Burst‐patterned stimulation promotes nicotinic transmission in isolated perfused rat sympathetic ganglia.

Birks, R. I.; Isacoff, Ehud Y.

doi:10.1113/jphysiol.1988.sp017218

Cited by 14 publications

(9 citation statements)

References 33 publications

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“…In two experiments the distribution of evoked EPSP amplitudes could be described by a simple binomial distribution, in agreement with previous reports where transmitter release at some SCG synapses was fitted successfully by a binomial model (McLachlan, 1975;Bennett, Florin & Pettigrew, 1976;Birks & Isacoff, 1988). Of these two cases, histamine potentiated EPSPs and increased p values in one (Fig.…”

Section: Mediation Of Synaptic Depression By Two Different Histamine supporting

confidence: 90%

Presynaptic histamine H1 and H3 receptors modulate sympathetic ganglionic synaptic transmission in the guinea‐pig.

Christian

Weinreich

1992

The Journal of Physiology

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SUMMARY1. To study the effects of histamine on the efficacy of sympathetic ganglionic synaptic transmission, extracellular recordings of the postganglionic compound action potential (CAP) and intracellular recordings of excitatory postsynaptic potentials (EPSPs) elicited by preganglionic electrical stimulation were obtained from isolated guinea-pig superior cervical ganglia (SCG).2. In different preparations, superfusion with histamine (0 1-100 /IM) either potentiated or depressed the postganglionic CAP elicited by electrical stimulation of the cervical sympathetic trunk (0-2-3-0 Hz). The direction of response produced by histamine did not depend on stimulation frequency or histamine concentration; potentiation and depression both showed concentration dependence over the range of histamine concentrations tested.3. Experiments employing a variety of histamine receptor agonists or antagonists revealed that histamine-induced potentiation of the postganglionic CAP could be attributed to histamine H1 receptor activation, and depression to H3 receptor activation.4. Histamine similarly potentiated or depressed the intracellularly recorded EPSP. However, these opposite effects occurred at different synapses. In agreement with the studies on the postganglionic CAP, histamine H1 antagonists prevented histamine-induced potentiation of the EPSP and H3 receptor antagonists prevented histamine-induced depression.5. Direct quantal analyses of histamine-induced synaptic potentiation and depression were implemented to determine the pre-and postsynaptic components of these effects. Quantal size was estimated by measuring the amplitude of spontaneous miniature EPSP amplitudes. Histamine-induced potentiation and depression of the evoked EPSP were found to be accompanied by increased or decreased quantal content respectively, and unchanged quantal size, providing evidence that presynaptic mechanisms were involved in mediating both effects.6. Some guinea-pigs were actively sensitized to ovalbumin. Subsequent exposure

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Section: Mediation Of Synaptic Depression By Two Different Histamine supporting

confidence: 90%

Presynaptic histamine H1 and H3 receptors modulate sympathetic ganglionic synaptic transmission in the guinea‐pig.

Christian

Weinreich

1992

The Journal of Physiology

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“…At relatively low frequencies (i.e., ≤1 Hz), repeatedly stimulating the afferent nerve has little effect on EPSP amplitude. However, with increasingly higher frequencies, EPSP amplitude passes the following three stages: (1) initial facilitation (or depression) (Birks and Isacoff ), which is followed by (2) depression due to the depletion of presynaptic ACh stores (Bennett and McLachlan ), followed by (3) steady‐state activity maintained by the synthesis of new ACh molecules (Bennett and McLachlan ). In addition, synaptic transmission can also be affected by receptor desensitization (Papke et al.…”

