Electrical activation of the pocket scratch central pattern generator in the turtle

1988 ◽  
Vol 60 (6) ◽  
pp. 2122-2137 ◽  
Author(s):  
S. N. Currie ◽  
P. S. Stein
Keyword(s):  
Receptive Field ◽  
Motor Activity ◽  
Central Pattern Generator ◽  
Motor Response ◽  
Tactile Stimulation ◽  
Motor Pattern ◽  
Pattern Generator ◽  
Motor Output ◽  
Stimulus Pulse ◽  
Stimulation Of

1. A low-spinal, immobilized turtle displays a fictive scratch reflex in hindlimb motor neurons in response to tactile stimulation of the shell (17, 19). Turtles exhibit three forms of the scratch reflex: rostral, pocket, and caudal. Each form is elicited by tactile stimulation of a different receptive field on the body surface. The ventral-posterior pocket (VPP) cutaneous nerve innervates the ventral-posterior portion of the pocket scratch receptive field (Fig. 1). Natural stimulation within the VPP nerve's receptive field evoked a pocket scratch reflex (Fig. 2A). Electrical stimulation of this nerve elicited robust pocket scratch reflexes (Fig. 2, B and C). 2. A single electrical pulse to the VPP nerve delivered at a voltage (greater than 5 V, 0.1 ms) that activated all the axons in the nerve was termed a "maximal" pulse. A single maximal pulse did not evoke a scratch motor response. It raised the excitability of the pocket scratch central pattern generator for several seconds, however. We revealed such excitability changes by applying maximal pulses to the VPP nerve at multisecond intervals (Figs. 5 and 6). When we delivered maximal pulses with interpulse intervals of less than or equal to 5 s, the first pulse produced no motor response and the second pulse evoked one or more cycles of pocket scratch. 3. A stimulus pulse applied to the VPP nerve was used as a probe for studying changes in the excitability of the pocket scratch CPG following scratch motor patterns. In a rested preparation, the stimulus pulse did not activate motor output. In contrast, the stimulus pulse evoked one or two cycles of pocket scratch activity if delivered within 2.5 s after the cessation of rhythmic pocket scratch motor activity (Figs. 7-9). These results are consistent with the hypothesis that the pocket scratch CPG has elevated excitability for seconds following the cessation of pocket scratch motor output. A single pulse applied to the VPP nerve evoked no response if delivered after the cessation of rostral scratch motor activity, however (Fig. 9D). 4. We used a train of maximal pulses to the VPP nerve to probe the form-specificity of the changes in the excitability following a rostral scratch motor pattern (Fig. 10). We set the stimulus parameters so that the train evoked one or two cycles of a pocket scratch motor pattern in a preparation that had rested for over 1 min.(ABSTRACT TRUNCATED AT 400 WORDS)

Plasticity in the multifunctional buccal central pattern generator of Helisoma illuminated by the identification of phase 3 interneurons

1996 ◽  
Vol 75 (2) ◽  
pp. 561-574 ◽  
Author(s):  
E. M. Quinlan ◽  
A. D. Murphy
Keyword(s):  
Motor Activity ◽  
Motor Neuron ◽  
Central Pattern Generator ◽  
Motor Neurons ◽  
Motor Pattern ◽  
Pattern Generator ◽  
Neuron Activity ◽  
Phase 2 ◽  
Phase 3 ◽  
Standard Pattern

