action potential would also be manifested by modulating repetitive firing and amplitude of calcium-dependent potassium currents.…”

Section: Erk Affects Neuronal Excitability By Direct Modulation Of Thmentioning

confidence: 99%

A Novel Role for Extracellular Signal-Regulated Kinase in Maintaining Long-Term Memory-Relevant Excitability Changes

Cohen-Matsliah

Brosh²,

Rosenblum³

et al. 2007

J. Neurosci.

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Pyramidal neurons in the piriform cortex from olfactory-discrimination-trained rats show enhanced intrinsic neuronal excitability that lasts for several days after learning. Such enhanced intrinsic excitability is mediated by long-term reduction in the postburst afterhyperpolarization (AHP), which is generated by repetitive spike firing. AHP reduction is attributable to decreased conductance of a calciumdependent potassium current, the sI AHP . We have previously shown that such learning-induced AHP reduction is maintained by PKC activation. However, the molecular machinery underlying such long-lasting modulation of intrinsic excitability is yet to be fully described. Here we examine whether the extracellular signal-regulated kinase I/II (ERKI/II) pathway, which is known to be crucial in learning, memory, and synaptic plasticity processes, is instrumental for the long-term maintenance of learning-induced AHP reduction. PD98059 or UO126, which selectively block MEK, the upstream kinase of ERK, increased the AHP in neurons from trained rats but not in neurons from naive and pseudo-trained rats. Consequently, the differences in AHP amplitude and neuronal adaptation between neurons from trained rats and controls were abolished. This effect was not mediated by modulation of basic membrane properties. In accordance with its effect on neuronal excitability, the level of activated ERK in the membranal fraction was significantly higher in piriform cortex samples taken from trained rats. In addition, the PKC activator OAG (1-oleoyl-20acety-sn-glycerol), which was shown to reduce the AHP in neurons from control rats, had no effect on these neurons in the presence of PD98059. Our data show that ERK has a key role in maintaining long-lasting learning-induced enhancement of neuronal excitability.

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Section: Erk Affects Neuronal Excitability By Direct Modulation Of Thmentioning

confidence: 99%

A Novel Role for Extracellular Signal-Regulated Kinase in Maintaining Long-Term Memory-Relevant Excitability Changes

Cohen-Matsliah

Brosh²,

Rosenblum³

et al. 2007

J. Neurosci.

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“…These channels are important targets for the actions of neurotransmitters, e.g. : dopamine, acetylcholine and somatostatin, among others (Pineda et al, 1995; Hernández-López et al, 1996; Vilchis et al, 2002; Pérez-Rosello et al, 2005; Galarraga et al, 2007). In dissociated neurons, Ca 2+ -activated K + -currents are preferentially activated by calcium entry through Ca V 2.1 and Ca V 2.2 channels.…”

Section: Introductionmentioning

confidence: 99%

Duration differences of corticostriatal responses in striatal projection neurons depend on calcium activated potassium currents

Arias-García¹,

Tapia²,

Flores-Barrera³

et al. 2013

Front. Syst. Neurosci.

