scholarly journals How does the Lamprey Central Nervous System make the Lamprey Swim?

1984 ◽  
Vol 112 (1) ◽  
pp. 337-357 ◽  
Author(s):  
STEN GRILLNER ◽  
PETER WALLÉN
Keyword(s):  
Spinal Cord ◽  
Nmda Receptor ◽  
Morphological Characteristics ◽  
Rhythmic Activity ◽  
The Body ◽  
Fictive Locomotion ◽  
Motor Patterns ◽  
Motor Neurones ◽  
Receptor Blockers

The lamprey spinal cord, in isolation or with the brainstem, can be used in vitro. The motor patterns underlying the swimming movements can be elicited by: (1) a pharmacological activation of a specific type of neuronal receptor (NMDA-receptor), that may in other systems give rise to an unstable membrane potential, (2) by stimulation of the brainstem or (3) by tactile activation of skin regions left innervated. In the latter case the initiation of ‘fictive’ swimming is partially caused by a release of a transmitter activating NMDA-receptors, as judged by the effect of NMDA-receptor blockers. The central pattern generator (CPG) is strongly influenced by feedback from mechanosensitive elements, which at least partially reside within the spinal cord. The edge cell in the lamprey spinal cord serves as an intraspinal mechanoreceptor. The ability to generate a coordinated motor output is distributed, since spinal cord sections down to 1.5–2 segments can be made to generate alternating activity. Motor neurones receive an approximately synchronous alternating excitatory and inhibitory drive in each swim cycle and do not appear to be part of the CPG. Motor neurones supplying different parts of the body wall on the same side of a body segment have different morphology with ramifications around different descending axons. The input drive signal during fictive locomotion to motor neurones located close to each other but with different morphological characteristics may differ substantially with regard to the γ-relationship (±25%) and the shape of the oscillation. This implies that even at a segmental level motor neurones may be further subdivided, and furthermore that the ipsilateral network generating the drive signal to ipsilateral motor neurones generates a more complex and individualized output than previously assumed. Motor neurones are not part of the rhythm-generating circuit. The large identifiable interneurones are not required for rhythmic activity to occur although they may be phasically active in the swim cycle. The small segmental interneurones have not yet been completely characterized. Many are phasically active during ‘fictive locomotion’ and lack an apparent axon. Their phase relationships in relation to the burst patterns vary over the entire swim cycle.

Ontogeny of Rhythmic Motor Patterns Generated in the Embryonic Rat Spinal Cord

2003 ◽  
Vol 89 (3) ◽  
pp. 1187-1195 ◽  
Author(s):  
Jun Ren ◽  
John J. Greer
Keyword(s):  
Spinal Cord ◽  
Spontaneous Activity ◽  
Developmental Stages ◽  
Rhythmic Activity ◽  
Late Gestation ◽  
Spatiotemporal Pattern ◽  
Rat Spinal Cord ◽  
Motor Patterns ◽  
Rhythmic Motor

Patterned spontaneous activity is generated in developing neuronal circuits throughout the CNS including the spinal cord. This activity is thought to be important for activity-dependent neuronal growth, synapse formation, and the establishment of neuronal networks. In this study, we examine the spatiotemporal distribution of motor patterns generated by rat spinal cord and medullary circuits from the time of initial axon outgrowth through to the inception of organized respiratory and locomotor rhythmogenesis during late gestation. This includes an analysis of the neuropharmacological control of spontaneous rhythms generated within the spinal cord at different developmental stages. In vitro spinal cord and medullary-spinal cord preparations isolated from rats at embryonic ages (E)13.5–E21.5 were studied. We found age-dependent changes in the spatiotemporal pattern, neurotransmitter control, and propensity for the generation of spontaneous rhythmic motor discharge during the prenatal period. The developmental profile of the neuropharmacological control of rhythmic bursting can be divided into three periods. At E13.5–E15.5, the spinal networks comprising cholinergic and glycinergic synaptic interconnections are capable of generating rhythmic activity, while GABAergic synapses play a role in supporting the spontaneous activity. At late stages (E18.5–E21.5), glutamate drive acting via non- N-methyl-d-aspartate (non-NMDA) receptors is primarily responsible for the rhythmic activity. During the middle stage (E16.5–E17.5), the spontaneous activity results from the combination of synaptic drive acting via non-NMDA glutamatergic, nicotinic acetylcholine, glycine, and GABAA receptors. The modulatory actions of chloride-mediated conductances shifts from predominantly excitatory to inhibitory late in gestation.