Section: Discussionmentioning

confidence: 99%

The role of the nAChR subunits α 5, β 2, and β 4 on synaptic transmission in the mouse superior cervical ganglion

et al. 2019

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Our previous immunoprecipitation analysis of nicotinic acetylcholine receptors ( nAChR s) in the mouse superior cervical ganglion ( SCG ) revealed that approximately 55%, 24%, and 21% of receptors are comprised of α 3 β 4, α 3 β 4 α 5, and α 3 β 4 β 2 subunits, respectively. Moreover, mice lacking β 4 subunits do not express α 5‐containing receptors but still express a small number of α 3 β 2 receptors. Here, we investigated how synaptic transmission is affected in the SCG of α 5 β 4‐ KO and α 5 β 2‐ KO mice. Using an ex vivo SCG preparation, we stimulated the preganglionic cervical sympathetic trunk and measured compound action potentials ( CAP s) in the postganglionic internal carotid nerve. We found that CAP amplitude was unaffected in α 5 β 4‐ KO and α 5 β 2‐ KO ganglia, whereas the stimulation threshold for eliciting CAP s was significantly higher in α 5 β 4‐ KO ganglia. Moreover, intracellular recordings in SCG neurons revealed no difference in EPSP amplitude. We also found that the ganglionic blocking agent hexamethonium was the most potent in α 5 β 4‐ KO ganglia ( IC 50 : 22.1 μ mol/L), followed by α 5 β 2‐ KO ( IC 50 : 126.7 μ mol/L) and WT ganglia ( IC 50 : 389.2 μ mol/L). Based on these data, we estimated an IC 50 of 568.6 μ mol/L for a receptor population consisting solely of α 3 β 4 α 5 receptors; and we estimated that α 3 β 4 α 5 receptors comprise 72% of nAChR s expressed in the mouse SCG . Similarly, by measuring the effects of hexamethonium on AC h‐induced currents in cultured SCG neurons, we found that α 3 β ...

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“…Thus, presynaptic depression may play a more dominant role in the short-term depression of cholinergic transmission onto GABAergic neurons. Indeed, repetitive stimulation at 2–20 Hz has been shown to cause short-term depression of nicotinic EPSPs via a presynaptic mechanism in cervical sympathetic ganglion neurons (Birks and Isacoff, 1988). …”

Section: Discussionmentioning

confidence: 99%

Recurrent Inhibitory Network among Striatal Cholinergic Interneurons

Sullivan¹,

Chen²,

Morikawa³

2008

J. Neurosci.

118

122

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The striatum plays a central role in sensorimotor learning and action selection. Tonically active cholinergic interneurons in the striatum give rise to dense axonal arborizations and significantly shape striatal output. However, it is not clear how the activity of these neurons is regulated within the striatal microcircuitry. In this study, using rat brain slices, we find that stimulation of intrastriatal cholinergic fibers evokes polysynaptic GABA A IPSCs in cholinergic interneurons. These polysynaptic GABA A IPSCs were abolished by general nicotinic acetylcholine receptor antagonists and also by a specific antagonist of nicotinic receptors containing ␤2 subunits. Dopamine receptor antagonists or dopamine depletion failed to block polysynaptic IPSCs, indicating that phasic dopamine release does not directly mediate the polysynaptic transmission. Dual recording from pairs of cholinergic interneurons revealed that activation of a single cholinergic interneuron is capable of eliciting polysynaptic GABA A IPSCs both in itself and in nearby cholinergic interneurons. Although polysynaptic transmission arising from a single cholinergic interneuron was depressed during repetitive 2 Hz firing, intrastriatal stimulation reliably evoked large polysynaptic IPSCs by recruiting many cholinergic fibers. We also show that polysynaptic GABAergic inhibition leads to a transient suppression of tonic cholinergic interneuron firing. We propose a novel microcircuit in the striatum, in which cholinergic interneurons are connected to one another through GABAergic interneurons. This may provide a mechanism to convert activation of cholinergic interneurons into widespread recurrent inhibition of these neurons via nicotinic excitation of striatal GABAergic neurons.

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Burst‐patterned stimulation promotes nicotinic transmission in isolated perfused rat sympathetic ganglia.

Cited by 14 publications

References 33 publications

Presynaptic histamine H1 and H3 receptors modulate sympathetic ganglionic synaptic transmission in the guinea‐pig.

Presynaptic histamine H1 and H3 receptors modulate sympathetic ganglionic synaptic transmission in the guinea‐pig.

The role of the nAChR subunits α 5, β 2, and β 4 on synaptic transmission in the mouse superior cervical ganglion

Recurrent Inhibitory Network among Striatal Cholinergic Interneurons

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