1. The mechanism for generating diverse patterns of buccal motor neuron activity was explored in the multifunctional central pattern generator (CPG) of Helisoma. The standard pattern of motor neuron activity, which results in typical feeding behavior, consists of three distinct phases of buccal motor neuron activity. We have previously identified CPG interneurons that control the motor neuron activity during phases 1 and 2 of the standard pattern. Here we identify a pair of interneurons responsible for buccal motor neuron activity during phase 3, and examine the variability in the interactions between this third subunit and other subunits of the CPG. 2. During the production of the standard pattern, phase 3 excitation in many buccal motor neurons follows a prominent phase 2 inhibitory postsynaptic potential. Therefore phase 3 excitation was previously attributed to postinhibitory rebound (PIR) in these motor neurons. Two classes of observations indicated that PIR was insufficient to account for phase 3 activity, necessitating phase 3 interneurons. 1) A subset of identified buccal neurons is inhibited during phase 3 by discrete synaptic input. 2) Other identified buccal neurons display discrete excitation during both phases 2 and 3. 3. A bilaterally symmetrical pair of CPG interneurons, named N3a, was identified and characterized as the source of phase 3 postsynaptic potentials in motor neurons. During phase 3 of the standard motor pattern, interneuron N3a generated bursts of action potentials. Stimulation of N3a, in quiescent preparations, evoked a depolarization in motor neurons that are excited during phase 3 and a hyperpolarization in motor neurons that are inhibited during phase 3. Hyperpolarization of N3a during patterned motor activity eliminated both phase 3 excitation and inhibition. Physiological and morphological characterization of interneuron N3a is provided to invite comparisons with possible homologues in other gastropod feeding CPGs. 4. These data support a model proposed for the organization of the tripartite buccal CPG. According to the model, each of the three phases of buccal motor neuron activity is controlled by discrete subsets of pattern-generating interneurons called subunit 1 (S1), subunit 2 (S2), and subunit 3 (S3). The standard pattern of buccal motor neuron activity underlying feeding is mediated by an S1-S2-S3 sequence of CPG subunit activity. However, a number of "nonstandard" patterns of buccal motor activity were observed. In particular, S2 and S3 activity can occur independently or be linked sequentially in rhythmic patterns other than the standard feeding pattern. Simultaneous recordings of S3 interneuron N3a with effector neurons indicated that N3a can account for phase-3-like postsynaptic potentials (PSPs) in nonstandard patterns. The variety of patterns of buccal motor neuron activity indicates that each CPG subunit can be active in the absence of, or in concert with, activity in any other subunit. 5. To explore how CPG activity may be regulated to generate a particular motor pattern from the CPG's full repertoire, we applied the neuromodulator serotonin. Serotonin initiated and sustained the production of an S2-S3 pattern of activity, in part by enhancing PIR in S3 interneuron N3a after the termination of phase 2 inhibition.

scholarly journals Nonspiking Stretch Receptors of the Crayfish Swimmeret Receive an Efference Copy of the Central Motor Pattern for the Swtmmeret

1989 ◽  
Vol 141 (1) ◽  
pp. 257-264 ◽  
Author(s):  
DOROTHY H. PAUL
Keyword(s):  
Central Pattern Generator ◽  
Synaptic Input ◽  
Lucifer Yellow ◽  
Motor Pattern ◽  
Pattern Generator ◽  
Efference Copy ◽  
Motor Output ◽  
Sensory Signal ◽  
Stretch Receptors

In crayfish, the movement of each swimmeret is monitored by a pair of nonspiking stretch receptors (NSR) with central somata and dendrites that are embedded in an elastic strand at the base of the appendage. I provide evidence that the neuropile segments of these primary sensory neurones receive synaptic input from the hemiganglionic central pattern generator for the swimmeret. In nonbursting isolated abdominal nerve cords of Pacifastacus leniusculus Dana, the membrane potentials of the NSRs (recorded in the neuropile) are stable; whenever the central pattern generator is active, they oscillate in phase with the motor output. Every perturbation of the central pattern generator's activity is precisely reflected in analogous changes (in phase and/or amplitude) of the NSRs' oscillations. This activity must arise via central, synaptic input to the NSRs, because it occurs when all ganglia except the sixth are deafferented. Lucifer Yellow dye-fills show that the neurites of the NSRs are confined to the ipsilateral lateral neuropile, which is the region of the hemiganglion where swimmeret functions are integrated. These results imply that during rhythmic beating of the swimmerets, the NSRs receive an efference copy of the motor output to the limb whose movements they monitor. In vivo, therefore, the incoming sensory signal must be subject to modulation (gating) by the limb's central pattern generator.

scholarly journals Feedforward discharges couple the singing central pattern generator and ventilation central pattern generator in the cricket abdominal central nervous system

2019 ◽  
Vol 205 (6) ◽  
pp. 881-895 ◽  
Author(s):  
Stefan Schöneich ◽  
Berthold Hedwig
Keyword(s):  
Motor Activity ◽  
Central Pattern Generator ◽  
Sensory Feedback ◽  
Motor Pattern ◽  
Pattern Generator ◽  
Abdominal Muscle ◽  
Excitatory Input ◽  
Intracellular Recordings ◽  
Motor Patterns ◽  
The Brain

