Muscarinic receptor regulation of synaptic transmission in airway parasympathetic ganglia

1996 ◽  
Vol 270 (4) ◽  
pp. L630-L636 ◽  
Author(s):  
A. C. Myers ◽  
B. J. Undem
Keyword(s):  
Synaptic Transmission ◽  
Vagus Nerve ◽  
Muscarinic Receptor ◽  
Physiological Role ◽  
Receptor Activation ◽  
Significant Inhibition ◽  
Receptor Regulation ◽  
Parasympathetic Ganglia ◽  
Ganglion Neurons

Muscarinic receptor regulation of synaptic transmission in guinea pig bronchial parasympathetic ganglia was evaluated with the use of intracellular recording of the intrinsic ganglion neurons. Methacholine (1 microM) decreased the amplitude of vagus nerve-stimulated fast excitatory postsynaptic potentials (fEPSP) by 33 and 46% (at 0.8 and 8.0 Hz, respectively) but had no effect on the amplitude of the depolarizations evoked by a bath-applied nicotinic receptor agonist. Methoctramine (1 microM) inhibited methacholine's effect on fEPSP but alone did not influence the magnitude of the fEPSP evoked by vagus nerve stimulation. Methacholine (10 microM) depolarized a subpopulation of neurons (approximately 4 mV), which was blocked by pirenzepine (0.1 microM). In other neurons, either no effect or a small (1-5 mV) hyperpolarization was noted. Cholinergic contractions of bronchial smooth muscle elicited by electrical field stimulation were potentiated by methoctramine to the same extent as those evoked by vagus nerve (preganglionic) stimulation. The data indicate that M2 receptor activation can lead to inhibition of presynaptic acetylcholine release and consequently a significant inhibition of synaptic transmission in bronchial parasympathetic ganglia. The physiological role of this neuromodulatory effect appears limited, however, when studied in the in vitro setting.

Electrophysiological properties of neurons in guinea pig bronchial parasympathetic ganglia

1990 ◽  
Vol 259 (6) ◽  
pp. L403-L409 ◽  
Author(s):  
A. C. Myers ◽  
B. J. Undem ◽  
D. Weinreich
Keyword(s):  
Guinea Pig ◽  
Vagus Nerve ◽  
Action Potentials ◽  
Receptor Activation ◽  
Membrane Properties ◽  
Constant Current ◽  
Parasympathetic Ganglia ◽  
Stimulation Of ◽  
Passive Membrane

Active and passive membrane membrane properties of parasympathetic neurons were examined in vitro in a newly localized ganglion on the right bronchus of the guinea pig. Neurons could be classified as “tonic” or “phasic” based on their action potential discharge response to suprathreshold depolarizing constant current steps. Tonic neurons (39%) responded with repetitive action potentials sustained throughout the current step, whereas phasic neurons (61%) responded with an initial burst of action potentials at the onset of the step but then accommodated. Tonic and phasic neurons could not be differentiated by other active or passive membrane properties. Electrical stimulation of the vagus nerve elicited one to three temporally distinct fast nicotinic excitatory potentials, and tetanic stimulation of the vagus nerve evoked slow depolarizing (10% of neurons) and hyperpolarizing (25% of neurons) potentials; the latter was mimicked by muscarinic receptor activation. Similar slow and fast postsynaptic potentials were observed in both tonic and phasic neurons. We suggest neurons within the bronchial ganglion possess membrane and synaptic properties capable of integrating presynaptic stimuli.

