Connexions Between a Movement-Detecting Visual Interneurone and Flight Motoneurones of a Locust

1980 ◽  
Vol 86 (1) ◽  
pp. 87-97
Author(s):  
PETER SIMMONS

Both of the descending contralateral movement detector (DCMD) neurones of Schistocerca americana gregaria, which respond to stimulation of the contralateral eye or to loud noises, mediate excitatory postsynaptic potentials in most ipsilateral flight motoneurones.

1991 ◽  
Vol 65 (1) ◽  
pp. 57-66 ◽  
Author(s):  
Z. G. Jiang ◽  
E. Shen ◽  
M. Y. Wang ◽  
N. J. Dun

1. Intracellular recordings were made from antidromically identified motoneurons in transverse (500 microns) lumbar spinal cord slices of neonatal (12-20 day) rats. 2. Electrical stimulation of ventral rootlets evoked, with or without an antidromic spike or initial segment potential, a depolarizing response (latency, 1-4.2 ms), a hyperpolarizing response (latency, 1.5-3.5 ms), or a combination of two preceding responses in 38, 6, and 8% of motoneurons investigated. 3. The hyperpolarizing response was reversibly eliminated by low Ca2+ (0.25 mM), d-tubocurarine (d-Tc; 10 microM) or strychnine (1 microM), suggesting that this response represents an inhibitory post-synaptic potential (IPSP) mediated by glycine or a related substance release from inhibitory interneurons subsequent to their activation by axon collaterals in a manner analogous to the Renshaw cell circuitry described for the cat motoneurons. 4. The depolarizing responses were excitatory postsynaptic potentials (EPSPs), because they could be graded by varying the stimulus intensity and were reversibly abolished in low Ca2+ solution. 5. Membrane hyperpolarization increased the amplitude of EPSPs, and the mean extrapolated reversal potential was -4 mV. 6. EPSPs were augmented, rather than diminished, by dihydro-beta-erythroidine (1 microM) or d-Tc, arguing against a role of recurrent motor axon collaterals in initiating the responses. 7. The conduction velocity of the fibers initiating the EPSPs ranged from 0.35 to 0.96 m/s, indicating that these fibers were unmyelinated. Furthermore, the EPSP exhibited a constant delay when the stimulus frequency was varied from 1 to 5 Hz, and the synaptic delay estimated by extrapolation was less than 1 ms, suggesting that it was a monosynaptic event. 8. After complete separation of the ventral and dorsal horns by a knife cut, stimulation of ventral rootlets could still evoke an EPSP in motoneurons. 9. Superfusion of the slices with the nonselective glutamate receptor antagonist kynurenic acid (0.2-1 mM) or the selective quisqualate/kainate receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX) (0.5-1 microM) reversibly diminished the EPSPs. 10. EPSPs evoked by stimulation of dorsal and ventral rootlets exhibited different latency and waveform in the same motoneurons. 11. The results provide evidence that activation of ventral root afferents evoked an EPSP mediated by glutamate or a related substance in a population of motoneurons. Furthermore, the afferent pathway mediating the EPSP appears to be monosynaptic and confined to the ventral horn.


2018 ◽  
Vol 120 (4) ◽  
pp. 2049-2058 ◽  
Author(s):  
Hongxia Wang ◽  
Richard B. Dewell ◽  
Markus U. Ehrengruber ◽  
Eran Segev ◽  
Jacob Reimer ◽  
...  

The locust is a widely used animal model for studying sensory processing and its relation to behavior. Due to the lack of genomic information, genetic tools to manipulate neural circuits in locusts are not yet available. We examined whether Semliki Forest virus is suitable to mediate exogenous gene expression in neurons of the locust optic lobe. We subcloned a channelrhodopsin variant and the yellow fluorescent protein Venus into a Semliki Forest virus vector and injected the virus into the optic lobe of locusts ( Schistocerca americana). Fluorescence was observed in all injected optic lobes. Most neurons that expressed the recombinant proteins were located in the first two neuropils of the optic lobe, the lamina and medulla. Extracellular recordings demonstrated that laser illumination increased the firing rate of medullary neurons expressing channelrhodopsin. The optogenetic activation of the medullary neurons also triggered excitatory postsynaptic potentials and firing of a postsynaptic, looming-sensitive neuron, the lobula giant movement detector. These results indicate that Semliki Forest virus is efficient at mediating transient exogenous gene expression and provides a tool to manipulate neural circuits in the locust nervous system and likely other insects.NEW & NOTEWORTHY Using Semliki Forest virus, we efficiently delivered channelrhodopsin into neurons of the locust optic lobe. We demonstrate that laser illumination increases the firing of the medullary neurons expressing channelrhodopsin and elicits excitatory postsynaptic potentials and spiking in an identified postsynaptic target neuron, the lobula giant movement detector neuron. This technique allows the manipulation of neuronal activity in locust neural circuits using optogenetics.