Abstract We investigated the central nervous coordination between singing motor activity and abdominal ventilatory pumping in crickets. Fictive singing, with sensory feedback removed, was elicited by eserine-microinjection into the brain, and the motor activity underlying singing and abdominal ventilation was recorded with extracellular electrodes. During singing, expiratory abdominal muscle activity is tightly phase coupled to the chirping pattern. Occasional temporary desynchronization of the two motor patterns indicate discrete central pattern generator (CPG) networks that can operate independently. Intracellular recordings revealed a sub-threshold depolarization in phase with the ventilatory cycle in a singing-CPG interneuron, and in a ventilation-CPG interneuron an excitatory input in phase with each syllable of the chirps. Inhibitory synaptic inputs coupled to the syllables of the singing motor pattern were present in another ventilatory interneuron, which is not part of the ventilation-CPG. Our recordings suggest that the two centrally generated motor patterns are coordinated by reciprocal feedforward discharges from the singing-CPG to the ventilation-CPG and vice versa. Consequently, expiratory contraction of the abdomen usually occurs in phase with the chirps and ventilation accelerates during singing due to entrainment by the faster chirp cycle.

Swim initiation in the leech by serotonin-containing interneurones, cells 21 and 61

1986 ◽  
Vol 122 (1) ◽  
pp. 277-302
Author(s):  
M. P. Nusbaum ◽  
W. B. Kristan
Keyword(s):  
Central Pattern Generator ◽  
Motor Pattern ◽  
Pattern Generator ◽  
The Other ◽  
Sensory Neurones ◽  
Segmental Nerve ◽  
Macrobdella Decora ◽  
Intracellular Stimulation ◽  
Retzius Cell ◽  
Stimulation Of

Two pairs of serotonin-containing neurones, designated cells 21 and 61, were characterized physiologically and anatomically in the hirudinid leeches Macrobdella decora and Hirudo medicinalis. Both of these cells are bilaterally paired interneurones and each cell is weakly electrically coupled to the other serotonin-containing cells both intra- and interganglionically. Cells 21 and 61 are excited polysynaptically by individual identified mechano-sensory neurones. Segmental nerve shock sufficient to elicit an episode of swimming strongly excites cells 21 and 61, which then tend to generate bursts of impulses that are phase-locked to the swim motor pattern. Intracellular stimulation of either cell 21 or cell 61 often causes the initiation of swimming, acting in parallel with the nonserotonergic swim-initiator cell 204. Cells 61 and 204 are also weakly electrically coupled. The latency to swim onset by stimulating cell 21 or 61 is similar to that of cell 204 and different from that of the serotonergic Retzius cell. This result, with those in the accompanying paper (Nusbaum, 1986), suggests that unlike the Retzius cell and similar to cell 204, cells 21 and 61 synaptically contact cells of the swim central pattern generator (CPG).

Gating of Afferent Input by a Central Pattern Generator

1999 ◽  
Vol 81 (2) ◽  
pp. 950-953 ◽  
Author(s):  
Ralph A. DiCaprio
Keyword(s):  
Central Pattern Generator ◽  
Sensory Input ◽  
Motor Pattern ◽  
Pattern Generator ◽  
Afferent Input ◽  
Inhibitory Input ◽  
Cycle Period ◽  
Intracellular Recordings ◽  
Afferent Fibers ◽  
Sufficient Magnitude

Gating of afferent input by a central pattern generator. Intracellular recordings from the sole proprioceptor (the oval organ) in the crab ventilatory system show that the nonspiking afferent fibers from this organ receive a cyclic hyperpolarizing inhibition in phase with the ventilatory motor pattern. Although depolarizing and hyperpolarizing current pulses injected into a single afferent will reset the ventilatory motor pattern, the inhibitory input is of sufficient magnitude to block afferent input to the ventilatory central pattern generator (CPG) for ∼50% of the cycle period. It is proposed that this inhibitory input serves to gate sensory input to the ventilatory CPG to provide an unambiguous input to the ventilatory CPG.