Role of cyclooxygenase activation and prostaglandins in antigen-induced excitability changes of bronchial parasympathetic ganglia neurons

2003 ◽  
Vol 284 (4) ◽  
pp. L581-L587 ◽  
Author(s):  
Radhika Kajekar ◽  
Bradley J. Undem ◽  
Allen C. Myers
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Synaptic Transmission ◽  
Cyclooxygenase Inhibitors ◽  
Antigen Challenge ◽  
Parasympathetic Nerve ◽  
Parasympathetic Ganglia ◽  
Parasympathetic Ganglion ◽  
Ganglion Neurons

In vitro antigen challenge has multiple effects on the excitability of guinea pig bronchial parasympathetic ganglion neurons, including depolarization, causing phasic neurons to fire with a repetitive action potential pattern and potentiating synaptic transmission. In the present study, guinea pigs were passively sensitized to the antigen ovalbumin. After sensitization, the bronchi were prepared for in vitro electrophysiological intracellular recording of parasympathetic ganglia neurons to investigate the contribution of cyclooxygenase activation and prostanoids on parasympathetic nerve activity. Cyclooxygenase inhibition with either indomethacin or piroxicam before in vitro antigen challenge blocked the change in accommodation. These cyclooxygenase inhibitors also blocked the release of prostaglandin D2 (PGD2) from bronchial tissue during antigen challenge. We also determined that PGE2 and PGD2 decreased the duration of the action potential after hyperpolarization, whereas PGF2α potentiated synaptic transmission. Thus prostaglandins released during antigen challenge have multiple effects on the excitability of guinea pig bronchial parasympathetic ganglia neurons, which may consequently affect the output from these neurons and thereby alter parasympathetic tone in the lower airways.

Cholinergic modulation of synaptic inhibition in the guinea pig hippocampus in vitro: excitation of GABAergic interneurons and inhibition of GABA-release

1993 ◽  
Vol 69 (2) ◽  
pp. 626-629 ◽  
Author(s):  
J. C. Behrends ◽  
G. ten Bruggencate
Keyword(s):  
Guinea Pig ◽  
Synaptic Transmission ◽  
Pyramidal Neurons ◽  
Gaba Release ◽  
Cholinergic Receptor ◽  
Receptor Activation ◽  
Release Mechanism ◽  
Gabaergic Interneurons ◽  
Gamma Aminobutyric Acid

1. The effect of cholinergic receptor activation on gamma-aminobutyric acid (GABA)-mediated inhibitory synaptic transmission was investigated in voltage-clamped CA1 pyramidal neurons (HPNs) in the guinea pig hippocampal slice preparation. 2. The cholinergic agonist carbachol (1-10 microM) induced a prominent and sustained increase in the frequency and amplitudes of spontaneous inhibitory postsynaptic currents (IPSCs) in Cl(-)-loaded HPNs. The potentiation of spontaneous IPSCs was not dependent on excitatory synaptic transmission but was blocked by atropine (1 microM). 3. Monosynaptically evoked IPSCs were reversibly depressed by carbachol (10 microM). 4. The frequency of miniature IPSCs recorded in the presence of tetrodotoxin (0.6 or 1.2 microM) was reduced by carbachol (10 or 20 microM) in an atropine-sensitive manner. 5. We conclude that, while cholinergic receptor activation directly excites hippocampal GABAergic interneurons, it has, in addition, a suppressant effect on the synaptic release mechanism at GABAergic terminals. This dual modulatory pattern could explain the suppression of evoked IPSCs despite enhanced spontaneous transmission.

Barbiturates depress vagal motor pathway to ferret trachea at ganglia

1982 ◽  
Vol 53 (1) ◽  
pp. 253-257 ◽  
Author(s):  
B. E. Skoogh ◽  
M. J. Holtzman ◽  
J. R. Sheller ◽  
J. A. Nadel
Keyword(s):  
Neuromuscular Junction ◽  
Vagus Nerve ◽  
Muscle Tension ◽  
Postsynaptic Membrane ◽  
Nerve Fibers ◽  
Motor Pathway ◽  
Parasympathetic Ganglia ◽  
Before And After ◽  
Nerve Muscle

