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S Grillner

Publications and source records attributed to S Grillner.

At least 181 records · Page 10Linked to original sources
PubMed1987

Single sensory neurons activate excitatory amino acid receptors in the lamprey spinal cord.

The effects of excitatory amino acid (EAA) antagonists were tested on sensory afferent excitation in the lamprey spinal cord. Paired intracellular recordings were made from mechanosensory neurons (dorsal cells) and second order sensory neurons (giant interneurons). Stimulation of individual dorsal cells evoked mono- and/or polysynaptic excitatory postsynaptic potentials (EPSPs) in giant interneurons. These EPSPs were depressed by the EAA antagonists cis-2,3-piperidine dicarboxylate and kynurenic acid. Small components of the synaptic potentials were due to electrical coupling since they were not depressed by EAA antagonists or by calcium-free solution. The N-methyl-D-aspartate antagonist 2-amino-5-phosphonovalerate did not depress short-latency EPSPs. Thus, mechanosensory neurons in the lamprey spinal cord activate EAA receptors (kainate/quisqualate receptors) on interneurons, via mixed chemical and electrical synapses.

Afferent Pathways↗
PubMed1987

N-methyl-D-aspartate receptor-induced, inherent oscillatory activity in neurons active during fictive locomotion in the lamprey.

Bath application of N-methyl-aspartate induces fictive locomotor activity in the isolated spinal cord preparation of the lamprey, as well as TTX-resistant membrane potential oscillations in many individual neurons. This inherent oscillatory activity is shown to depend on a specific activation of N-methyl-D-aspartate (NMDA) receptors. This activation initiates voltage-dependent, magnesium-requiring membrane potential bistability, presumably due to a development of a region of negative slope conductance in the current-voltage relation of the neuron. When sodium ions were removed from the bathing solution, oscillations disappeared, and the membrane potential was maintained at a hyperpolarized level, suggesting that the depolarizing current during the oscillatory cycle is mainly carried by sodium ions. Replacing Ca2+ with Ba2+ also leads to a cessation of oscillatory activity, with the membrane potential remaining at the more depolarized level. This indicates an involvement of a Ca2+-dependent K+ current during the repolarization phase. These findings, together with the voltage dependence, can account for the main characteristics of the NMDA receptor-induced, TTX-resistant membrane potential oscillations. This oscillatory behavior has been demonstrated in motoneurons and in several interneurons including CC interneurons but has not been found in edge cells, dorsal cells, or lateral interneurons. The possibility that inherent oscillatory membrane properties may contribute to the activity pattern during fictive locomotion was investigated in experiments with intracellular current injection in the absence of TTX. The stimulation effects obtained required the presence of magnesium ions and were analogous to the stimulation effects seen during oscillations after TTX blockade. Together with similarities in, for instance, frequency and amplitude between the locomotor oscillatory activity and the TTX-resistant oscillations, the results are compatible with an involvement of inherent, oscillatory membrane properties during fictive locomotion in the lamprey spinal cord.

Animals↗
PubMed1986

Müller cells and other reticulospinal neurones are phasically active during fictive locomotion in the isolated nervous system of the lamprey.

Reticulospinal neurones were studied during fictive locomotion in the lamprey brainstem-spinal cord in vitro preparation. Intracellular recordings were made from the large reticulospinal Müller cells located in the mesencephalon (M1-3), rostral (I1) and middle (B1-5) rhombencephalon, the Mauthner cells, and the V cells located within the posterior reticular nucleus during fictive locomotor activity. All cells were depolarized during motor activity on either the ipsilateral (M1-3, I1, B1-5 and V cells) or the contralateral (Mauthner cell (crossed axon] side. During locomotor activity and long-lasting burst activity, phasic membrane potential oscillations occurred well correlated to the ventral root activity.

Action Potentials↗
PubMed1986

Effects of magnesium on fictive locomotion induced by activation of N-methyl-D-aspartate (NMDA) receptors in the lamprey spinal cord in vitro.

