The effects of nitric oxide on long-term potentiation at the crayfish neuromuscular junction (original) (raw)
Related papers
2017
We conducted this research to determine how synaptic activity, namely post-tetanic potentiation (PTP) amplitude and duration, in crayfish muscle cells is affected by differing levels of nitric oxide (NO). We hypothesized that, relative to control conditions, medium (100 μm sodium nitroprusside) levels of NO would have no effect on PTP, high (200 μm sodium nitroprusside) and low (50 μm sodium nitroprusside) levels of NO would negatively impact PTP, and an absence of NO would result in a lack of PTP. Through the use of two drugs, L-NAME and sodium nitroprusside, we exposed a dissected crayfish to various levels of NO before using intracellular recording to measure PTP several times for each NO concentration. Compared to control levels, we found that all NO concentrations below or equal to that provided by 100 μm nitroprusside resulted in a decrease of PTP while high NO levels resulted in an increase in PTP thus disproving our hypothesis.
Synaptic inputs onto spiking local interneurons in crayfish are depressed by nitric oxide
Journal of Neurobiology, 2002
We have analyzed the action of nitric oxide on the synaptic inputs of spiking local interneurons that form part of the local circuits in the terminal abdominal ganglion of the crayfish, Pacifastacus leniusculus. Increasing the availability of NO in the ganglion by bath applying the NO donor SNAP, or the substrate for its synthesis, L‐arginine, caused a depression of synaptic inputs onto the interneurons evoked by electrically stimulating mechanosensory neurons in nerve 2 of the terminal ganglion. Conversely, reducing the availability of NO by bath application of an NO scavenger, PTIO, and an inhibitor of nitric oxide synthase, L‐NAME, increased the amplitude of the evoked potentials. These results suggest that elevated NO concentration causes a depression of the synaptic inputs to spiking local interneurons. To determine whether these effects could be mediated through an NO/cGMP signaling pathway we bath applied a membrane permeable analogue of cGMP, 8‐br‐cGMP, which decreased the a...
The effects of exogenous nitric oxide on the function of neuromuscular synapses
2002
Extracellular recording experiments using neuromuscular skin/chest muscle preparations from lake frogs were performed at low extracellular Ca 2+ ion concentrations to study the effect of L-arginine (the substrate for nitric oxide synthesis) and N G -nitro-L-arginine methyl ester (a blocker of NO synthase) on the parameters of evoked transmitter secretion and ion currents in motor nerve endings. L-arginine at a concentration of 100 µM decreased the amplitude of endplate currents as well as their quantum composition, and also increased the amplitude of the third phase of the evoked nerve ending response, which reflects the kinetics of potassium influx currents. N G -nitro-L-arginine methyl ester at a condition of 100 µM led to increases in the amplitude and quantum composition of endplate currents and decreased the amplitude of the third phase of the evoked nerve ending response. It is suggested that endogenous nitric oxide is produced in frog neuromuscular synapses, which in normal conditions suppresses transmitter secretion and modulates the function of potassium channels in the nerve ending.
Nitric Oxide Potentiation of Locomotor Activity in the Spinal Cord of the Lamprey
The Journal of Neuroscience, 2009
To understand the intrinsic operation of spinal networks generating locomotion, we need to not only characterize the constituent neurons and their connectivity, but also determine the role of intrinsic modulation in shaping the final motor output. We have focused on the effects of nitric oxide (NO) on the locomotor frequency and the underlying synaptic mechanisms in the lamprey spinal cord. To identify the source of NO, we used NADPH-diaphorase histochemistry and nNOS immunocytochemistry. Gray matter and sensory neurons were positively labeled using both methods. Preparations preincubated with NO synthase inhibitors displayed slower locomotor frequency that increased upon washout of the inhibitors, suggesting that NO is an endogenous neuromodulator in the spinal cord. Application of NO donors increased the locomotor frequency that was blocked by an NO scavenger and partially reduced by an inhibitor of sGC. To analyze the synaptic modulation underlying the NO-induced increase of the ...
