Muscarinic slow excitation and muscarinic inhibition of synaptic transmission in the rat neostriatum.

Dodt, Hans Ulrich; Misgeld, U.

doi:10.1113/jphysiol.1986.sp016304

Cited by 70 publications

(38 citation statements)

References 36 publications

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“…In a substantial number of non-histamine-responding neurones, however, ACh induced a net inward current, possibly resulting from the reduction of IM. This is consistent with the report that ACh reduces a voltage-dependent K+ conductance that is identical to IM in principal neurones (Dodt & Misgeld, 1986). Therefore, the reduction of K+ current might be elicited in large aspiny neurones which serve as cholinergic interneurones.…”

Section: Discussionsupporting

confidence: 92%

“…Most interneurones are known to be cholinergic and project to principal neurones in the neostriatum. Endogenous and exogenous ACh modifies the activities of rat neostriatal neurones through the reduction of K+ conductance (Dodt & Misgeld, 1986), which has been partly shown in the present study. Moreover, a voltage-dependent transient K+ conductance in cultured neurones of the rat neostriatum is also affected by ACh (Akins, Surmeier & Kitai, 1990).…”

supporting

confidence: 73%

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Regulation of K+ conductance by histamine H1 and H2 receptors in neurones dissociated from rat neostriatum.

Munakata¹,

Akaike²

1994

The Journal of Physiology

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1. The effects of histamine on dissociated neostriatal neurones of the rat were investigated in the whole-cell mode using the nystatin-perforated patch recording technique. 2. Histamine evoked a net inward current accompanied by a decrease in the membrane conductance at a holding potential (Vh) of -44 mV. This response was observed in neurones considered to be interneurones based on morphology, membrane properties and the responsiveness to acetylcholine.3. A net inward current evoked by 10'-to 106 M histamine was inhibited in a concentration-dependent manner by the H1 receptor antagonists, pyrilamine and triprolidine. The H1 receptor agonists, 2-methylhistamine and 2-thiazolylethylamine, mimicked the histamine response, indicating that this response was mediated by the H, receptor.4. Histamine, at high concentrations between 10-6 and 10'-M, evoked an additional net inward current with a decrease in the membrane conductance, which was inhibited by the H2 receptor antagonists, cimetidine, ranitidine and famotidine. The H2 receptor agonist, impromidine, partially mimicked the response. Thus, this additional current was considered to be mediated by the H2 receptor. 5. The reversal potentials for H1 and H2 receptor-operated currents shifted 56-9 and 59.3 mV for a 10-fold change in [K+]O, respectively, suggesting that these currents were carried by K+.6. An analysis of change in current fluctuations mediated by H1 and H2 receptors suggested that the unitary current amplitudes of K+ channels linked to H1 and H2 receptors were 0-29 + 0-06 (n = 4) and 0'27 + 0 07 pA (n = 4), respectively. There was no significant difference between these values. The estimated mean life times (r) for both channels were also identical (1 1 ms). 7. It was concluded that histamine reduces K+ currents in neostriatal interneurones and that both H1 and H2 receptors are involved in the response.

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Section: Discussionsupporting

confidence: 92%

supporting

confidence: 73%

Regulation of K+ conductance by histamine H1 and H2 receptors in neurones dissociated from rat neostriatum.

Munakata¹,

Akaike²

1994

The Journal of Physiology

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“…2A and B, right panels) but not by hexamethonium (10-50 /LM, n = 8). In addition, both actions of carbachol were mimicked by superfusion of muscarine (1)(2)(3)(4)(5)(6)(7)(8)(9)(10) JtM, n = 8), oxotremorine (1 JtM, n = 3) and oxotremorine-M (1 /,M, n = 8), but not by the nicotinic agonist DMPP (10 /IM, n = 5), consistent with their mediation via a muscarinic receptor. Previous studies have suggested that the M1 receptor is involved in the muscarinic reduction of the AHP in hippocampal pyramidal cells (Dutar & Nicoll, 1988) and myenteric plexus neurons (Galligan, North & Tokimasa, 1989).…”

Section: S Washburn and H C Moisesmentioning

confidence: 99%

Muscarinic responses of rat basolateral amygdaloid neurons recorded in vitro.

Washburn

Moises

1992

The Journal of Physiology

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SUMMARY1. Intracellular recordings were obtained from pyramidal-type neurons in the basolateral amygdaloid nucleus (BLA) in slices of rat ventral forebrain and used to compare the actions of exogenously applied cholinomimetics to the effects produced by electrical stimulation of amygdalopetal cholinergic afferents from basal forebrain.2. Bath application of carbachol depolarized pyramidal cells with an associated increase in input resistance (Ri), reduced the slow after-hyperpolarization (AHP)that followed a series of current-evoked action potentials and blocked spike frequency accommodation. All of these effects were reversed by the muscarinic antagonist atropine but not by the nicotinic antagonist hexamethonium. 3. Electrical stimulation of amygdaloid afferents within the external capsule evoked a series of synaptic potentials consisting of a non-cholinergic fast excitatory postsynaptic potential (EPSP), followed by early and late inhibitory postsynaptic potentials (IPSPs). Each of these synaptic potentials was reduced by carbachol in an atropine-sensitive manner.4. Local application of carbachol to pyramidal cells produced a short-latency hyperpolarization followed by a prolonged depolarization. The hyperpolarization and depolarization to carbachol were blocked by atropine but not hexamethonium.5. The carbachol-induced hyperpolarization was associated with a decrease in Ri and had a reversal potential nearly identical to that of the early IPSP. The inhibitory response was blocked by perfusion of medium containing tetrodotoxin (TTX), bicuculline or picrotoxin, while the subsequent depolarization was unaffected. On the basis of these data, it is concluded that the muscarinic hyperpolarization is mediated through the rapid excitation of presynaptic GABAergic interneurons in the slice.6. The findings that the carbachol-induced depolarization was associated with an increase in Ri, often had a reversal potential below -80 mV, was sensitive to changes in extracellular potassium concentration and was blocked by intracellular ionophoresis of the potassium channel blocker caesium suggest that it resulted from a muscarinic blockade of one or more potassium conductances. M. S. WASHBURN AND H. C MOISES evoked a series of fast EPSPs followed by IPSPs. These non-cholinergic potentials were followed by a slow EPSP that lasted from 10 s-4 min. The slow EPSP was enhanced by eserine and blocked by atropine. It was also blocked by TTX or cadmium, indicating that it was dependent on spike propagation and calciumdependent release of acetylcholine (ACh).8. Stimulation of cholinergic afferents in the slice mimicked other effects produced by carbachol including blockade of the slow AHP and accommodation of action potential discharge and these actions were potentiated by eserine and blocked by atropine.9. The present results provide the first demonstration of muscarinic cholinergic actions in an area of the amygdala known to receive cholinergic innervation. These effects appear to involve both direct and indirect mechanisms.

