Serotonergic modulation of locust motor neurons

1995 ◽  
Vol 73 (3) ◽  
pp. 923-932 ◽  
Author(s):  
D. Parker
Keyword(s):  
Cyclic Amp ◽  
Motor Neurons ◽  
Schistocerca Gregaria ◽  
Phosphodiesterase Inhibitor ◽  
Membrane Resistance ◽  
Excitatory Postsynaptic Potential ◽  
Metathoracic Ganglion ◽  
Bath Application ◽  
Potassium Conductances ◽  
5 Ht Uptake

1. The effects of the putative endogenous neuromodulator serotonin (5-HT) on the fast extensor and flexor tibiae motor neurons in the locust (Schistocerca gregaria) metathoracic ganglion, were analyzed. 2. 5-HT consistently increased the duration of the fast extensor spike and usually reduced the afterhyperpolarization, although this effect was less consistent. The spike broadening in the fast extensor was associated with an increase in the amplitude of the excitatory postsynaptic potential (EPSP) evoked monosynaptically in the flexor motor neurons by fast extensor stimulation. 5-HT also increased the membrane resistance of the fast extensor and flexor tibiae motor neurons. 3. The effects of 5-HT were mimicked by bath application of the 5-HT uptake inhibitor imipramine, and blocked by the 5-HT receptor antagonist ketanserin. The effects were also mimicked by dibutryl cyclic AMP, a membrane permeant analogue of cyclic AMP, and by the phosphodiesterase inhibitor 3-isobutyl-1-methyl-xanthine, but not by dibutryl cyclic GMP. The 5-HT-dependent modulation was blocked by the protein kinase A inhibitor H8. In addition, injection of cyclic AMP into the fast extensor or a flexor motor neuron could mimic the effects of 5-HT on these neurons. 4. 5-HT probably broadened the FETi action potential by modulating potassium conductances responsible for spike repolarization. 5. These results show that 5-HT modulates both the fast extensor and flexor tibiae motor neurons, resulting in potentiation of synaptic transmission between these neurons. In addition, the increase in flexor membrane resistance will potentiate other inputs onto these cells, which will affect the output of the motor neurons during locomotion.

Enhancement of Platelet Sensitivity to ADP-Aggregation by Isometric Exercise in Arteriosclerotic Patients and its Prevention

1977 ◽  
Vol 37 (02) ◽  
pp. 329-338 ◽  
Author(s):  
Tadahiro Sano ◽  
Takeshi Motomiya ◽  
Hiroh Yamazaki ◽  
Takio Shimamoto
Keyword(s):  
Cyclic Amp ◽  
Mechanical Stress ◽  
Optical Density ◽  
Platelet Function ◽  
Isometric Exercise ◽  
Phosphodiesterase Inhibitor ◽  
New Method ◽  
Platelet Aggregability ◽  
Control Subjects ◽  
Healthy Control

SummaryA new method for assessment of platelet sensitivity to ADP-aggregation was devised. Its reproducibility and the correlations between the values obtained by this method, the optical density (O. D.) method, and the screen filtration pressure (SFP) method were assessed. In summary, this method may be said to have three main points:1. It can be performed without centrifugation, avoiding mechanical stress to platelets, using only 0.8 ml. of blood and inexpensive equipment.2. It may reflect different aspects of platelet function from the O. D. method and the SFP method, despite the positive significant correlations between the values obtained by these three methods.3. It was proved to be highly reproducible and is thought to be useful clinically.By using this method, the effect of sustained isometric exercise by handgripping on platelet aggregability was assessed in coronary sclerotic and cerebral arteriosclerotic patients on placebo and EG-626, a newly synthesized cyclic AMP phosphodiesterase inhibitor. On placebo, an enhancement of platelet sensitivity was observed after isometric exercise in coronary and cerebral arteriosclerotic patients but not in healthy control subjects. The enhancement was prevented by pretreatment of EG-626, administered orally 1.5 hours prior to exercise.

Forskolin and phosphodiesterase inhibitors release adenosine but inhibit morphine-evoked release of adenosine from spinal cord synaptosomes

1991 ◽  
Vol 69 (6) ◽  
pp. 877-885 ◽  
Author(s):  
D. Nicholson ◽  
T. D. White ◽  
J. Sawynok
Keyword(s):  
Spinal Cord ◽  
Cyclic Amp ◽  
Phosphodiesterase Inhibitor ◽  
Phosphodiesterase Inhibitors ◽  
Dorsal Spinal Cord ◽  
Adenosine Release ◽  
Basal Release ◽  
Phosphodiesterase Isoenzymes ◽  
Dorsal Spinal ◽  
Ventral Spinal Cord