Fast Synaptic Connections From CBIs to Pattern-Generating Neurons in Aplysia: Initiation and Modification of Motor Programs

2003 ◽  
Vol 89 (4) ◽  
pp. 2120-2136 ◽  
Author(s):  
Itay Hurwitz ◽  
Irving Kupfermann ◽  
Klaudiusz R. Weiss
Keyword(s):  
Central Pattern Generator ◽  
Motor Pattern ◽  
Aplysia Californica ◽  
Pattern Generator ◽  
Synaptic Connections ◽  
Motor Patterns ◽  
Motor Programs ◽  
Postsynaptic Potentials ◽  
Buccal Ganglia ◽  
Very High

Consummatory feeding movements in Aplysia californica are organized by a central pattern generator (CPG) in the buccal ganglia. Buccal motor programs similar to those organized by the CPG are also initiated and controlled by the cerebro-buccal interneurons (CBIs), interneurons projecting from the cerebral to the buccal ganglia. To examine the mechanisms by which CBIs affect buccal motor programs, we have explored systematically the synaptic connections from three of the CBIs (CBI-1, CBI-2, CBI-3) to key buccal ganglia CPG neurons (B31/B32, B34, and B63). The CBIs were found to produce monosynaptic excitatory postsynaptic potentials (EPSPs) with both fast and slow components. In this report, we have characterized only the fast component. CBI-2 monosynaptically excites neurons B31/B32, B34, and B63, all of which can initiate motor programs when they are sufficiently stimulated. However, the ability of CBI-2 to initiate a program stems primarily from the excitation of B63. In B31/B32, the size of the EPSPs was relatively small and the threshold for excitation was very high. In addition, preventing firing in either B34 or B63 showed that only a block in B63 firing prevented CBI-2 from initiating programs in response to a brief stimulus. The connections from CBI-2 to the buccal ganglia neurons showed a prominent facilitation. The facilitation contributed to the ability of CBI-2 to initiate a BMP and also led to a change in the form of the BMP. The cholinergic blocker hexamethonium blocked the fast EPSPs induced by CBI-2 in buccal ganglia neurons and also blocked the EPSPs between a number of key CPG neurons within the buccal ganglia. CBI-2 and B63 were able to initiate motor patterns in hexamethonium, although the form of a motor pattern was changed, indicating that non-hexamethonium-sensitive receptors contribute to the ability of these cells to initiate bursts. By contrast to CBI-2, CBI-1 excited B63 but inhibited B34. CBI-3 excited B34 and not B63. The data indicate that CBI-1, -2, and -3 are components of a system that initiates and selects between buccal motor programs. Their behavioral function is likely to depend on which combination of CBIs and CPG elements are activated.

Motor reflexes of stomach elicited by phenyldiguanide in the rat

1980 ◽  
Vol 58 (4) ◽  
pp. 352-359 ◽  
Author(s):  
K. S. Rao
Keyword(s):  
Motor Activity ◽  
Motor Response ◽  
Sympathetic Nerves ◽  
Vagal Afferents ◽  
Intragastric Pressure ◽  
Motor Responses ◽  
Efferent System ◽  
Efferent Pathway ◽  
Cervical Vagotomy ◽  
Stimulation Of

Intragastric pressure (IGP) as an index of gastric motor activity was used to investigate gastric motor responses elicited by phenyldiguanide (PDG) in rats under pentobarbitone anaesthesia. Phenyldiguanide injected into the atrium produced an inhibitory gastric motor response whereas an aortic injection resulted in an increase in IGP. Intracarotid injections were without effect. Atropine reduced the response to atrial PDG but not to aortic PDG. Cervical vagotomy abolished the response to both atrial and aortic PDG. Guanethidine and spinal transection abolished the response to atrial PDG only. It is concluded that PDG acts by stimulation of nonmedullated vagal afferents. The efferent pathway for PDG-evoked gastric relaxation is through sympathetic nerves and the efferent system for gastric contraction involves a noncholinergic, nonadrenergic excitatory mechanism.

scholarly journals Output variability across animals and levels in a motor system

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Angela Wenning ◽  
Brian J Norris ◽  
Cengiz Günay ◽  
Daniel Kueh ◽  
Ronald L Calabrese
Keyword(s):  
Life History ◽  
Central Pattern Generator ◽  
Motor Neurons ◽  
Motor System ◽  
Motor Pattern ◽  
Pattern Generator ◽  
Phase Relations ◽  
The Other ◽  
Output Variability ◽  
Rhythmic Behaviors

