Intracellular transduction mechanisms for the slow synaptic events

1992 ◽  
Vol 70 (S1) ◽  
pp. S44-S50 ◽  
Author(s):  
Haruo Kobayashi ◽  
Sumiko Mochida ◽  
Susumu Y. Takahashi
Keyword(s):  
Superior Cervical Ganglion ◽  
Action Potentials ◽  
Acetylcholine Receptors ◽  
Second Messengers ◽  
Muscarinic Acetylcholine Receptors ◽  
Characteristic Change ◽  
Receptor Subtypes ◽  
Cervical Ganglion ◽  
Cervical Ganglia ◽  
Ganglion Neurons

Electrical activities of the postganglionic neurons in the superior cervical ganglia of rabbits are modulated in various ways following activation of the subtypes of muscarinic acetylcholine receptors, (i) M1 receptors mediate a slow depolarization consisting of at least three types of ionic conductance changes, and one of these is possibly mediated by cyclic GMP. (ii) M2 receptors mediate a slow hyperpolarization that seems to be generated by inositol triphosphate derived from phosphatidylinositol breakdown. (iii) M2 receptors also cause, through an activation of C kinase, a suppression of Ca entry during action potentials that results in a characteristic change in the action potentials and thereby modulates excitability of superior cervical ganglion neurons. Each subtype of muscarinic receptors thus regulates different pathways of intracellular transduction and modulates the electrical signaling of sympathetic neurons.Key words: superior cervical ganglion, electrical signals, muscarinic responses, muscarinic receptor subtypes, second messengers.

M1 and M2 Muscarinic Acetylcholine Receptor Subtypes Mediate Ca2+ Channel Current Inhibition in Rat Sympathetic Stellate Ganglion Neurons

2006 ◽  
Vol 96 (5) ◽  
pp. 2479-2487 ◽  
Author(s):  
Qing Yang ◽  
Andrew D. Sumner ◽  
Henry L. Puhl ◽  
Victor Ruiz-Velasco
Keyword(s):  
Acetylcholine Receptors ◽  
Stellate Ganglion ◽  
Muscarinic Acetylcholine Receptor ◽  
Muscarinic Acetylcholine Receptors ◽  
Receptor Subtypes ◽  
Muscarinic Acetylcholine ◽  
Peripheral Neurons ◽  
Voltage Dependent ◽  
Ganglion Neurons ◽  
Channel Currents

Muscarinic acetylcholine receptors (mAChRs) are known to mediate the acetylcholine inhibition of Ca2+ channels in central and peripheral neurons. Stellate ganglion (SG) neurons provide the main sympathetic input to the heart and contribute to the regulation of heart rate and myocardial contractility. Little information is available regarding mAChR regulation of Ca2+ channels in SG neurons. The purpose of this study was to identify the mAChR subtypes that modulate Ca2+ channel currents in rat SG neurons innervating heart muscle. Accordingly, the modulation of Ca2+ channel currents by the muscarinic cholinergic agonist, oxotremorine-methiodide (Oxo-M), and mAChR blockers was examined. Oxo-M–mediated mAChR stimulation led to inhibition of Ca2+ currents through voltage-dependent (VD) and voltage-independent (VI) pathways. Pre-exposure of SG neurons to the M1 receptor blocker, M1-toxin, resulted in VD inhibition of Ca2+ currents after Oxo-M application. On the other hand, VI modulation of Ca2+ currents was observed after pretreatment of cells with methoctramine (M2 mAChR blocker). The Oxo-M–mediated inhibition was nearly eliminated in the presence of both M1 and M2 mAChR blockers but was unaltered when SG neurons were exposed to the M4 mAChR toxin, M4-toxin. Finally, the results from single-cell RT-PCR and immunofluorescence assays indicated that M1 and M2 receptors are expressed and located on the surface of SG neurons. Overall, the results indicate that SG neurons that innervate cardiac muscle express M1 and M2 mAChR, and activation of these receptors leads to inhibition of Ca2+ channel currents through VI and VD pathways, respectively.