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“…In the case of the amygdala, selective inhibition of these neurons could be helpful in certain epilepsies; the amygdala is among the most readily kindled of brain regions, and this is blocked by muscarinic antagonists (27,28). Conversely, selective agonists at M1 receptors would be expected to excite the principal cells of these regions by direct excitation (11,29) and by reduction of GABA-mediated feedback inhibition, while having no effect on the excitatory drive to the cells mediated by glutamate. The cholinergic innervation of the amygdala from the nucleus basalis is one site of the typical neurodegenerative changes associated with Alzheimer disease (1,30), and the present findings therefore point to the possible value of M1 agonists and M3 antagonists in this disease.…”

mentioning

confidence: 99%

Distinct muscarinic receptors inhibit release of gamma-aminobutyric acid and excitatory amino acids in mammalian brain.

Sugita

Uchimura

Jiang

et al. 1991

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

147

117

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Intracellular recordings were made from neurons of rat lateral amygdala, nucleus accumbens, and striatum in vitro. Synaptic potentials mediated by Y-aminobutyric acid and by excitatory amino acids were isolated pharmacologically by using receptor antagonists, and their amplitudes were used as a measure oftransmitter release. Mucanrne and acetylcholine inhibited the release of both y-aminobutyric acid and excitatory amino acids, but measurements of the dissociation equilibrium constants for the antagonists piren- ,4]benzodiazepine-6-one, methoctramine, and hexahydrosiladifenidol indicated clearly that different muscarinic receptors were involved (MI and probably M3, respectively). The differential localization of distinct muscarinc receptor subtypes on terminals releasing the major inhibitory and excitatory transmitters of the brain could be exploited therapeutically in some movement disorders and Alzheimer disease.Acetylcholine (AcCho) has diverse functional roles in the mammalian brain, including actions at muscarinic receptors that are important for memory (1). Cholinergic neurons are lost in Alzheimer disease, and one therapeutic approach has been to develop drugs that mimic the neurotransmitter action of missing AcCho (1). However, such drugs, like AcCho itself, will have different effects at different muscarinic receptors in the brain, and not all of these effects may be desired. Three muscarinic receptors (M1-M3) can be distinguished pharmacologically, but five (ml-mS) have been identified by molecular cloning (ml-m3 correspond to M1-M3) (2-8).Fibers containing 'y-aminobutyric acid (GABA) and excitatory amino acids such as glutamate provide synaptic inputs to virtually all central neurons; therefore, in addition to their direct effects on neurons (9, 10), muscarinic agonists will also excite or inhibit cells by acting presynaptically to change release of these neurotransmitters. In the present experiments, the release of GABA and excitatory amino acids (glutamate) was assayed by recording the amplitude of depolarizing synaptic potentials from neurons in three brain regions where AcCho is known to play an important functional role-the amygdala, nucleus accumbens, and striatum. METHODSAdult rats were anesthetized with halothane and killed by a heavy blow to the chest. The brain was rapidly removed, and a block of tissue containing nucleus accumbens, dorsal striatum, or amygdaloid complex was sectioned with a Vibratome. Intracellular recordings were made from slices (300 ,am thick) by using electrodes containing 2 M KCI (11-13).The superfusing solution was a bicarbonate buffer gassed with 95% 02/5% CO2 and contained 2.5 mM KCI, 2.4 mM CaC12, 1.3 mM MgCl2, 1.2 mM NaH2PO4, 26 mM NaHCO3, 126 mM NaCi, and 10 mM glucose. The slice was completely submerged in this flowing solution, which was prewarmed to 370C. Drugs were applied by changing this solution to one that contained the drug. A bipolar tungsten-in-glass stimulating electrode was used for focal stimulation. The components of the synaptic potential...

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Muscarinic slow excitation and muscarinic inhibition of synaptic transmission in the rat neostriatum.

Cited by 70 publications

References 36 publications

Regulation of K+ conductance by histamine H1 and H2 receptors in neurones dissociated from rat neostriatum.

Regulation of K+ conductance by histamine H1 and H2 receptors in neurones dissociated from rat neostriatum.

Muscarinic responses of rat basolateral amygdaloid neurons recorded in vitro.

Distinct muscarinic receptors inhibit release of gamma-aminobutyric acid and excitatory amino acids in mammalian brain.

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