It has previously been demonstrated that an activation of N-methyl-D-aspartate (NMDA) receptors can induce fictive locomotion as well as tetrodotoxin (TTX)-resistant membrane potential oscillations in certain types of neurones in the in vitro preparation of the lamprey spinal cord. These oscillations in individual neurones depend on voltage-sensitive properties of NMDA-activated channels which are only manifested in the presence of Mg2+. To evaluate the role of these pacemaker-like oscillations in the generation of locomotion, the motor patterns induced by N-methyl-D,L-aspartate (NMA) before and after removal of Mg2+ were compared. It was found that the ventral root burst pattern of fictive locomotion was more irregular after removal of Mg2+, particularly at low burst rates. This suggests that the membrane properties underlying the NMDA-induced TTX-resistant membrane potential oscillations are of importance for the generation of a stable and regular locomotor activity in particular at low rates of fictive locomotion. When fictive locomotion was induced instead by an activation of kainate receptors a removal of Mg2+ had no effect on the motor pattern. The effects of the two K+-channel blockers, tetraethylammonium (TEA) and gallamine were also tested on NMA-induced fictive locomotion. Both compounds caused an increase in the burst frequency. The Mg2+-dependent NMDA-induced bistable membrane properties thus appear to be of importance for the operation of the network which generates the locomotor pattern.

Animals↗
PubMed1986

A spinal projection of 5-hydroxytryptamine neurons in the lamprey brainstem; evidence from combined retrograde tracing and immunohistochemistry.

To investigate whether there is a descending contribution to the spinal 5-hydroxytryptamine (5-HT) innervation in the lamprey, a primitive vertebrate, a study using retrograde transport of the fluorescent tracer Fast blue combined with 5-HT immunohistochemistry was conducted. Two to 4 weeks after an injection of Fast blue into the rostral spinal cord, retrogradely labelled cells were seen throughout the brainstem. Two groups of these cells, one within the posterior reticular nucleus of the rhombencephalon and another rostral to the trigeminal motor nucleus, were labelled after incubation with 5-HT antiserum. These findings suggest that in addition to the well-described local intraspinal 5-HT system, there is also, as in higher vertebrates, a descending 5-HT projection from the brainstem which extends at least 20 segments into the spinal cord.

Animals↗
PubMed1986

5-Hydroxytryptamine (serotonin) causes a reduction in the afterhyperpolarization following the action potential in lamprey motoneurons and premotor interneurons.

The actions of 5-hydroxytryptamine (5-HT) on single neurons in the lamprey spinal cord have been investigated by intracellular recordings in vitro. Administration of 5-HT either by pressure ejection or by perfusion in the bath caused a reversible reduction of the late phase of the afterhyperpolarization (AHP) following the action potentials. This effect was antagonized by methysergide. A reduction of the late AHP was observed in lateral interneurons, motoneurons and some unclassified cells.

Action Potentials↗
PubMed1986

Dual-component synaptic potentials in the lamprey mediated by excitatory amino acid receptors.

The synaptic mechanisms underlying amino acid-mediated excitation in the lamprey spinal cord have been investigated. Fine stimulating electrodes were used to stimulate single axons in the spinal cord and evoke unitary EPSPs in lamprey motoneurons and one type of premotor interneuron, the CC interneuron. Three types of EPSP, distinguished by their time course and sensitivity to amino acid antagonists, were seen. Fast EPSPs had a fast rise time (mean, 6.5 msec) and a short half-decay time (mean, 22.5 msec). Slow EPSPs lasted at least 200 msec, had a slow rise time (mean, 28 msec), and a long half-decay time (mean, 109 msec). The third type of unitary potential, called "mixed" EPSP, also lasted at least 200 msec, had a fast rise time (mean, 12 msec), and a long half-decay time (mean, 105 msec). Lamprey neurons were found to possess 3 types of excitatory amino acid receptor: N-methyl-D-aspartate (NMDA), kainate, and quisqualate receptors. 2-Amino-5-phosphonovaleric acid (APV) or Mg2+ blocked the depolarizations caused by N-methyl-D,L-aspartate (NMA) but not those of kainate or quisqualate. Cis-2, 3-piperidine dicarboxylic acid (PDA) blocked the depolarizations caused by NMA and kainate but not those of quisqualate. Fast EPSPs were unaffected by the bath application of APV or Mg2+ but were greatly reduced by PDA, suggesting that these EPSPs were mediated by non-NMDA, possibly kainate receptors. Both APV and Mg2+ blocked the slow EPSPs, suggesting that they were mediated by NMDA receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

