scholarly journals Evidence that acetylcholine is an inhibitory transmitter of heart interneurons in the leech

1992 ◽  
Vol 171 (1) ◽  
pp. 329-347
Author(s):  
J. Schmidt ◽  
R. L. Calabrese
Keyword(s):  
Membrane Potential ◽  
Motor Neurons ◽  
Membrane Conductance ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Bicuculline Methiodide ◽  
Postsynaptic Receptors ◽  
Postsynaptic Potential ◽  
Inhibitory Transmitter ◽  
Cl Conductance

1. In the leech, synaptic transmission between heart interneurons (HN cells) and between HN cells and heart motor neurons (HE cells) is blocked by bicuculline methiodide. 2. Gamma-aminobutyric acid, when applied focally onto the somata of HN cells or when added to the superfusate, has no effect on the membrane potential of HN cells. 3. Both acetylcholine (ACh) and the ACh agonist carbachol hyperpolarize HN cells and HE cells when applied focally onto their somata or into the neuropil or when added to the superfusate. 4. Inhibitory postsynaptic-potential-like responses elicited by focal application of carbachol onto the somata of HN cells and HE cells are blocked by bicuculline methiodide and are reversed when Cl- is injected into the cells. 5. Focal application of carbachol onto the somata of HN cells and HE cells increases membrane conductance. 6. The results indicate that HN cells use ACh as an inhibitory transmitter, that the postsynaptic receptors for ACh are blocked by bicuculline methiodide and that inhibition of HN cells and HE cells is mediated by an increased Cl- conductance.

scholarly journals GABA-like immunoreactivity in nonspiking interneurons of the locust metathoracic ganglion

2002 ◽  
Vol 205 (23) ◽  
pp. 3651-3659 ◽  
Author(s):  
M. Wildman ◽  
S. R. Ott ◽  
M. Burrows
Keyword(s):  
Membrane Potential ◽  
Motor Neurons ◽  
Lucifer Yellow ◽  
Current Injection ◽  
Aminobutyric Acid ◽  
Homogeneous Population ◽  
Metathoracic Ganglion ◽  
Nonspiking Interneurons ◽  
Intracellular Microelectrodes ◽  
Gaba Immunohistochemistry

SUMMARYNonspiking interneurons are important components of the premotor circuitry in the thoracic ganglia of insects. Their action on postsynaptic neurons appears to be predominantly inhibitory, but it is not known which transmitter(s) they use. Here, we demonstrate that many but not all nonspiking local interneurons in the locust metathoracic ganglion are immunopositive for GABA (γ-aminobutyric acid). Interneurons were impaled with intracellular microelectrodes and were shown physiologically to be nonspiking. They were further characterized by defining their effects on known leg motor neurons when their membrane potential was manipulated by current injection. Lucifer Yellow was then injected into these interneurons to reveal their cell bodies and the morphology of their branches. Some could be recognised as individuals by comparison with previous detailed descriptions. Ganglia were then processed for GABA immunohistochemistry. Fifteen of the 17 nonspiking interneurons studied were immunopositive for GABA, but two were not. The results suggest that the majority of these interneurons might exert their well-characterized effects on other neurons through the release of GABA but that some appear to use a transmitter other than GABA. These nonspiking interneurons are therefore not an homogeneous population with regard to their putative transmitter.

A comparison of similar ionic responses to gamma-aminobutyric acid and acetylcholine

1978 ◽  
Vol 41 (3) ◽  
pp. 531-541 ◽  
Author(s):  
J. Yarowsky ◽  
D. O. Carpenter
Keyword(s):  
Gaba Receptor ◽  
Aminobutyric Acid ◽  
Identified Neurons ◽  
Ionic Conductance ◽  
Gamma Aminobutyric Acid ◽  
Gaba Antagonists ◽  
Conductance Increase ◽  
Alpha Bungarotoxin ◽  
Cl Conductance

1. Fast Na+-, Cl-, and K+-Conductance increase responses to gamma-aminobutyric acid (GABA) show times to peak similar to the comparable ionic responses to acetylcholine (ACh). 2. On some identified neurons, both putative transmitters elicit responses due to the same conductance change. For example, in cell R2 both substances cause an increase in Cl- conductance. Receptors for GABA and ACh on R2 do not cross desensitize and therefore are distinct. The ACh but not the GABA response is blocked by alpha-bungarotoxin and strychnine. 3. In R2 both responses reverse at -58 mV, and the Cl- ionophore (for both responses) appears to be partially permeant to propionate and isethionate, but impermeant to acetate, sulfate, and methylsulfate. 4. The Cl- responses but not the Na+ responses to both ACh and GABA are blocked by both picrotoxin and bicuculline, the classical GABA antagonists. 5. These results are compatible with the hypothesis that the ionophores associated with receptors to different neurotransmitters but mediating the same ionic conductance change have many common properties and may, in fact, be identical. Bicuculline and picrotoxin may be specific blockers of the Cl- ionophore, not the GABA receptor.

