Synaptic inhibition of the M‐current: slow excitatory post‐synaptic potential mechanism in bullfrog sympathetic neurones.

Adams, Patrick W.; Brown, David A.

doi:10.1113/jphysiol.1982.sp014412

Cited by 145 publications

(55 citation statements)

References 22 publications

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“…In an attempt to isolate the KCNQ channel currents from other voltage-gated K ϩ currents, the membrane potential was held at a relatively depolarized potential (V H , Ϫ30 mV) to activate KCNQ channels (Brown and Adams, 1980;Adams and Brown, 1982) and to inactivate many of the other K ϩ channels that activate in this membrane potential region (Nisenbaum et al, 1996;Tkatch et al, 2000;Shen et al, 2004). The membrane potential was then stepped down to more hyperpolarized potentials for 4 s to deactivate the KCNQ channels ( Fig.…”

Section: Resultsmentioning

confidence: 99%

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Cholinergic Suppression of KCNQ Channel Currents Enhances Excitability of Striatal Medium Spiny Neurons

Shen¹,

Hamilton²,

Nathanson³

et al. 2005

J. Neurosci.

205

165

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In response to glutamatergic synaptic drive, striatal medium spiny neurons in vivo transition to a depolarized "up state" near spike threshold. In the up state, medium spiny neurons either depolarize enough to spike or remain below spike threshold and are silent before returning to the hyperpolarized "down state." Previous work has suggested that subthreshold K ϩ channel currents were responsible for this dichotomous behavior, but the channels giving rise to the current and the factors determining its engagement have been a mystery. To move toward resolution of these questions, perforated-patch recordings from medium spiny neurons in tissue slices were performed.

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Section: Resultsmentioning

confidence: 99%

“…They were originally called "M-channels" because of their suppression by muscarinic receptor signaling (Brown and Adams, 1980;Adams and Brown, 1982;Jones, 1985). One of the most prominent modulators of medium spiny neurons is acetylcholine (Bolam et al, 1984;Kawaguchi, 1993).…”

Section: Introductionmentioning

confidence: 99%

Cholinergic Suppression of KCNQ Channel Currents Enhances Excitability of Striatal Medium Spiny Neurons

Shen¹,

Hamilton²,

Nathanson³

et al. 2005

J. Neurosci.

205

165

View full text Add to dashboard Cite

show abstract

“…NEUROPSYCHOPHARMACOLOGY 1993-VOL. 9, NO.3 Similarly, the muscarinic responses, the slow EPSP and EPSC, whether at the ganglia or in the CNS, in volve diverse currents that include several types of K + and Ca + + currents; particularly well studied is the voltage-dependent Paul Adam's K + current (M -cur rent; Adams and Brown 1982; see also Schimerlik 1990). Second-messenger mechanisms mediate these mus carinic responses (see the section Second Messengers), and these mechanisms and the currents that they gener ate are specifIc for the different muscarinic channel receptor macromolecule subtypes.…”

Section: Electrophysiological Postsynaptic Aspects Of Cholinergic Synmentioning

confidence: 99%

Brief Presentation of the Story and Present Status of Studies of the Vertebrate Cholinergic System

Karczmar

1993

Neuropsychopharmacol

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This year marks the seventieth anniversary of Otto Loewi's demonstration of chemical transmission generally and autonomic cholinergic transmission specifically and the fortieth anniversary of John Eccles's proof of the existence of central cholinergic transmission. Following these epochal findings, the subsequent studies of the cholinergic system led to discoveries of similarly important phenomena. This review concerns these phenomena, including chemical structure and molecular biology of cholinergic receptors; electrophysiologic and ionic aspects of pre-and postsynaptic cholinergic events; the quantal expression of cholinergic postsynaptic events and activities of their subunits, the elementary events; and teratology; trophic phenomena; and the clinical aspects of the cholinergic system. This review refers to the history as well as the present status of each of these phenomena; furthermore, it describes briefly the nineteenth-century work with calabar bean, pilocarpine, muscarine, and nicotine, that is, the work performed before the promulgation of the cholinergic era.[ Neuropsychopharmacology 9:181-199, 1993J included the frrst descriptions of the trophic phenomena, the quantal nature of the biological events, the recep tors and their chemical structure, the role of a trans mittive system in arousal and memory, and so on. So, it is appropriate to sketch at this time the history and the present status of the vertebrate cholinergic studies.

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“…In bullfrog sympathetic neurons, activation of muscarinic receptors by acetylcholine released presynaptically causes the slow excitatory postsynaptic potential, due to suppression of the M-current (Z,) (Adams and Brown, 1982), a noninactivating voltage-dependent potassium current (Brown and Adams, 1980;Adams et al, 1982a,b). Blockade of Z, leads to depolarization of the membrane potential, an increase in cell input resistance, and an increase in neuronal excitability (reviewed in Adams et al, 1986).…”

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confidence: 99%

On the role of arachidonic acid in M-current modulation by muscarine in bullfrog sympathetic neurons

Villarroel

1994

J. Neurosci.

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The modulation by muscarine or LHRH of the potassium M-current (IM) in whole-cell voltage-clamped bullfrog sympathetic neurons presents an initial phase of current reduction, followed, after agonist removal, by a transient enhancement or “overrecovery.” Employing a fast solution exchange system, an inhibitory process and an enhancing process were distinguished kinetically. The extent of overrecovery increased with the extent of the preceding inhibition. The rate and degree of inhibition increased with the concentration of agonist. In contrast, the rate of recovery and the extent of overrecovery were independent. The half-lives of the inhibitory and enhancing processes were 21 and 53 sec, respectively. Several observations suggest that arachidonic acid (AA) may be involved in overrecovery: (1) AA enhanced IM in a dose- dependent and reversible manner, with an IC50 of 2.8 microM. (2) Muscarine inhibited the A-current (IA), a potassium current that is blocked by AA. (3) Phospholipase A2 inhibitors (quinacrine and bromophenacyl bromide) and a lipoxygenase inhibitor (nordihydroguaiaretic acid) prevented overrecovery, without affecting the rate or extent of IM inhibition significantly. However, kinetic analysis indicates that these drugs were preventing overrecovery by prolonging the half-life of the inhibitory process to > 80 sec (e.g., not necessarily by blocking the enhancing pathway). In addition, the extent of IA inhibition was less than expected if AA was mediating both IM enhancement and IA inhibition. The observed relation between extent and rate of overrecovery, and the action of arachidonic acid metabolism inhibitors can be accounted for by a model proposing that the agonist alters the equilibrium between three pools of M-channels.

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Synaptic inhibition of the M‐current: slow excitatory post‐synaptic potential mechanism in bullfrog sympathetic neurones.

Cited by 145 publications

References 22 publications

Cholinergic Suppression of KCNQ Channel Currents Enhances Excitability of Striatal Medium Spiny Neurons

Cholinergic Suppression of KCNQ Channel Currents Enhances Excitability of Striatal Medium Spiny Neurons

Brief Presentation of the Story and Present Status of Studies of the Vertebrate Cholinergic System

On the role of arachidonic acid in M-current modulation by muscarine in bullfrog sympathetic neurons

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