1986 ◽  
Vol 55 (3) ◽  
pp. 569-586 ◽  
Author(s):  
S. Vanden Noven ◽  
T. M. Hamm ◽  
D. G. Stuart

Experiments were conducted to test the hypothesis that a partitioning of Ia monosynaptic excitatory postsynaptic potentials (Ia EPSPs) is present in motor nuclei supplying muscles with regions capable of different mechanical actions. Intracellular recordings of synaptic potentials were made in lateral gastrocnemius (LG) motoneurons in anesthetized low-spinal cats. The effects were tested of stimuli (group I range) to the four primary nerve branches of the LG nerve supplying muscle compartments LGm, LG1, LG2, and LG3 (terminology of English, Ref. 26) and the nerve to a heteronymous muscle, soleus. Stimulation of a given LG nerve branch produced monosynaptic Ia EPSPs of greater amplitude in "own-branch" motoneurons than "other-branch" cells. A significant partitioning of mean Ia EPSPs was found in three (LG1, LG2, LG3) out of the four homonymous pathways studied. An EPSP normalization (7) was performed to eliminate potential differences in cell type that might affect the amplitudes of the EPSPs between these four cell groups (e.g., differences in the number of cells supplying FF, FR, and S muscle units). This normalization confirmed that the partitioning of monosynaptic Ia inputs upon stimulation of LG1, LG2, and LG3 could not be attributed to differences in cell type. In addition, the effects of LGm stimulation were found to be significantly greater in the LGm motoneurons compared with the other cell groups. Heteronymous input (from soleus) to the LG motor nucleus showed some partitioned effects. Motoneurons innervating compartment LG2 received larger EPSPs from soleus than did the cells supplying compartments LG1, LG3, and LGm. The contributions of location specificity and species specificity (terminology of Scott and Mendell, Ref. 55) in the establishment of these Ia-afferent-motoneuronal connections were examined. Cell location sites within the spinal cord were consistent with location specificity making some contribution to the observed pattern of homonymous Ia connections. A more prominent role for species specificity was indicated by species-dependent differences in EPSP amplitude in pairs of LG motoneurons (e.g., LGm vs. LG2) at similar rostrocaudal locations upon stimulation of a given homonymous or heteronymous nerve/branch.


1998 ◽  
Vol 275 (3) ◽  
pp. G490-G497 ◽  
Author(s):  
B. A. Moore ◽  
S. Vanner

Electrophysiological techniques were employed to examine the organization of the projections of submucosal neurons in the submucosal plexus of guinea pig ileum. These neurons were activated by focal pressure-pulse application of 5-hydroxytryptamine (5-HT) to single ganglia in submucosal preparations in vitro, and resulting fast excitatory postsynaptic potentials (EPSPs) were recorded intracellularly in S-type neurons. 5-HT-evoked fast EPSPs were blocked by TTX, hexamethonium, and ICS-205-930 (tropisetron). 5-HT was applied either directly to the ganglion containing the neuron recorded intracellularly or to adjacent ganglia positioned at increasing distances on either side of the impaled cell in circumferential or longitudinal orientations. All S-type neurons recorded in this study ( n = 103) received nicotinic fast EPSPs from cholinergic neurons when 5-HT was applied directly to the ganglion containing the impaled neuron. Stimulation of adjacent ganglia also evoked nicotinic fast EPSPs, but the number of neurons that received this input decreased as the distance between the stimulus and the impaled cell increased. Maximal projections were 3 mm in the circumferential and orad-to-aborad orientations. There were no significant projections in the aborad-to-orad direction. These findings suggest that S-type neurons in the submucosal plexus are innervated by intrinsic cholinergic neurons that project over relatively short distances and have a distinct orad-to-aborad polarity.


1981 ◽  
Vol 45 (3) ◽  
pp. 501-515 ◽  
Author(s):  
K. G. Pearson ◽  
C. S. Goodman

1. Intracellular recordings near the output terminals of an identified interneuron (the descending contralateral movement detector, DCMD) in the locust revealed the occurrence of depolarizing synaptic potentials. These presynaptic depolarizing potentials were evoked by spikes in both DCMDs, by auditory stimuli, and by electrical stimulation of the pro- to mesothoracic connectives. The occurrence of the depolarizing potentials decreased the amplitude of the action potentials close to the output terminals. 2. The stimuli that produced depolarizing potentials in the presynaptic terminals reduced the amplitude of the monosynaptic excitatory postsynaptic potentials evoked by the DCMDs in identified follower interneurons. We conclude that at least part of this reduction in transmission from the DCMDs results from presynaptic inhibition and that the presynaptic inhibition is related to a reduction in the amplitude of the presynaptic action potentials. 3. We propose that the function of the presynaptic inhibition of the DCMDs is to ensure that the interneurons triggering a jump are never activated by the DCMDs in the absence of proprioceptive signals from the legs indicating the animal's readiness to jump.