The effects of forskolin, Ro 20-1724, rolipram, and 3-isobutyl-1-methylxanthine (IBMX) on morphine-evoked release of adenosine from dorsal spinal cord synaptosomes were evaluated to examine the potential involvement of cyclic AMP in this action of morphine. Ro 20-1724 (1–100 μM), rolipram (1–100 μM), and forskolin (1–10 μM) increased basal release of adenosine, and at 1 μM inhibited morphine-evoked release of adenosine. Release of adenosine by Ro 20-1724, rolipram, and forskolin was reduced 42–77% in the presence of α, β-methylene ADP and GMP, which inhibits ecto-5′-nucleotidase activity by 81%, indicating that this adenosine originated predominantly as nucleotide(s). Significant amounts of adenosine also were released from the ventral spinal cord by these agents. Ro 20-1724 and rolipram did not significantly alter the uptake of adenosine into synaptosomes. Although Ro 20-1724 and rolipram had only limited effects on the extrasynaptosomal conversion of added cyclic AMP to adenosine, IBMX, a phosphodiesterase inhibitor with a broader spectrum of inhibitory activity for phosphodiesterase isoenzymes, significantly inhibited the conversion of cyclic AMP to adenosine and resulted in recovery of a substantial amount of cyclic AMP. As with the non-xanthine phosphodiesterase inhibitors, IBMX increased basal release of adenosine and reduced morphine-evoked release of adenosine. Adenosine released by IBMX was reduced 70% in the presence of α, β-methylene ADP and GMP, and release from the ventral spinal cord was 61% of that from the dorsal spinal cord. Collectively, these results indicate that forskolin and phosphodiesterase inhibitors release nucleotide(s) which is (are) converted extrasynaptosomally to adenosine. For forskolin, Ro 20-1724, and rolipram, the nucleotide released could be cyclic AMP. Morphine releases adenosine per se, and forskolin and phosphodiesterase inhibitors reduce this release. The lack of increase in the action of morphine with phosphodiesterase inhibitors in particular does not support a role for stimulation of cyclic AMP production by morphine in the release of adenosine. The reduction in morphine-evoked release of adenosine by forskolin and phosphodiesterase inhibitors suggests either (a) that a reduction in cyclic levels by morphine promotes adenosine release, or (b) that cyclic AMP interferes with the release process.Key words: forskolin, Ro 20-1724, 3-isobutyl-1-methylxanthine, cyclic AMP, morphine, adenosine release, spinal cord.

THE HISTOLOGY OF THE GIANT FIBRE SYSTEM IN THE ABDOMINAL VENTRAL NERVE CORD OF THE DESERT LOCUST

1970 ◽  
Vol 102 (9) ◽  
pp. 1163-1168 ◽  
Author(s):  
W. D. Seabrook
Keyword(s):  
Single Cell ◽  
Nerve Cord ◽  
Ventral Nerve Cord ◽  
Schistocerca Gregaria ◽  
Desert Locust ◽  
Giant Fibre ◽  
Metathoracic Ganglion ◽  
Giant Fibres ◽  
Giant Fibre System

AbstractSchistocerca gregaria possess four neurones of giant fibre proportions within the abdominal ventral nerve cord. These fibres arise from single cell bodies in the terminal ganglionic mass and pass without interruption to the metathoracic ganglion. Fibres become reduced in diameter when passing through a ganglion. Branching of the giant fibres occurs in abdominal ganglia 6 and 7.

The role of interneurons in controlling the tail-withdrawal reflex in Aplysia: a network model

1993 ◽  
Vol 70 (5) ◽  
pp. 1777-1786 ◽  
Author(s):  
J. A. White ◽  
I. Ziv ◽  
L. J. Cleary ◽  
D. A. Baxter ◽  
J. H. Byrne
Keyword(s):  
Synaptic Plasticity ◽  
Sensory Neurons ◽  
Network Model ◽  
Motor Neurons ◽  
Excitatory Postsynaptic Potential ◽  
Layer Model ◽  
Neural Network Models ◽  
Plastic Properties ◽  
Withdrawal Reflex ◽  
Long Duration

1. The contributions of monosynaptic and polysynaptic circuitry to the tail-withdrawal reflex in the marine mollusk Aplysia californica were assessed by the use of physiologically based neural network models. Effects of monosynaptic circuitry were examined by the use of a two-layer network model with four sensory neurons in the input layer and one motor neuron in the output layer. Results of these simulations indicated that the monosynaptic circuit could not account fully for long-duration responses of tail motor neurons elicited by tail stimulation. 2. A three-layer network model was constructed by interposing a layer of two excitatory interneurons between the input and output layers of the two-layer network model. These interneurons had properties mimicking those of the recently described interneuron LP117, receiving excitatory input from pleural sensory neurons and evoking a biphasic excitatory postsynaptic potential (EPSP) in pedal motor neurons (Cleary and Byrne 1993). The three-layer model could account for long-duration responses in motor neurons. 3. Sensory neurons are a known site of plasticity in Aplysia. Synaptic plasticity was incorporated into the three-layer model by altering the magnitudes of conductance changes evoked in motor neurons and interneurons by presynaptic sensory neurons. In these simulations the excitatory interneurons converted an amplitude-coded input into an amplitude- and duration-coded output, allowing the three-layer network to support a large range of output amplitudes and durations. 4. Synaptic plasticity at more than one locus modified dramatically the input-output relationship of the three-layer network model. This feature gave the model redundancy in its plastic properties and points to the possibility of distributed memory in the circuitry mediating withdrawal reflexes in Aplysia. Multiple sites of control over the response of the network would likely allow a more diverse repertoire of responses.