scholarly journals Fictive Rhythmic Motor Patterns Induced by NMDA in an In Vitro Brain Stem–Spinal Cord Preparation From an Adult Urodele

1999 ◽  
Vol 82 (2) ◽  
pp. 1074-1077 ◽  
Author(s):  
Isabelle Delvolvé ◽  
Pascal Branchereau ◽  
Réjean Dubuc ◽  
Jean-Marie Cabelguen
Keyword(s):  
Spinal Cord ◽  
Brain Stem ◽  
Rhythm Generation ◽  
Motor Patterns ◽  
Rhythmic Motor ◽  
Bath Application ◽  
The Neural Networks ◽  
Ventral Roots ◽  
Pleurodeles Waltl

An in vitro brain stem–spinal cord preparation from an adult urodele ( Pleurodeles waltl) was developed in which two fictive rhythmic motor patterns were evoked by bath application of N-methyl-d-aspartate (NMDA; 2.5–10 μM) with d-serine (10 μM). Both motor patterns displayed left-right alternation. The first pattern was characterized by cycle periods ranging between 2.4 and 9.0 s (4.9 ± 1.2 s, mean ± SD) and a rostrocaudal propagation of the activity in consecutive ventral roots. The second pattern displayed longer cycle periods (8.1–28.3 s; 14.2 ± 3.6 s) with a caudorostral propagation. The two patterns were inducible after a spinal transection at the first segment. Preliminary experiments on small pieces of spinal cord further suggested that the ability for rhythm generation is distributed along the spinal cord of this preparation. This study shows that the in vitro brain stem–spinal cord preparation from Pleurodeles waltl may be a useful model to study the mechanisms underlying the different axial motor patterns and the flexibility of the neural networks involved.

NMDA Receptor-Dependent Periodic Oscillations in Cultured Spinal Cord Networks

2001 ◽  
Vol 86 (6) ◽  
pp. 3030-3042 ◽  
Author(s):  
Edward W. Keefer ◽  
Alexandra Gramowski ◽  
Guenter W. Gross
Keyword(s):  
Spinal Cord ◽  
Nmda Receptor ◽  
Rhythmic Activity ◽  
Network Size ◽  
Observation Time ◽  
Network Activity ◽  
Early Postnatal Development ◽  
Bath Application ◽  
Coefficients Of Variation ◽  
Burst Patterns

Cultured spinal cord networks grown on microelectrode arrays display complex patterns of spontaneous burst and spike activity. During disinhibition with bicuculline and strychnine, synchronized burst patterns routinely emerge. However, the variability of both intra- and interculture burst periods and durations are typically large under these conditions. As a further step in simplification of synaptic interactions, we blocked excitatory AMPA synapses with 2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzoquinoxaline-7-sulphonamide (NBQX), resulting in network activity mediated through the N-methyl-d-aspartate (NMDA) receptor (NMDAONLY). This activity was APV sensitive. The oscillation under NMDAONLY conditions at 37°C was characterized by a period of 2.9 ± 0.3 s (16 separate cultures). More than 98% of all neurons recorded participated in this highly rhythmic activity. The temporal coefficients of variation, reflecting the rhythmic nature of the oscillation, were 3.7, 4.7, and 4.9% for burst rate, burst duration, and interburst interval, respectively [mean coefficients of variation (CVs) for 16 cultures]. The oscillation persisted for at least 12 h without change (maximum observation time). Once established, it was not perturbed by agents that block mGlu receptors, GABABreceptors, cholinergic receptors, purinergic receptors, tachykinin receptors, serotonin (5-HT) receptors, dopamine receptors, electrical synapses, burst afterhyperpolarization, NMDA receptor desensitization, or the hyperpolarization-activated current. However, the oscillation was destroyed by bath application of NMDA (20–50 μM). These results suggest a presynaptic mechanism underlying this periodic rhythm that is solely dependent on the NMDA synapse. When the AMPA/kainate synapse was the sole driving force ( n = 6), the resulting burst patterns showed much higher variability and did not develop the highly periodic, synchronized nature of the NMDAONLYactivity. Network size or age did not appear to influence the reliability of expression of the NMDAONLYactivity pattern. For this reason, we suggest that the NMDAONLY condition unmasks a fundamental rhythmogenic mechanism of possible functional importance during periods of NMDA receptor-dominated activity, such as embryonic and early postnatal development.

