D1 dopaminergic control of G protein–dependent inward rectifier K+ (GIRK)–like channel current in pyramidal neurons of the medial prefrontal cortex

Witkowski, Grzegorz; Szulczyk, Bartłomiej; Rola, Rafał; Szulczyk, Paweł

doi:10.1016/j.neuroscience.2008.05.021

Cited by 49 publications

(27 citation statements)

References 56 publications

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“…Thus, although the present study provides no direct evidence, our results are compatible with a dopaminergic modulation of potassium channels. Indeed, dopamine modulates potassium inward rectifiers in medium spiny neurons of the nucleus accumbens (Perez et al 2006;Podda et al 2010) and in fast spiking interneurons and pyramidal neurons of the prefrontal cortex (Gorelova et al 2002;Witkowski et al 2008). Future experiments using specific dopaminergic antagonists and/or inward rectifier K ϩ channel blockers will test the hypothesis that such a regulation is present in the M-cell.…”

Section: Discussionmentioning

confidence: 99%

Dopaminergic-induced changes in Mauthner cell excitability disrupt prepulse inhibition in the startle circuit of goldfish

Medan

Preuss

2011

Journal of Neurophysiology

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Medan V, Preuss T. Dopaminergic-induced changes in Mauthner cell excitability disrupt prepulse inhibition in the startle circuit of goldfish. J Neurophysiol 106: 3195-3204, 2011. First published September 28, 2011 doi:10.1152/jn.00644.2011.-Prepulse inhibition (PPI) is a widespread sensorimotor gating phenomenon characterized by a decrease in startle magnitude if a nonstartling stimulus is presented 20 -1,000 ms before a startling stimulus. Dopaminergic agonists disrupt behavioral PPI in various animal models. This provides an important neuropharmacological link to schizophrenia patients that typically show PPI deficits at distinct (60 ms) prepulsepulse intervals. Here, we study time-dependent effects of dopaminergic modulation in the goldfish Mauthner cell (M-cell) startle network, which shows PPI-like behavioral and physiological startle attenuations. The unique experimental accessibility of the M-cell system allows investigating the underlying cellular mechanism with physiological stimuli in vivo. Our results show that the dopaminergic agonist apomorphine (2 mg/kg body wt) reduced synaptic M-cell PPI by 23.6% (n ϭ 18; P ϭ 0.009) for prepulse-pulse intervals of 50 ms, whereas other intervals showed no reduction. Consistently, application of the dopamine antagonist haloperidol (0.4 mg/kg body wt) restored PPI to control level. Current ramp injections while recording M-cell membrane potential revealed that apomorphine acts through a postsynaptic, time-dependent mechanism by deinactivating a M-cell membrane nonlinearity, effectively increasing input resistance close to threshold. This increase is most pronounced for prepulse-pulse intervals of 50 ms (47.9%, n ϭ 8; P Ͻ 0.05) providing a timedependent, cellular mechanism for dopaminergic disruption of PPI. These results provide, for the first time, direct evidence of dopaminergic modulation of PPI in the elementary startle circuit of vertebrates and reemphasize the potential of characterizing temporal aspects of PPI at the physiological level to understand its underlying mechanisms.sensorimotor-gating; dopamine; cellular mechanisms; input resistance; time-specific neuromodulation THE CENTRAL NERVOUS SYSTEM has to filter the overwhelming stream of information provided by the various sense organs while optimizing detection of behaviorally relevant information. One prominent filtering phenomenon is prepulse inhibition (PPI), which is thought of as an early sensory gate that reduces the sensory information of a secondary event (pulse) while a preceding event (prepulse) is being processed (Graham 1975;Hoffman and Ison 1980;Koch 1999). Experimentally, PPI is produced when a startling stimulus (pulse) is preceded within 20 -1,000 ms by a subthreshold stimulus (prepulse) of the same or another modality (Graham 1975;Hoffman and Ison 1980;Koch 1999). The multimodal nature of PPI distinguishes it from unimodal synaptic modulations such as pairedpulse depression and short-term habituation (Aubert et al. 2006;Campeau and Davis 1995;Simons-Weidenmaier et al. 2006). The majority ...