Electrically coupled pacemaker neurons respond differently to same physiological inputs and neurotransmitters

1984 ◽  
Vol 51 (6) ◽  
pp. 1362-1374 ◽  
Author(s):  
E. Marder ◽  
J. S. Eisen
Keyword(s):  
Motor Neurons ◽  
Slow Wave ◽  
Lucifer Yellow ◽  
Electrical Coupling ◽  
Excitatory Postsynaptic Potential ◽  
Panulirus Interruptus ◽  
Bursting Neuron ◽  
Postsynaptic Potential ◽  
Pyloric Dilator ◽  
Muscarinic Cholinergic

The two pyloric dilator (PD) motor neurons and the single anterior burster (AB) interneuron are electrically coupled and together comprise the pacemaker for the pyloric central pattern generator of the stomatogastric ganglion of the lobster, Panulirus interruptus. Previous work (31) has shown that the AB neuron is an endogenously bursting neuron, while the PD neuron is a conditional burster. In this paper the effects of physiological inputs and neurotransmitters on isolated PD neurons and AB neurons were studied using the lucifer yellow photoinactivation technique (33). Stimulation of the inferior ventricular nerve (IVN) fibers at high frequencies elicits a triphasic response in AB and PD neurons: a rapid excitatory postsynaptic potential (EPSP) followed by a slow inhibitory postsynaptic potential (IPSP), followed by an enhancement of the pacemaker slow-wave depolarizations. Photoinactivation experiments indicate that the enhancement of the slow wave is due primarily to actions of the IVN fibers on the PD neurons but not on the AB neuron. Bath-applied dopamine dramatically alters the motor output of the pyloric system. Photoinactivation experiments show that 10(-4) M dopamine increases the amplitude and frequency of the slow-wave depolarizations recorded in the AB neurons but hyperpolarizes and inhibits the PD neurons. Bath-applied serotonin increases the frequency and amplitude of the slow-wave depolarizations in the AB neuron but has no effect on PD neurons. Pilocarpine, a muscarinic cholinergic agonist, stimulates slow-wave depolarization production in both PD neurons and the AB neuron, but the waveform and frequency of the slow waves elicited are quite different. These results show that although the electrically coupled PD and AB neurons always depolarize synchronously and act together as the pacemaker for the pyloric system, they respond differently to a neuronal input and to several putative neuromodulators. Thus, despite electrical coupling sufficient to ensure synchronous activity, the PD and AB neurons can be modulated independently.

Innervation pattern of a pool of nine excitatory motor neurons in the flexor tibiae muscle of a locust hind leg

1998 ◽  
Vol 201 (12) ◽  
pp. 1885-1893 ◽  
Author(s):  
K Sasaki ◽  
M Burrows
Keyword(s):  
Motor Neurons ◽  
Muscle Fibres ◽  
Main Body ◽  
Intracellular Recordings ◽  
Innervation Pattern ◽  
Flexor Muscle ◽  
Fibre Bundles ◽  
Metathoracic Ganglion ◽  
Overlapping Sets ◽  
Individual Motor

The flexor tibiae muscle of a locust hind leg consists of 10-11 pairs of fibre bundles in the main body of the muscle and a distal pair of bundles that form the accessory flexor muscle, all of which insert onto a common tendon. It is much smaller than the antagonistic extensor tibiae muscle and yet it is innervated by nine excitatory motor neurons, compared with only two for the extensor. To determine the pattern of innervation within the muscle by individual motor neurons, branches of the nerve (N5B2) that supplies the different muscle bundles were backfilled to reveal somata in the metathoracic ganglion. This showed that different muscle bundles are innervated by different numbers of excitatory motor neurons. Physiological mapping of the innervation was then carried out by intracellular recordings from the somata of flexor motor neurons in the metathoracic ganglion using microelectrodes. Spikes were evoked in these neurons by the injection of current, and matching junctional potentials were sought in fibres throughout the muscle using a second intracellular electrode. Each motor neuron innervates only a restricted array of muscle fibres and, although some innervate a larger array than others, none innervates fibres throughout the muscle. Some motor neurons innervate only proximal fibres and others only more distal fibres, so that the most proximal and most distal bundles of muscle fibres are innervated by non-overlapping sets of motor neurons. More motor neurons innervate proximal bundles than distal ones, and there are some asymmetries in the number of motor neurons innervating corresponding bundles on either side of the tendon. Individual motor neurons cause slow, fast or intermediate movements of the tibia, but their patterns of innervation overlap in the different muscle bundles. Furthermore, individual muscle fibres may also be innervated by motor neurons with different properties.

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