Selective Depression of the Spinal Polysynaptic Reflex by the NMDA Receptor Antagonists in an Isolated Spinal Cord in vitro

1997 ◽  
Vol 29 (4) ◽  
pp. 645-649 ◽  
Author(s):  
Yoshimi Maruoka ◽  
Yukihiro Ohno ◽  
Hiroyasu Tanaka ◽  
Hirokazu Yasuda ◽  
Ken-Ichi Ohtani ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Nmda Receptor ◽  
Nmda Receptor Antagonists ◽  
Receptor Antagonists ◽  
Polysynaptic Reflex

scholarly journals Retracing your footsteps: developmental insights to spinal network plasticity following injury

2018 ◽  
Vol 119 (2) ◽  
pp. 521-536 ◽  
Author(s):  
C. Jean-Xavier ◽  
S. A. Sharples ◽  
K. A. Mayr ◽  
A. P. Lognon ◽  
P. J. Whelan
Keyword(s):  
Spinal Cord ◽  
Neuronal Excitability ◽  
Weight Bearing ◽  
Rhythmic Activity ◽  
Motor Output ◽  
Parallel Mechanisms ◽  
Sensory Afferents ◽  
Motor Patterns ◽  
Network Function ◽  
Cord Injury

During development of the spinal cord, a precise interaction occurs between descending projections and sensory afferents, with spinal networks that lead to expression of coordinated motor output. In the rodent, during the last embryonic week, motor output first occurs as regular bursts of spontaneous activity, progressing to stochastic patterns of episodes that express bouts of coordinated rhythmic activity perinatally. Locomotor activity becomes functionally mature in the 2nd postnatal wk and is heralded by the onset of weight-bearing locomotion on the 8th and 9th postnatal day. Concomitantly, there is a maturation of intrinsic properties and key conductances mediating plateau potentials. In this review, we discuss spinal neuronal excitability, descending modulation, and afferent modulation in the developing rodent spinal cord. In the adult, plastic mechanisms are much more constrained but become more permissive following neurotrauma, such as spinal cord injury. We discuss parallel mechanisms that contribute to maturation of network function during development to mechanisms of pathological plasticity that contribute to aberrant motor patterns, such as spasticity and clonus, which emerge following central injury.

Activity of commissural interneurons in spinal cord of Xenopus embryos

1984 ◽  
Vol 51 (6) ◽  
pp. 1257-1267 ◽  
Author(s):  
S. R. Soffe ◽  
J. D. Clarke ◽  
A. Roberts
Keyword(s):  
Spinal Cord ◽  
Rhythmic Activity ◽  
Excitatory Input ◽  
Cycle Period ◽  
Fictive Locomotion ◽  
Anatomy And Physiology ◽  
Postsynaptic Potential ◽  
Natural Stimulation ◽  
Xenopus Laevis Embryos ◽  
Stimulation Of

Horseradish peroxidase- (HRP) filled microelectrodes have been used to examine the anatomy and physiology of "commissural interneurons," a morphologically defined class of spinal cord interneuron in Xenopus laevis embryos. Commissural interneurons have unipolar cell bodies in the dorsal half of the spinal cord. Their dendrites lie in the mid to ventral parts of the lateral tracts and their axons cross the cord ventrally, T branch, and ascend and descend on the opposite side of the cord. Recordings were made from animals immobilized in tubocurarine and responding to natural stimulation with three patterns of fictive motor activity. During episodes of fictive swimming, commissural interneurons are phasically excited to fire 1 spike/cycle in phase with motor discharge on the same side and receive a midcycle inhibitory postsynaptic potential (IPSP) in phase with motor discharge on the opposite side. Rhythmic activity is superimposed on a background depolarization. During periods of synchrony, phasic excitatory input doubles in frequency so that cells fire with half the swimming cycle period. The background depolarization is generally stronger than during swimming. During periods of fictive struggling, evoked by electrical stimulation of the skin, commissural interneurons fire a burst of spikes per cycle, cells being relatively hyperpolarized when motoneurons on the opposite side are active. In response to ipsilateral skin stimulation, some cells receive an IPSP at a latency of 12-20 ms. This precedes the onset of fictive locomotion. We discuss how anatomy and activity of commissural interneurons is suitable for a reciprocal inhibitory role.