To determine which site in the vagal motor pathway to airway smooth muscle is most sensitive to depression by barbiturates, we recorded isometric muscle tension in vitro and stimulated the vagal motor pathway at four different sites before and after exposure to barbiturates. In isolated tracheal rings from ferrets, we stimulated muscarinic receptors in the neuromuscular junction by exogenous acetylcholine, postganglionic nerve fibers by electrical fluid stimulation, and the postsynaptic membrane in ganglia by 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP). We also developed a tracheal nerve-muscle preparation to stimulate preganglionic fibers in the vagus nerve electrically. Activation of ganglia by DMPP or by vagus nerve stimulation was depressed by barbiturates at 10-fold lower concentrations than those depressing the activation of postganglionic nerves or the neuromuscular junction. These findings suggest that the postsynaptic membrane in parasympathetic ganglia is the site in the vagal motor pathway most sensitive to depression by barbiturates.

A muscarinic receptor subtype modulates vagally stimulated bronchial contraction

1988 ◽  
Vol 65 (5) ◽  
pp. 2144-2150 ◽  
Author(s):  
J. W. Bloom ◽  
C. Baumgartener-Folkerts ◽  
J. D. Palmer ◽  
H. I. Yamamura ◽  
M. Halonen
Keyword(s):  
Smooth Muscle ◽  
Muscarinic Receptor ◽  
Vagal Stimulation ◽  
Receptor Subtype ◽  
Inhibitory Effects ◽  
Main Stem Bronchus ◽  
Parasympathetic Ganglia ◽  
Excitatory Neurotransmission ◽  
Inhibition Studies

An in vitro preparation was developed to study vagus nerve-stimulated (preganglionic) and field-stimulated (post-ganglionic) contraction of the rabbit main stem bronchus and to compare the inhibitory effects of muscarinic antagonists on that contraction. The maximal contractile responses (20 V, 0.5 ms, 64 Hz) for either field or vagal stimulation were completely abolished by atropine (60 nM). Hexamethonium (0.1 mM) abolished the response to vagal stimulation but did not affect the field-stimulated response. To compare the effectiveness of atropine and pirenzepine as antagonists at the nerve-smooth muscle junction, inhibition studies of field-stimulated contractions were performed. Pirenzepine was 102- to 178-fold less potent than atropine when compared at the inhibitory concentration of antagonist that produced 25, 50, and 75% inhibition (IC25, IC50, and IC75, respectively), indicating that the muscarinic receptor at the nerve-smooth muscle junction is a muscarinic receptor with low affinity for pirenzepine (M2 subtype). Atropine had similar inhibitory effects on vagal- and field-stimulated contractions. In contrast, pirenzepine was more potent in inhibiting vagally stimulated contraction than field-stimulated contraction, especially at the IC25 where pirenzepine was only 8- to 22-fold less potent than atropine in inhibiting vagally stimulated contraction. These data suggest that an M1 subtype of muscarinic receptor modulates excitatory neurotransmission through bronchial parasympathetic ganglia.

Prevention of diminished parasympathetic control of the heart in experimental heart failure

2004 ◽  
Vol 287 (4) ◽  
pp. H1780-H1785 ◽  
Author(s):  
Steve Bibevski ◽  
Mark E. Dunlap
Keyword(s):  
Heart Failure ◽  
Synaptic Transmission ◽  
Sinus Node ◽  
Parasympathetic Ganglia ◽  
Sinus Cycle Length ◽  
Parasympathetic Control ◽  
The Right ◽  
Parasympathetic Function ◽  
Nicotinic Agonist