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The firing of striatal projection neurons (SPNs) exhibits afterhyperpolarizing potentials (AHPs) that determine discharge frequency. They are in part generated by Ca2+-activated K+-currents involving BK and SK components. It has previously been shown that suprathreshold corticostriatal responses are more prolonged and evoke more action potentials in direct pathway SPNs (dSPNs) than in indirect pathway SPNs (iSPNs). In contrast, iSPNs generate dendritic autoregenerative responses. Using whole cell recordings in brain slices, we asked whether the participation of Ca2+-activated K+-currents plays a role in these responses. Secondly, we asked if these currents may explain some differences in synaptic integration between dSPNs and iSPNs. Neurons obtained from BAC D1 and D2 GFP mice were recorded. We used charybdotoxin and apamin to block BK and SK channels, respectively. Both antagonists increased the depolarization and delayed the repolarization of suprathreshold corticostriatal responses in both neuron classes. We also used NS 1619 and NS 309 (CyPPA), to enhance BK and SK channels, respectively. Current enhancers hyperpolarized and accelerated the repolarization of corticostriatal responses in both neuron classes. Nevertheless, these drugs made evident that the contribution of Ca2+-activated K+-currents was different in dSPNs as compared to iSPNs: in dSPNs their activation was slower as though calcium took a diffusion delay to activate them. In contrast, their activation was fast and then sustained in iSPNs as though calcium flux activates them at the moment of entry. The blockade of Ca2+-activated K+-currents made iSPNs to look as dSPNs. Conversely, their enhancement made dSPNs to look as iSPNs. It is concluded that Ca2+-activated K+-currents are a main intrinsic determinant causing the differences in synaptic integration between corticostriatal polysynaptic responses between dSPNs and iSPNs.

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“…There are numerous examples of enhanced cellular excitability caused by a decrease in the spike afterhyperpolarization (Fung and Barnes, 1987;McCormick et al, 1991;Shepard and Bunney, 1991;Womble and Moises, 1993;Cox et al, 1994;Pineda et al, 1995;Gorelova and Reiner, 1996). Furthermore, calciumactivated potassium conductances have been shown to underlie afterhyperpolarizations in a number of other systems, including sympathetic neurons in mammals and amphibians (McAfee and Yarowsky, 1979;MacDermott and Weight, 1982), lamprey spinal Higher amplification of the top trace shows that DSI stimulation decreased the afterhyperpolarization that followed the C2 spikes (middle trace).…”

Section: Potential Mechanisms Underlying Modulation Of Spike Frequencmentioning

confidence: 99%

Removal of Spike Frequency Adaptation via Neuromodulation Intrinsic to theTritoniaEscape Swim Central Pattern Generator

Katz

Frost²

1997

J. Neurosci.

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For the mollusc Tritonia diomedea to generate its escape swim motor pattern, interneuron C2, a crucial member of the central pattern generator (CPG) for this rhythmic behavior, must fire repetitive bursts of action potentials. Yet, before swimming, repeated depolarizing current pulses injected into C2 at periods similar those in the swim motor program are incapable of mimicking the firing rate attained by C2 on each cycle of a swim motor program. This resting level of C2 inexcitability is attributable to its own inherent spike frequency adaptation (SFA). Clearly, this property must be altered for the swim behavior to occur. The pathway for initiation of the swimming behavior involves activation of the serotonergic dorsal swim interneurons (DSIs), which are also intrinsic members of the swim CPG. Physiologically appropriate DSI stimulation transiently decreases C2 SFA, allowing C2 to fire at higher rates even when repeatedly depolarized at short intervals. The increased C2 excitability caused by DSI stimulation is mimicked and occluded by serotonin application. Furthermore, the change in excitability is not caused by the depolarization associated with DSI stimulation or serotonin application but is correlated with a decrease in C2 spike afterhyperpolarization. This suggests that the DSIs use serotonin to evoke a neuromodulatory action on a conductance in C2 that regulates its firing rate. This modulatory action of one CPG neuron on another is likely to play a role in configuring the swim circuit into its rhythmic pattern-generating mode and maintaining it in that state.

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Muscarinic receptors modulate the afterhyperpolarizing potential in neostriatal neurons

Cited by 33 publications

References 29 publications

A Novel Role for Extracellular Signal-Regulated Kinase in Maintaining Long-Term Memory-Relevant Excitability Changes

A Novel Role for Extracellular Signal-Regulated Kinase in Maintaining Long-Term Memory-Relevant Excitability Changes

Duration differences of corticostriatal responses in striatal projection neurons depend on calcium activated potassium currents

Removal of Spike Frequency Adaptation via Neuromodulation Intrinsic to theTritoniaEscape Swim Central Pattern Generator

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