Neuroscience and behavioral physiology
Experiments on rat diaphragm muscle showed that the nitric oxide (NO) donors sodium nitroprusside SNP) and S-nitroso-N-acetylpenicillamine (SNAP). as well as L-arginine. a substrate for NO synthesis. decreased the level of muscle fiber hyperpolarization (the H effect) after blockade of cholinoceptors on the postsynaptic membrane by d-tubocurarine in conditions of irreversible inhibition of acetylcholinesterase with armine. Conversely, disruptions to NO synthesis in muscle fibers by the NO synthase blocker NG-nitro-L-arginine methyl ester (L-NAME) led to increases in the H effect both in vitro and in vivo. Inactivated solutions of sodium nitroprusside and inactive forms of arginine and NAME (D-arginine. D-NAME) had no effect on the magnitude of the H effect, while hemoglobin, which efficiently binds NO molecules, blocked the inhibitory effects of sodium nitroprusside. SNAP, and L-arginine on the magnitude of the H effect. All these points provide evidence that NO can function as a mo...
Nitric Oxide Activates Voltage-Dependent Potassium Currents of Crustacean Skeletal Muscle
Nitric Oxide, 2001
Nitric oxide (NO), a radical gas, acts as a multifunctional intra-and intercellular messenger. In the present study we investigated the effects of NO on muscle membrane potassium currents of isolated single muscle fibers from the marine isopods, Idotea baltica, using two-electrode voltage clamp recording techniques. Voltage-activated potassium currents consist of an outward current with fast activation and inactivation kinetics and a delayed, persistent outward current. Both currents were blocked by extracellular 4-aminopyridine and tetraethylammonium; the currents were not blocked by charybdotoxin or apamin. Application of the NO donors S-nitroso-N-acetylpenicillamine (SNAP) or hydroxylamine increased both the early and the delayed outward current in a dose-and time-dependent manner. PTIO, a NO scavenger, suppressed the effect of SNAP. N-Acetyl-DL-penicillamine, a related control compound which does not liberate NO, had no significant effect on outward currents. Methylene blue, a guanylyl cyclase inhibitor, prevented the increase of the outward current while 8-bromo-cGMP increased the current. Our experiments show that potassium currents of Idotea muscle are increased by NO donors. They suggest that NO by stimulating cGMP production mediates the effects on membrane currents involved in regulation of invertebrate muscle excitability.
The Journal of Comparative Neurology, 2003
Nitric oxide (NO) and carbon monoxide (CO) have been shown to serve neuromodulatory roles in both vertebrates and invertebrates. Here, we use antibodies to their respective biosynthetic enzymes, nitric oxide synthase (NOS) and heme oxygenase 2 (HO-2), to map the distribution of putative gas-producing neurons in the stomatogastric nervous system (STNS) of the crayfish Cherax quadricarinatus. In this species, NOS immunolabeling is found in the neuropil of the stomatogastric ganglion (STG). This staining originates from two immunopositive axons that project to the STG through the superior oesophageal and stomatogastric nerves, presumably from cell bodies located in the commissural ganglia (CoGs). HO-2 immunoreactivity is present in small diameter fibers and varicosities in the periphery of nerves located in the anterior portion of the STNS. This labeling originates from approximately 12 somata in each CoG. Transmission electron microscopy done on the nerves of the anterior STNS shows they contain a neuroendocrine plexus. Collectively, our results indicate that NO-and CO-producing neurons are likely to exist in the crayfish STNS. Moreover, these gases appear to be produced by distinct subsets of the neurons present there. The localization of NO to the STG neuropil suggests that it serves as a locally released modulator or is involved in the local release of other substances within this ganglion. The presence of CO in the neurohemal plexus of the anterior STNS suggests that it serves as a circulating hormone or is involved in the control of neuroendocrine release from this plexus.