Decreased synaptic transmission in parasympathetic ganglia contributes to abnormal parasympathetic function in heart failure (HF). Because nicotinic ACh receptors (nAChR) mediate synaptic transmission at the ganglion and upregulate in response to chronic exposure to agonist in vitro, we tested the hypothesis that repeated exposures of ganglionic neurons to a nAChR agonist can prevent a loss of parasympathetic control in HF. Two sets of experiments were performed. In set 1, unpaced control dogs and dogs undergoing pacing-induced HF were treated with a repeated intravenous nicotinic agonist during the development of HF. Under conditions of sympathetic blockade, R-R responses to a bolus injection of 200 μg 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP; nicotinic agonist) were found to be increased five times over the untreated group after 6 wk. In experimental set 2, dogs treated with weekly DMPP injections and in HF were anesthetized and underwent electrical stimulation of the right vagus nerve, which showed sinus cycle length responses >10 times that of controls ( P < 0.05). Complete ganglionic blockade with hexamethonium abolished all responses, confirming that synaptic transmission was mediated entirely by nAChRs in both controls and HF. Despite decreased ganglionic function leading to reduced parasympathetic control of the heart in HF, repeated exposure with a nicotinic agonist during the development of HF results in not only preserved but also supranormal effects of parasympathetic stimulation on the sinus node.

scholarly journals RTP801 REGULATES MOTOR CORTEX SYNAPTIC TRANSMISSION AND LEARNING

2020 ◽  
Author(s):  
L Pérez-Sisqués ◽  
N Martín-Flores ◽  
M Masana ◽  
J Solana ◽  
A Llobet ◽  
...  
Keyword(s):  
Motor Cortex ◽  
Motor Learning ◽  
Synaptic Transmission ◽  
Neuronal Plasticity ◽  
Brain Slices ◽  
Physiological Role ◽  
Neuronal Cultures ◽  
Spine Density

ABSTRACTRTP801/REDD1 is a stress-regulated protein whose upregulation is necessary and sufficient to trigger neuronal death in in vitro and in vivo models of Parkinson’s and Huntington’s diseases and is up regulated in compromised neurons in human postmortem brains of both neurodegenerative disorders. Indeed, in both Parkinson’s and Huntington’s disease mouse models, RTP801 knockdown alleviates motor-learning deficits.Here, we investigated the physiological role of RTP801 in neuronal plasticity. RTP801 is found in rat, mouse and human synapses. The absence of RTP801 enhanced excitatory synaptic transmission in both neuronal cultures and brain slices from RTP801 knock-out (KO) mice. Indeed, RTP801 KO mice showed improved motor learning, which correlated with lower spine density but increased basal filopodia and mushroom spines in the motor cortex layer V. This paralleled with higher levels of synaptosomal GluA1 and TrkB receptors in homogenates derived from KO mice motor cortex, proteins that are associated with synaptic strengthening. Altogether, these results indicate that RTP801 has an important role modulating neuronal plasticity in motor learning.

Abstract 1623: Reactive Oxygen Species increases Intracellular Calcium, alters the Electrophysiological Properties and Synaptic Transmission in Intrinsic Cardiac Ganglion Neurons: in vitro

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Jhansi Dyavanapalli ◽  
Katrina Rimmer ◽  
Alexander A Harper
Keyword(s):  
Reactive Oxygen Species ◽  
Synaptic Transmission ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Simultaneous Recording ◽  
Oxygen Species ◽  
Home Office ◽  
Electrophysiological Properties ◽  
Ganglion Neurons