Identification of excitatory interneurons contributing to generation of locomotion in lamprey: structure, pharmacology, and function

1989 ◽  
Vol 62 (1) ◽  
pp. 59-69 ◽  
Author(s):  
J. T. Buchanan ◽  
S. Grillner ◽  
S. Cullheim ◽  
M. Risling
Keyword(s):  
Spinal Cord ◽  
Membrane Potential ◽  
Excitatory Amino Acid ◽  
Postsynaptic Membrane ◽  
Fictive Locomotion ◽  
Potential Oscillations ◽  
And Function ◽  
Spherical Vesicles ◽  
Membrane Potential Oscillations

1. In the in vitro preparation of the lamprey spinal cord, paired intracellular recordings of membrane potential were used to identify interneurons producing excitatory postsynaptic potentials (EPSPs) on myotomal motoneurons. 2. Seventy-nine interneurons (8.4% of all neuron-motoneuron pairs tested) elicited unitary EPSPs that followed one-for-one at short, constant latencies and were therefore considered monosynaptic according to conventional criteria. Evidence was obtained for selectivity and divergence of excitatory interneuron (EIN) outputs and for convergence of EIN input to motoneurons. 3. The neurotransmitter released by EINs may be an excitatory amino acid such as glutamate, because the EPSPs were depressed by antagonists of excitatory amino acids. 4. Intracellular dye injection revealed that EINs have small cell bodies (average 11 x 27 microns), transversely oriented dendrites, and thin (less than 3 microns) slowly conducting axons (0.7 m/s) that project caudally and ipsilaterally. One EIN exhibited a system of thin multi-branching axon collaterals with periodic swellings. Ultrastructurally, these swellings contained clear spherical vesicles, and they apposed postsynaptic membrane specializations. 5. During fictive locomotion, the membrane-potential oscillations of EINs were greater in amplitude than, but similar in shape and timing to, those of their postsynaptic motoneurons. EINs fired action potentials during fictive locomotion and contributed to the depolarization of motoneurons. 6. These interneurons are proposed to be a source of excitation to motoneurons and interneurons in the lamprey spinal cord, participating in motor activity including locomotion.

Extracellular K+ Induces Locomotor-Like Patterns in the Rat Spinal Cord In Vitro: Comparison With NMDA or 5-HT Induced Activity

1998 ◽  
Vol 79 (5) ◽  
pp. 2643-2652 ◽  
Author(s):  
E. Bracci ◽  
M. Beato ◽  
A. Nistri
Keyword(s):  
Spinal Cord ◽  
Threshold Concentration ◽  
Pattern Generation ◽  
Neonatal Rat ◽  
Rat Spinal Cord ◽  
Motor Patterns ◽  
Pattern Frequency ◽  
High K ◽  
In Vitro Comparison