The role of putative excitatory amino acid neurotransmitters in the initiation of locomotion in the lamprey spinal cord. I. The effects of excitatory amino acid antagonists.

The activation of N-methyl-D-aspartate (NMDA) and kainate receptors will evoke fictive locomotion in the appropriate motor pattern for locomotion in the isolated lamprey spinal cord, but not a selective activation of quisqualate receptors. The present experiments test whether the initiation of locomotion in response to sensory stimulation depends on these types of receptors. An in vitro preparation of the lamprey spinal cord with part of its tailfin left innervated has been used. In this preparation a sequence of fictive locomotion (i.e. alternating bursts in the segmental ventral roots with a rostrocaudal phase lag) can be elicited by continual sensory stimulation of the tailfin. The effects of excitatory amino acid antagonists were studied by recordings from ventral roots (extracellularly) and motoneurones (intracellularly). It was found that the strong initial bursts of each swimming sequence induced by sensory stimulation were depressed by combined NMDA/kainate antagonists (cis-2,3-piperidine dicarboxylate (PDA) and gamma-D-glutamylglycine (gamma-DGG] whereas the less intense burst activity, occurring particularly towards the end of each swimming sequence, was depressed by a selective NMDA antagonist, 2-amino-5-phosphonovalerate (2-APV). This condition could be mimicked in an isolated spinal cord preparation by an application of L-glutamate; the low-level fictive locomotion induced by low doses of L-Glu (less than 100 microM) was depressed by a NMDA antagonist (2-APV), and, if higher doses were applied, the activity was only depressed by PDA/gamma-DGG. The mode and time course of the depression (by excitatory amino acid antagonists) of fictive locomotion, induced by sensory stimulation, shows that the putative excitatory amino acid neurotransmitter directly or indirectly acts at the pattern generating circuitry within the spinal cord.

Amino Acids↗
PubMed1985

The role of putative excitatory amino acid neurotransmitters in the initiation of locomotion in the lamprey spinal cord. II. The effects of amino acid uptake inhibitors.

Fictive locomotion can be evoked in an in vitro preparation of the lamprey spinal cord by an activation of N-methyl-D-aspartate (NMDA) or kainate receptors. To obtain further knowledge of the putative transmitters underlying this activation the effects of L-glutamate and L-aspartate were examined. These endogenous amino acids exerted a distinctly different effect as compared to the synthetic amino acids (N-methyl-D,L-aspartate and kainate) previously tested. In a wide dose range L-glutamate and L-aspartate elicited fictive locomotion only when the bathing solution was rapidly circulated over the spinal cord surface. In the absence of fluid circulation the activity rapidly ceased. To test if this effect was due to an uptake of amino acids, two amino acid uptake inhibitors were administered. After exposure to p-chloromercuriphenylsulphonate (pCMS) or dihydrokainate (DHK), L-glutamate and L-aspartate elicited continuous fictive locomotion independently of whether the bathing fluid was circulated or not. This treatment also markedly lowered the threshold doses of L-glutamate and L-aspartate, while the effects of NMA and kainate were barely affected. Fictive locomotion induced by sensory stimulation of the tailfin was also prolonged by dihydrokainate. These findings suggest that a highly effective amino acid uptake system is present in the lamprey spinal cord and furthermore that it takes part in the inactivation of synaptically released acidic amino acid neurotransmitters, which are of importance for the initiation of locomotion.