Anerobic metabolism generates reactive oxygen species (ROS) as by-products and this is increased during ischemia. ROS have been shown to interact with and impair the functioning of membrane proteins such as ion channels and transporters and cause disturbances in intracellular Ca 2+ homeostasis. We have investigated the effects of ROS upon [Ca 2+ ] i , the intrinsic electrophysiological characteristics and synaptic transmission in neurons of the ICG regulating the sinoatrial node. The hypothesis is that ROS-induced damage increases [Ca 2+ ] i and attenuates synaptic transmission in ICG. used a whole-mount adult rat ICG preparation, in vitro (rats were killed by stunning and cervical dislocation, according to current UK Home Office guidelines). Intracellular recordings were made using sharp glass microelectrodes filled with Oregon Green 488 BAPTA-1, allowing simultaneous recording of electrical properties and measurement of [Ca 2+ ] i . Signals resulting from [Ca 2+ ] i changes were expressed as the ratio of fluorescence changes over baseline fluorescence, (f-fo)/fo . The ROS-donors hydrogen peroxide (H 2 O 2 , 1 mM) and tert-butyl hydroperoxide ( t -BHP, 1mM) had broadly similar actions on postganglionic somata, both producing membrane potential hyperpolarization (from −48.4 mV ± 6.5 S.D control to −69.9 mV ± 7.9 H 2 O 2 , n=7; and from −51.9 mV ± 7.1 control to −59.2 mV ± 7.9 t -BHP, n=17, p<0.001). Considering the somatic action potential (AP), t -BHP decreased the rate of rise (from 159 V/sec ± 79 control to 117 V/sec ± 53, n=6, p<0.05), but did not alter the rate of fall and increased AP duration (measured at 0 mV) from 0.7ms (± 0.2) control to 1.1ms (± 0.3, n=5, p<0.05). In addition, t -BHP reduced the AP afterhyper-polarization (AHP) amplitude (from 15.5 mV ± 5.2 control to 9.9 mV ± 4.5, n=10, p<0.001) but had no impact on AP overshoot or AHP duration. t -BHP and H 2 O 2 markedly increased resting [Ca 2+ ] i to 1.59 (± 0.03, n=8,p<0.001) and 2.36 (± 0.04, n=3, p<0.05) respectively, of control values (~ 60 nM ). H 2 O 2 blocked synaptic transmission in 3 /4 neurons. In contrast, t -BHP had no significant action on synaptic transmission. Together, these data demonstrate that ROS alters the excitability of ICG neurons attenuating parasympathetic control of the heart during ischemia/ reperfusion.

GABAB receptors presynaptically modulate excitatory synaptic transmission in the rat supraoptic nucleus in vitro

1996 ◽  
Vol 76 (2) ◽  
pp. 1166-1179 ◽  
Author(s):  
S. B. Kombian ◽  
J. A. Zidichouski ◽  
Q. J. Pittman
Keyword(s):  
Synaptic Transmission ◽  
Receptor Agonist ◽  
Supraoptic Nucleus ◽  
Gabab Receptor ◽  
Synaptic Depression ◽  
Receptor Activation ◽  
Excitatory Synaptic Transmission ◽  
Gabab Receptors ◽  
Dependent Manner

1. The effect of gamma-aminobutyric acid-B (GABAB)-receptor activation on excitatory synaptic transmission in the rat supraoptic nucleus (SON) was examined using the nystatin perforated-patch whole cell recording technique in coronal hypothalamic slices. 2. Stimulation of the hypothalamic region dorso-medial to the SON elicited glutamate and GABAA-receptor-mediated synaptic responses in electrophysiologically identified magnocellular neurosecretory cells. 3. Bath application of the GABAB-receptor agonist, +/- -baclofen reversibly reduced pharmacologically isolated, glutamate-mediated excitatory postsynaptic currents (EPSCs) in a concentration-dependent manner. At the concentrations used, baclofen altered neither the postsynaptic conductances of these cells nor their response to bath applied alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA). 4. The baclofen-induced synaptic depression was accompanied by an increase in paired pulse facilitation (PPF). This increase in PPF, as well as the synaptic depression, was blocked by the GABAB-receptor antagonists CGP36742 and saclofen. 5. In addition to blocking the actions of baclofen in this nucleus, CGP36742 caused an increase in the evoked EPSC amplitude without altering postsynaptic cell conductances or responses induced by bath-applied AMPA. Contrary to the action of CGP36742, saclofen caused a baclofen-like depression of the evoked EPSC, suggesting that it may act as a partial GABAB receptor agonist. 6. These results indicate that the activation of presynaptic GABAB receptors reduces fast excitatory synaptic transmission in the SON. They further suggest that presynaptic GABAB receptors may be tonically activated in vitro. Thus GABAB receptors may influence the level of activity and excitation of SON neurons and hence modulate the secretion of the regulatory neuropeptides vasopressin and oxytocin.

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