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Section: Discussionmentioning

confidence: 99%

Dopaminergic-induced changes in Mauthner cell excitability disrupt prepulse inhibition in the startle circuit of goldfish

Medan

Preuss

2011

Journal of Neurophysiology

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“…Thus, GIRK channels are important regulators of electrical excitability in neurons. Neuronal GIRK channels mediate the inhibitory effect of numerous neurotransmitters including opioids, acetylcholine, adenosine, dopamine, γ-aminobutyric acid (GABA), glutamate, serotonin, norepinephrine, somatostatin, and neuropeptide Y ( Jaén & Doupnik, 2005;Lüscher et al, 1997;North, 1989;Sosulina, Schwesig, Seifert, & Pape, 2008;Witkowski, Szulczyk, Rola, & Szulczyk, 2008) by stimulating their cognate GPCRs, which couple to the G i/o family of G proteins. The opening of GIRK channels following GPCR activation decreases membrane excitability by hyperpolarizing the membrane potential and opposing membrane depolarization (Dascal, 1997).…”

Section: Molecular Organization and Heterogeneity Of Girk Channelsmentioning

confidence: 99%

Localization and Targeting of GIRK Channels in Mammalian Central Neurons

Luján

Aguado

2015

International Review of Neurobiology

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“…kinases that regulate ion channel conductances independent of AC-cAMP (15). Ultimately, K-channel conductance is decreased and conductances of Ca-channels, Na-channels, and nonspecific cation-channels are increased (2,11,32,50).…”

Section: Discussionmentioning

confidence: 99%

D1/D2-dopamine receptor agonist dihydrexidine stimulates inspiratory motor output and depresses medullary expiratory neurons

Lalley

2009

American Journal of Physiology-Regulatory, Integrative and Comp

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It is now accepted that dopamine plays an important neuromodulatory role in the central nervous control of respiration. D1, D2, and D4 subtypes of the receptor seem to be important players, but the assignment of various respiratory tasks to specific subtypes of the dopamine receptor is a work in progress. In the present investigation, dihydrexidine (DHD), a full dopamine receptor agonist with affinity for both D1- and D2-subtypes of receptor, was tested for its effects on inspiratory neurons and motor output and on membrane potential properties of medullary bulbospinal expiratory augmenting expiratory neurons in the pentobarbital anesthetized adult cat. The effects of DHD were compared with those of the highly selective D1-dopamine receptor (D1R) agonists SKF-38393 and 6-chloro-APB. DHD increased the intensity and duration of inspiratory motor output. Phrenic nerve discharge intensity was increased and prolonged, contributing to elevated inspiratory effort and duration when spontaneous breathing was monitored with tracheal pressure measurements. Intracellular recording from rostral medullary inspiratory neurons revealed that DHD, like SKF-38393, increases and prolongs inspiratory phase membrane depolarization, resulting in a longer and more intense discharge of action potentials. Remarkably, DHD had opposite effects on Aug-E neurons. Membrane potential was hyperpolarized, and action potential discharges were suppressed or abolished. In association with reduction of discharge intensity, action potential half width was reduced and after-hyperpolarization increased. The stimulatory action of DHD on inspiratory motor output is attributed to D1R effects, while the depression of Aug-E neurons seems to be linked to D2R actions on the postsynaptic membrane.

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D1 dopaminergic control of G protein–dependent inward rectifier K+ (GIRK)–like channel current in pyramidal neurons of the medial prefrontal cortex

Cited by 49 publications

References 56 publications

Dopaminergic-induced changes in Mauthner cell excitability disrupt prepulse inhibition in the startle circuit of goldfish

Dopaminergic-induced changes in Mauthner cell excitability disrupt prepulse inhibition in the startle circuit of goldfish

Localization and Targeting of GIRK Channels in Mammalian Central Neurons

D1/D2-dopamine receptor agonist dihydrexidine stimulates inspiratory motor output and depresses medullary expiratory neurons

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