scholarly journals THE METABOLISM OF GAMMA AMINOBUTYRIC ACID IN THE LOBSTER NERVOUS SYSTEM

1970 ◽  
Vol 46 (2) ◽  
pp. 290-299 ◽  
Author(s):  
Z. W. Hall ◽  
M. D. Bownds ◽  
E. A. Kravitz
Keyword(s):  
Aminobutyric Acid ◽  
Inhibitory Neurons ◽  
Decarboxylase Activity ◽  
Succinic Semialdehyde ◽  
Gamma Aminobutyric Acid ◽  
Succinic Semialdehyde Dehydrogenase ◽  
Gaba Metabolism ◽  
Semialdehyde Dehydrogenase ◽  
Electrophoretic Behavior ◽  
Inhibitory Transmitter

γ-aminobutyric acid (GABA) is the inhibitory transmitter compound at the lobster neuromuscular junction. This paper presents a comparison of the enzymes of GABA metabolism in single identified inhibitory and excitatory axons from lobster walking legs. Inhibitory axons contain more than 100 times as much glutamic decarboxylase activity as do excitatory axons. GABA-glutamic transaminase is found in both excitatory and inhibitory axons, but about 50% more enzyme is present in inhibitory axons. The kinetic and electrophoretic behavior of the transaminase activity in excitatory and inhibitory axons is similar. Succinic semialdehyde dehydrogenase is found in both axon types, as is an unknown enzyme which converts a contaminant in radioactive glutamic acid to GABA. In lobster inhibitory neurons, therefore, the ability to accumulate GABA ultimately rests on the ability of the neuron to accumulate the enzyme glutamic decarboxylase.

Enflurane Directly Depresses Glutamate AMPA and NMDA Currents in Mouse Spinal Cord Motor Neurons Independent of Actions on GABAAor Glycine Receptors

2000 ◽  
Vol 93 (4) ◽  
pp. 1075-1084 ◽  
Author(s):  
Gong Cheng ◽  
Joan J. Kendig
Keyword(s):  
Spinal Cord ◽  
Nmda Receptor ◽  
Glutamate Receptors ◽  
Dorsal Horn ◽  
Motor Neurons ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Excitatory Postsynaptic Currents ◽  
Postsynaptic Currents ◽  
Anesthetic Concentration

Background The spinal cord is an important anatomic site at which volatile agents act to prevent movement in response to a noxious stimulus. This study was designed to test the hypothesis that enflurane acts directly on motor neurons to inhibit excitatory synaptic transmission at glutamate receptors. Methods Whole-cell recordings were made in visually identified motor neurons in spinal cord slices from 1- to 4-day-old mice. Excitatory postsynaptic currents (EPSCs) or potentials (EPSPs) were evoked by electrical stimulation of the dorsal root entry area or dorsal horn. The EPSCs were isolated pharmacologically into glutamate N-methyl-d-aspartate (NMDA) receptor- and non-NMDA receptor-mediated components by using selective antagonists. Currents also were evoked by brief pulse pressure ejection of glutamate under various conditions of pharmacologic blockade. Enflurane was made up as a saturated stock solution and diluted in the superfusate; concentrations were measured using gas chromatography. Results Excitatory postsynaptic currents and EPSPs recorded from motor neurons by stimulation in the dorsal horn were mediated by glutamate receptors of both non-NMDA and NMDA subtypes. Enflurane at a general anesthetic concentration (one minimum alveolar anesthetic concentration) reversibly depressed EPSCs and EPSPs. Enflurane also depressed glutamate-evoked currents in the presence of tetrodotoxin (300 nm), showing that its actions are postsynaptic. Block of inhibitory gamma-aminobutyric acid A and glycine receptors by bicuculline (20 micrometer) or strychnine (2 micrometer) or both did not significantly reduce the effects of enflurane on glutamate-evoked currents. Enflurane also depressed glutamate-evoked currents if the inhibitory receptors were blocked and if either D,L-2-amino-5-phosphonopentanoic acid (50 micrometer) or 6-cyano-7-nitroquinoxaline-2,3-dione disodium (10 micrometer) was applied to block NMDA or alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-kainate receptors respectively. Conclusions Enflurane exerts direct depressant effects on both alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and NMDA glutamate currents in motor neurons. Enhancement of gamma-aminobutyric acid A and glycine inhibition is not needed for this effect. Direct depression of glutamatergic excitatory transmission by a postsynaptic action on motor neurons thus may contribute to general anesthesia as defined by immobility in response to a noxious stimulus.