Amino Acids↗
PubMed1985

Ionic mechanisms of 3 types of functionally different neurons in the lamprey spinal cord.

Action potentials and afterpotentials were compared in giant interneurons, sensory dorsal cells and large intraspinal axons in the lamprey spinal cord. Afterpotentials of giant interneurons and dorsal cells consisted of two hyperpolarizing phases, an early and a late one, which were separated by a delayed depolarization. The afterpotentials of axons had a single hyperpolarizing phase also followed by a delayed depolarization. Tetraethyl ammonium chloride (TEA+) eliminated the early phase of the afterhyperpolarization in giant interneurons, only partially reduced the early phase in dorsal cells and did not affect the single phase of axons. The delayed depolarization of dorsal cells was attenuated by TEA+ but in axons it was unaltered. The heavy metal ions Mn2+ and Co2+ (2 mM) eliminated the late phase in giant interneurons but did not reduce the late phase in dorsal cells. The delayed depolarization remained in both types of cell in the presence of these ions. Action potentials of giant interneurons and dorsal cells, but not those of axons, were broadened by TEA+. The TEA-prolonged action potentials were narrowed by Mn2+ applied in combination with TEA+. The afterhyperpolarizations of all 3 cells were reduced by injection of negative current and enhanced by positive current. Repetitive stimulation resulted in summation of the afterhyperpolarization in giant interneurons and dorsal cells. The results suggest that different sets of potassium channels are responsible for the afterhyperpolarizations in each type of cell. In giant interneurons fast channels which are sensitive to TEA+ may underlie the early phase and slow channels activated by calcium entry may underlie the slow phase. The early phase of dorsal cells may be caused by two types of fast channel, one similar to that in giant interneurons and another less sensitive to external TEA+. This latter type may also cause the afterhyperpolarization in axons. Although calcium channels appear to contribute to the action potentials of giant interneurons and dorsal cells, the late phase of the latter neurons does not seem to be activated by calcium entry. The delayed depolarizations of the neurons appear to be due to an inward current which is not carried by calcium.

Action Potentials↗
PubMed1985

The ionic mechanisms underlying N-methyl-D-aspartate receptor-induced, tetrodotoxin-resistant membrane potential oscillations in lamprey neurons active during locomotion.

Activation of N-methyl-D-aspartate (NMDA) receptors can induce tetrodotoxin (TTX)-resistant membrane potential oscillations as well as fictive locomotion in the in vitro preparation of the lamprey spinal cord. The ionic basis of these oscillations were investigated in the presence of N-methyl-D,L-aspartate and TTX. Addition of blocking agents (2-amino-5-phosphonovalerate and tetraethylammonium (TEA)) and selective removal or substitution of certain ions (Mg2+, Ca2+, Na+, Ba2+) were used in the analysis of the oscillations. The depolarizing phase of the oscillation requires Na+ ions but not Ca2+ ions. The depolarization becomes larger if TEA is administered in the bath, which presumably is due to a blockade of potassium (K+) channels activated during the depolarizing phase. The repolarization appears to depend on a Ca2+ entry, which presumably acts indirectly by an activation of Ca2+-dependent K+ channels. Together with the NMDA-induced voltage dependence, this will bring the membrane potential back down to a hyperpolarized level.

Animals↗
PubMed1985

Activation of NMDA receptors elicits fictive locomotion and bistable membrane properties in the lamprey spinal cord.

The motor pattern underlying locomotion in the lamprey can be elicited in the spinal cord in vitro by applying excitatory amino acids that activate NMDA receptors. When this is done oscillatory membrane potentials phase-linked with the locomotory rhythm can be recorded in different types of neurones. In some spinal neurones large amplitude oscillation continues after elimination of synaptic input with application of TTX. This oscillatory pacemaker-like activity is dependent on an activation of NMDA receptors, and is probably important in the generation of locomotion.