Bracci, E., M. Beato, and A. Nistri. Extracellular K+ induces locomotor-like patterns in the rat spinal cord in vitro: comparison with NMDA or 5-HT induced activity. J. Neurophysiol. 79: 2643–2652, 1998. Bath-application of increasing concentrations of extracellular K+ elicited alternating motor patterns recorded from pairs of various lumbar ventral roots of the neonatal rat (0–2 days old) spinal cord in vitro. The threshold concentration of K+ for this effect was 7.9 ± 0.8 mM (mean ± SD). The suprathreshold concentration range useful to evoke persistent motor patterns (lasting ≥10 min) was very narrow (∼1 mM) as further increments elicited only rhythmic activity lasting from 20 s to a few minutes. On average, the fastest period of rhythmic patterns was 1.1 ± 0.3 s. Intracellular recording from lumbar motoneurons showed that raised extracellular K+ elicited membrane potential oscillations with superimposed repetitive firing. In the presence of N-methyl-d-aspartate (NMDA) or non-NMDA receptor blockers [ R(−)-2-amino-phosphonovaleric acid or 6-cyano-7-nitroquinoxaline-2,3-dione, respectively] extracellular K+ increases could still induce motor patterns although the threshold concentration was raised. Serotonin (5-HT) also induced alternating motor patterns (threshold 15 ± 7 μM) that were consistently slower than those induced by high K+ or NMDA. Ritanserin (1 μM) prevented the locomotor-like activity of 5-HT but not that of high K+ provided the concentration of the latter was further increased. Subthreshold concentrations of K+ became effective in the presence of subthreshold doses of 5-HT or NMDA, indicating mutual facilitation between these substances. The fastest pattern frequency was observed by raising K+ or by adding NMDA. In the presence of 5-HT, the pattern frequency was never as fast even if NMDA (or high K+) was coapplied. Furthermore, application of 5-HT significantly slowed down the K+- or NMDA-induced rhythm, an effect strongly potentiated in the presence of ritanserin. It is suggested that the operation of the spinal locomotor network was activated by rises in extracellular K+, which presumably led to a broad increase in neuronal excitability. Whenever the efficiency of excitatory synaptic transmission was diminished (for example by glutamate receptor antagonism), a larger concentration of K+ was required to evoke locomotor-like patterns. The complex effect (comprising stimulation and inhibition) of 5-HT on alternating pattern generation appeared to result from a dual action of this substance on the spinal locomotor network.

Synaptic transmission between ventrolateral funiculus axons and lumbar motoneurons in the isolated spinal cord of the neonatal rat

1994 ◽  
Vol 72 (5) ◽  
pp. 2406-2419 ◽  
Author(s):  
M. Pinco ◽  
A. Lev-Tov
Keyword(s):  
Spinal Cord ◽  
Nmda Receptor ◽  
Gabaa Receptor ◽  
Gabab Receptor ◽  
Short Latency ◽  
Neonatal Rat ◽  
Gamma Aminobutyric Acid ◽  
Long Latency ◽  
Ventrolateral Funiculus

1. We studied the projections of ventrolateral funiculus (VLF) axons to lumbar motoneurons in the in vitro spinal cord preparation of 1- to 6-day-old rats using extracellular and sharp-electrode intracellular recordings. 2. Ipsilateral and contralateral VLF projections to lumbar motoneurons (L4-L5) could be activated in the neonatal rat by stimulation of the surgically peeled VLF at the rostral (L1-L2) and caudal lumbar (L6) cord. Motoneurons were activated ipsilaterally through short- and long-latency projections in all cases and contralaterally through long-latency projections in most cases. 3. Suppression of the excitatory components of VLF postsynaptic potentials (PSPs) by application of the specific antagonists of N-methyl D-aspartate (NMDA) and non-NMDA receptors, 2-amino-5-phosphonovaleric acid (APV) and 6-cyano-7-nitroquin-oxaline-2,3-dione (CNQX), revealed depolarizing PSPs that could be reversed at -55 to -60 mV by injection of depolarizing current steps to the motoneurons. These depolarizing PSPs were blocked by addition of strychnine and bicuculline and are therefore suggested to be glycine and gamma-aminobutyric acid-A (GABAA) receptor-mediated inhibitory PSPs. The identity of a small (< or = 0.2 mV) residual depolarizing component that persisted in the presence of APV, CNQX, strychnine, and bicuculline remains to be determined. 4. Short-latency excitatory PSPs (EPSPs) could be resolved from the ipsilaterally elicited VLF PSPs after the reduction of the polysynaptic activity in the preparation by administration of mephenesin, which was followed by suppression of the glycine and GABAA receptor-mediated components of the PSPs by bath application of strychnine and bicuculline. The latencies of these EPSPs were similar to those of the monosynaptic dorsal root afferent EPSPs recorded from the same motoneurons. These short-latency VLF EPSPs were shortened by the NMDA antagonist APV and revealed an NMDA receptor-mediated component after administration of the non-NMDA receptor antagonist CNQX. Addition of the GABAB receptor agonist L-(-) baclofen or the glutamate analogue L-2-amino-4-phosphonobutyric acid (L-AP4) attenuated the pharmacologically resolved short-latency EPSPs.(ABSTRACT TRUNCATED AT 400 WORDS)

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