Sodium valproate and clonazepam for epilepsy

1975 ◽  
Vol 13 (25) ◽  
pp. 97-98
Keyword(s):  
Sodium Valproate ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Gaba A ◽  
Naturally Occurring ◽  
Inhibitory Transmitter ◽  
The Brain

Sodium valproate (Epilim - Reckitt-Labaz) and clonazepam (Rivotril - Roche) are two anti-epileptic drugs recently promoted in this country. Sodium valproate has been used elsewhere in Europe for several years. So far they have been employed predominantly for patients whose epilepsy is not controlled with conventional drugs. Sodium valproate and clonazepam are chemically unrelated. Clonazepam is a benzodiazepine, while the structure of sodium valproate is novel for an anticonvulsant. Sodium valproate appears to raise the concentration in the brain of gamma-aminobutyric acid (GABA), a naturally occurring inhibitory transmitter.1

scholarly journals Neural Mechanisms of Sevoflurane-induced Respiratory Depression in Newborn Rats

2008 ◽  
Vol 109 (2) ◽  
pp. 233-242 ◽  
Author(s):  
Junya Kuribayashi ◽  
Shigeki Sakuraba ◽  
Masanori Kashiwagi ◽  
Eiki Hatori ◽  
Miki Tsujita ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Respiratory Depression ◽  
Motor Neurons ◽  
Type A ◽  
Aminobutyric Acid ◽  
Respiratory Neurons ◽  
Gamma Aminobutyric Acid ◽  
Inspiratory Neurons ◽  
Acid Type ◽  
Bötzinger Complex

Background Sevoflurane-induced respiratory depression has been reported to be due to the action on medullary respiratory and phrenic motor neurons. These results were obtained from extracellular recordings of the neurons. Here, the authors made intracellular recordings of respiratory neurons and analyzed their membrane properties during sevoflurane application. Furthermore, they clarified the role of gamma-aminobutyric acid type A receptors in sevoflurane-induced respiratory depression. Methods In the isolated brainstem-spinal cord of newborn rat, the authors recorded the C4 nerve burst as an index of inspiratory activity. The preparation was superfused with a solution containing sevoflurane alone or sevoflurane plus the gamma-aminobutyric acid type A receptor antagonist picrotoxin or bicuculline. Neuronal activities were also recorded using patch clamp techniques. Results Sevoflurane decreased C4 burst rate and amplitude. Separate perfusion of sevoflurane to the medulla and to the spinal cord decreased C4 burst rate and amplitude, respectively. Both picrotoxin and bicuculline attenuated the reduction of C4 burst rate. Sevoflurane reduced both intraburst firing frequency and membrane resistance of respiratory neurons except for inspiratory neurons. Conclusion Under the influence of sevoflurane, the region containing inspiratory neurons, i.e., the pre-Bötzinger complex, may determine the inspiratory rhythm, because reduced C4 bursts were still synchronized with the bursts of inspiratory neurons within the pre-Bötzinger complex. In contrast, the sevoflurane-induced decrease in C4 burst amplitude is mediated through the inhibition of phrenic motor neurons. gamma-Aminobutyric acid type A receptors may be involved in the sevoflurane-induced respiratory depression within the medulla, but not within the spinal cord.

Histamine activates chloride conductance in motor neurons of the lobster cardiac ganglion

1992 ◽  
Vol 68 (1) ◽  
pp. 9-15 ◽  
Author(s):  
H. Hashemzadeh-Gargari ◽  
J. E. Freschi
Keyword(s):  
Motor Neurons ◽  
Equilibrium Potential ◽  
Gamma Aminobutyric Acid ◽  
Cardiac Ganglion ◽  
Voltage Dependent ◽  
The Mean ◽  
Histamine Response ◽  
Current Polarity ◽  
Cl Conductance ◽  
Individual Motor

1. Individual motor neurons of the lobster cardiac ganglion were voltage clamped with two microelectrodes. Superfusion of histamine evoked a concentration-dependent membrane current. The mean effective concentration (EC50) for the concentration-effect relationship was 28 microM. 2. The amplitude and polarity of the histamine-activated current depended on intracellular and extracellular Cl- concentration. The membrane potential at which the current polarity reversed was a function of the Cl- equilibrium potential. 3. The histamine-activated Cl- conductance was voltage dependent, increasing with depolarization. As a consequence, the histamine-evoked current showed outward rectification. 4. We conclude that histamine activates a Cl- conductance with biophysical properties similar to the crustacean Cl- conductance activated by gamma-aminobutyric acid (GABA) and to the histamine responses described in lobster olfactory and stomatogastric neurons. 5. The response to histamine was competitively inhibited (IC50 = 7 microM) by cimetidine, an H2 subtype inhibitor in mammals. Ranitidine, pyrilamine, chlorpheniramine, diphenhydramine, and cyproheptadine were 50-100 times less potent than cimetidine. Tubocurarine, a Cl- channel blocker, blocked with an IC50 of 20 microM, but picrotoxin did not begin to inhibit the histamine response until concentrations exceeded 0.1 mM. 6. These results suggest that the response cannot easily be classified with the use of the pharmacological categories developed in mammals. Like the Cl(-)-dependent responses to various neurotransmitters in a number of invertebrates, the histamine response in the lobster cardiac ganglion was inhibited by tubocurarine. 7. Both GABA and histamine had similar effects on the motor neurons, but only GABA inhibited pacemaker bursts. In this respect, GABA more resembles the endogenous inhibitory postsynaptic potential.(ABSTRACT TRUNCATED AT 250 WORDS)

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