Activity of in situ middle cervical ganglion neurons in dogs, using extracellular recording techniques

1985 ◽  
Vol 63 (6) ◽  
pp. 704-716 ◽  
Author(s):  
J. A. Armour
Keyword(s):  
Neuronal Activity ◽  
Action Potentials ◽  
Vena Cava ◽  
Extracellular Recording ◽  
Cervical Ganglion ◽  
Cervical Ganglia ◽  
Ganglion Neurons ◽  
Stimulation Of ◽  
Recording Techniques

Neuronal activity in the in situ middle cervical ganglion of dogs was investigated using extracellular recording techniques. The recorded action potentials were frequently active during specific phases of the cardiac cycle, particularly during systole, and this activity persisted following acute decentralization of the ganglion. The activity of these action potentials was modified when systemic arterial pressure was altered by isoproterenol, noradrenaline, adrenaline, or partial occlusion of the aorta, whether in the intact or acutely decentralized preparation. These neurons were active between systolic pressures of 70 and 180 mmHg (1 mmHg = 133.322 Pa). Action potentials were frequently modified by mechanical distortion of the superior vena cava, ventricular epicardium, or adventitia of the aorta, whether the preparation was acutely decentralized or not. Seventy percent of these action potentials were unaffected by stimulation (1 ms, 4 V, 0.5 Hz) of a cardiopulmonary nerve and 27% were suppressed by such stimulation. Five of the neurons were activated by such stimulation. It is presumed that the latter neurons had axons in a cardiopulmonary nerve and most likely were efferent sympathetic postganglionic neurons. Sixty-three percent of these spontaneously active phase-locked units were modified by stimulation of a ramus or an ansa. It is postulated that some of the neurons in the middle cervical ganglia can be modified by afferent axons arising from receptors in thoracic organs, in particular from the great vessels and heart, whether in an intact or acutely decentralized preparation. The majority of these neurons are presumed not to be afferent neurons or efferent postganglionic neurons, as they are not activated directly by electrical stimulation of axons in cardiopulmonary nerves. Rather they are presumed to be interneurons. These results lend support to the thesis that considerable integration of neuronal activity related to thoracic cardiovascular dynamics occurs within the middle cervical ganglia of dogs.

Evidence for a Blood Ganglion Barrier in the Superior Cervical Ganglion of the Rat

1982 ◽  
Vol 40 ◽  
pp. 204-204
Author(s):  
D. M. DePace
Keyword(s):  
Blood Vessels ◽  
Superior Cervical Ganglion ◽  
Peripheral Nerves ◽  
Time Schedule ◽  
Transmission Electron ◽  
Cervical Ganglion ◽  
The Central Nervous System ◽  
Cervical Ganglia ◽  
Capillary Circulation ◽  
And Control

The majority of blood vessels in the superior cervical ganglion possess a continuous endothelium with tight junctions. These same features have been associated with the blood brain barrier of the central nervous system and peripheral nerves. These vessels may perform a barrier function between the capillary circulation and the superior cervical ganglion. The permeability of the blood vessels in the superior cervical ganglion of the rat was tested by intravenous injection of horseradish peroxidase (HRP). Three experimental groups of four animals each were given intravenous HRP (Sigma Type II) in a dosage of.08 to.15 mg/gm body weight in.5 ml of.85% saline. The animals were sacrificed at five, ten or 15 minutes following administration of the tracer. Superior cervical ganglia were quickly removed and fixed by immersion in 2.5% glutaraldehyde in Sorenson's.1M phosphate buffer, pH 7.4. Three control animals received,5ml of saline without HRP. These were sacrificed on the same time schedule. Tissues from experimental and control animals were reacted for peroxidase activity and then processed for routine transmission electron microscopy.

Neuromodulation of Dendritic Action Potentials

1999 ◽  
Vol 81 (1) ◽  
pp. 408-411 ◽  
Author(s):  
Dax A. Hoffman ◽  
Daniel Johnston
Keyword(s):  
Protein Kinase ◽  
Action Potential ◽  
Action Potentials ◽  
Acetylcholine Receptors ◽  
Muscarinic Acetylcholine Receptors ◽  
Action Potential Amplitude ◽  
Neurotransmitter System ◽  
Potential Amplitude ◽  
Hippocampal Ca1 ◽  
Dopaminergic Neurotransmitter

Hoffman, Dax A. and Daniel Johnston. Neuromodulation of dendritic action potentials. J. Neurophysiol. 81: 408–411, 1999. The extent to which regenerative action potentials invade hippocampal CA1 pyramidal dendrites is dependent on both recent activity and distance from the soma. Previously, we have shown that the amplitude of back-propagating dendritic action potentials can be increased by activating either protein kinase A (PKA) or protein kinase C (PKC) and a subsequent depolarizing shift in the activation curve for dendritic K+ channels. Physiologically, an increase in intracellular PKA and PKC would be expected upon activation of β-adrenergic and muscarinic acetylcholine receptors, respectively. Accordingly, we report here that activation of either of these neurotransmitter systems results in an increase in dendritic action-potential amplitude. Activation of the dopaminergic neurotransmitter system, which is also expected to raise intracellular adenosine 3′,5′-cyclic monophosphate (cAMP) and PKA levels, increased action-potential amplitude in only a subpopulation of neurons tested.

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