2007 ◽  
Vol 292 (2) ◽  
pp. G492-G500 ◽  
Author(s):  
Na Gao ◽  
Hong-Zhen Hu ◽  
Sumei Liu ◽  
Chuanyun Gao ◽  
Yun Xia ◽  
...  

Actions of adenosine 5′-monophosphate (AMP) on electrical and synaptic behavior of submucosal neurons in guinea pig small intestine were studied with “sharp” intracellular microelectrodes. Application of AMP (0.3–100 μM) evoked slowly activating depolarizing responses associated with increased excitability in 80.5% of the neurons. The responses were concentration dependent with an EC50 of 3.5 ± 0.5 μM. They were abolished by the adenosine A2A receptor antagonist ZM-241385 but not by pyridoxal-phosphate-6-azophenyl-2,4-disulfonic acid, trinitrophenyl-ATP, 8-cyclopentyl-1,3-dimethylxanthine, suramin, or MRS-12201220. The AMP-evoked responses were insensitive to AACOCF3 or ryanodine. They were reduced significantly by 1) U-73122, which is a phospholipase C inhibitor; 2) cyclopiazonic acid, which blocks the Ca2+ pump in intraneuronal membranes; and 3) 2-aminoethoxy-diphenylborane, which is an inositol ( 1 , 4 , 5 )-trisphosphate receptor antagonist. Inhibitors of PKC or calmodulin-dependent protein kinase also suppressed the AMP-evoked excitatory responses. Exposure to AMP suppressed fast nicotinic ionotropic postsynaptic potentials, slow metabotropic excitatory postsynaptic potentials, and slow noradrenergic inhibitory postsynaptic potentials in the submucosal plexus. Inhibition of each form of synaptic transmission reflected action at presynaptic inhibitory adenosine A1 receptors. Slow excitatory postsynaptic potentials, which were mediated by the release of ATP and stimulation of P2Y1 purinergic receptors in the submucosal plexus, were not suppressed by AMP. The results suggest an excitatory action of AMP at adenosine A2A receptors on neuronal cell bodies and presynaptic inhibitory actions mediated by adenosine A1 receptors for most forms of neurotransmission in the submucosal plexus, with the exception of slow excitatory purinergic transmission mediated by the P2Y1 receptor subtype.


1992 ◽  
Vol 67 (3) ◽  
pp. 728-737 ◽  
Author(s):  
G. G. Hwa ◽  
M. Avoli

1. Intracellular recording techniques were used to investigate the physiological and pharmacological properties of stimulus-induced excitatory postsynaptic potentials (EPSPs) recorded in regular-spiking cells located in layers II/III of rat sensorimotor cortical slices maintained in vitro. 2. Depending on the strength of the extracellular stimuli, a pure EPSP or an EPSP-inhibitory postsynaptic potential sequence was observed under perfusion with normal medium. The EPSPs displayed short latency of onset [2.4 +/- 0.7 (SD) ms] and were able to follow repetitive stimulation (tested less than or equal to 5 Hz). Variation of the membrane potential (Vm) revealed two types of voltage behavior for the short-latency EPSP. The first type decreased in amplitude with depolarization and increased in amplitude with hyperpolarization. In contrast, the second type behaved anomalously by increasing and decreasing in size after depolarization and hyperpolarization, respectively. 3. Several experimental procedures were carried out to investigate the mechanism underlying the anomalous voltage behavior of the EPSP. Results indicated that this type of Vm dependency could be mimicked by an intrinsic response evoked by a brief pulse of depolarizing current and could be abolished by N-(2,6-dimethylphenylcarbamoylmethyl)triethylammonium bromide (50 mM). Furthermore, the EPSP was not sensitive to the N-methyl-D-aspartate (NMDA) receptor antagonist 3-((+-)-2-carboxypiperazin-4-yl)-propyl-1-phosphonate (CPP, 10 microM). Thus the anomalous voltage relationship of the neuronal membrane. 4. The involvement of non-NMDA receptors in excitatory synaptic transmission was investigated with their selective antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 1-10 microM). This drug greatly reduced or completely blocked the EPSP in a dose-dependent manner (1-10 microM). The IC50 for the CNQX effect was approximately 2 microM. In the presence of CNQX (10 microM) and glycine (10 microM), synaptic stimulation failed to elicit firing of action potential. However, a CPP-sensitive EPSP was observed. 5. When synaptic inhibition was reduced by low concentration of bicuculline methiodide (BMI, 1-2 microM), extracellular stimulation revealed late EPSPs (latency to onset: 10-30 ms) that were not discernible in normal medium. Similar to the short-latency EPSP, the Vm dependency displayed by this late EPSP could be modified by inward membrane rectifications. The late EPSP appeared to be polysynaptic in origin because 1) its latency of onset was long and variable and 2) it failed to follow repetitive stimuli delivered at a frequency that did not depress the short-latency EPSP.(ABSTRACT TRUNCATED AT 400 WORDS)


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