Rhythmic behaviors vary across individuals. We investigated the sources of this output variability across a motor system, from the central pattern generator (CPG) to the motor plant. In the bilaterally symmetric leech heartbeat system, the CPG orchestrates two coordinations in the bilateral hearts with different intersegmental phase relations (Δϕ) and periodic side-to-side switches. Population variability is large. We show that the system is precise within a coordination, that differences in repetitions of a coordination contribute little to population output variability, but that differences between bilaterally homologous cells may contribute to some of this variability. Nevertheless, much output variability is likely associated with genetic and life history differences among individuals. Variability of Δϕ were coordination-specific: similar at all levels in one, but significantly lower for the motor pattern than the CPG pattern in the other. Mechanisms that transform CPG output to motor neurons may limit output variability in the motor pattern.

scholarly journals Behaviour and Motor Output for an Insect Walking on a Slippery Surface: II. Backward Walking

1985 ◽  
Vol 118 (1) ◽  
pp. 287-296 ◽  
Author(s):  
D. GRAHAM ◽  
S. EPSTEIN
Keyword(s):  
Motor Activity ◽  
Motor Pattern ◽  
Motor Output ◽  
Retractor Muscle ◽  
Backward Walking ◽  
Stick Insects ◽  
Weak Activity ◽  
Slippery Surface ◽  
Walking Recovery ◽  
Simple Phase

Coordination of the legs and the motor activity of four muscles in a middle leg were recorded in adult stick insects walking on a slippery glass surface. Backward walking was not achieved by a simple phase shift of levators and depressors. In all muscles examined, there was a considerable disturbance of motor activity during backward walking when compared with that found in forward walking. In backward walking, recovery was performed, in the middle leg, by strong fast unit activity in the retractor muscle and all muscles showed weak activity at inappropriate times. Fast motor output appeared to be superimposed on the forward walking motor pattern to produce the movements required for backward walking in this insect.

Isoflurane Disrupts Central Pattern Generator Activity and Coordination in the Lamprey Isolated Spinal Cord

2005 ◽  
Vol 103 (3) ◽  
pp. 567-575 ◽  
Author(s):  
Steven L. Jinks ◽  
Richard J. Atherley ◽  
Carmen L. Dominguez ◽  
Karen A. Sigvardt ◽  
Joseph F. Antognini
Keyword(s):  
Spinal Cord ◽  
Central Pattern Generator ◽  
Motor Neurons ◽  
Central Pattern Generators ◽  
Volatile Anesthetics ◽  
Pattern Generator ◽  
Motor Output ◽  
Petroleum Jelly ◽  
Burst Frequency ◽  
Generator Activity

Background Although volatile anesthetics such as isoflurane can depress sensory and motor neurons in the spinal cord, movement occurring during anesthesia can be coordinated, involving multiple limbs as well as the head and trunk. However, it is unclear whether volatile anesthetics depress locomotor interneurons comprising central pattern generators or disrupt intersegmental central pattern generator coordination. Methods Lamprey spinal cords were excised during anesthesia and placed in a bath containing artificial cerebrospinal fluid and D-glutamate to induce fictive swimming. The rostral, middle, and caudal regions were bath-separated using acrylic partitions and petroleum jelly, and in each compartment, the authors recorded ventral root activity. The authors selectively delivered isoflurane (0.5, 1, and 1.5%) only to the middle segments of the spinal cord. Spectral analyses were then used to assess isoflurane effects on central pattern generator activity and coordination. Results Isoflurane dose-dependently reduced fictive locomotor activity in all three compartments, with 1.5% isoflurane nearly eliminating activity in the middle compartment and reducing spectral amplitudes in the anesthetic-free rostral and caudal compartments to 23% and 31% of baseline, respectively. Isoflurane decreased burst frequency in the caudal compartment only, to 53% of baseline. Coordination of central pattern generator activity between the rostral and caudal compartments was also dose-dependently decreased, to 42% of control at 1.5% isoflurane. Conclusion Isoflurane disrupts motor output by reducing interneuronal central pattern generator activity in the spinal cord. The effects of isoflurane on motor output outside the site of isoflurane application were presumably independent of effects on sensory or motor neurons.

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