Animals↗
PubMed1985

The effect of current passage on N-methyl-D-aspartate-induced, tetrodotoxin-resistant membrane potential oscillations in lamprey neurons active during locomotion.

In lamprey spinal cord neurons, N-methyl-aspartate (NMA) can elicit tetrodotoxin (TTX)-resistant membrane potential oscillations (10-25 mV), that are of similar frequency to those recorded during NMA-induced fictive locomotion before TTX. The frequency of the oscillations was progressively reduced when increasing the amount of hyperpolarizing DC current. Brief de- or hyperpolarizing pulses gave phase-dependent effects on the duration of the oscillation cycle and rhythm resetting. Periodic stimuli could entrain the oscillatory activity. Under normal conditions, these oscillations will be influenced by synaptic activity, leading to an adequate coordination between neurons active during locomotion.

Animals↗
PubMed1985

Immunohistochemical demonstration of some putative neurotransmitters in the lamprey spinal cord and spinal ganglia: 5-hydroxytryptamine-, tachykinin-, and neuropeptide-Y-immunoreactive neurons and fibers.

The distribution of some putative neurotransmitters was investigated in the spinal cord and spinal ganglia of the lamprey, a primitive vertebrate, by using immunohistochemical methods. In the spinal cord a midline row of 5-hydroxytryptamine (5-HT)-immunoreactive neurons was present immediately ventral to the central canal over the entire length of the spinal cord. The ventral processes of these neurons formed a dense ventromedial plexus of varicosities. In the dorsal, lateral, and ventral spinal axon columns, several longitudinal 5-HT fibers were present. After chronic spinal transections the distribution of 5-HT fibers was unchanged; it is therefore concluded that there was no substantial descending 5-HT contribution and that the spinal 5-HT neurons supplied the regional 5-HT innervation. The spinal 5-HT cells sent fibers into the dorsal and ventral roots; 5-HT cell bodies and fibers were also present in the spinal dorsal root ganglia, in their dorsal, ventral, and lateral nerve branches, and in the dorsal and ventral branches of the ventral roots. Neurons and fibers containing peptides of the tachykinin (TK) family (to which, amongst others, substance P belongs) were found in the spinal cord. TK neurons in the spinal cord supplied the local TK innervation, as well as TK fibers in the dorsal and ventral roots. Fibers have been found containing either TK, or 5-HT, or both compounds. Neurons containing neuropeptide-Y (NPY)-immunoreactive material were present in a medial column just dorsal to the central canal. The NPY neurons have longitudinal, mainly descending, fibers that provide the local NPY innervation of the lamprey spinal cord. The present results provide evidence for local spinal systems containing 5-HT, TK, 5-HT and TK, or NPY, but in contrast to mammals, these compounds do not seem to arise from supraspinal neurons.

Animals↗
PubMed1985

Possible target neurons of 5-hydroxytryptamine fibers in the lamprey spinal cord: immunohistochemistry combined with intracellular staining with Lucifer yellow.

Intracellular recordings were made from 76 neurons belonging to various cell types in the lamprey spinal cord, and these neurons were subsequently stained with Lucifer yellow. Sections were made of spinal cords containing Lucifer-yellow-filled neurons, and in the same sections 5-hydroxytryptamine (5-HT)-containing neurons and fibers were made visible with immunohistochemical methods. Motoneurons and lateral cells appeared to send part of their dendrites into a dense ventromedial 5-HT plexus, and these dendrites were adjacent to 5-HT varicosities. No or few 5-HT varicosities have been found adjacent to cell bodies or dendrites of sensory dorsal cells, giant interneurons, and edge cells. The combined application of intracellular staining and immunohistochemistry appeared to be suited to screen for possible transmitter-identified contacts on morphologically identified neurons.

Animals↗
PubMed1985

Neurobiological bases of rhythmic motor acts in vertebrates.

The general principles governing the nervous control of innate motor acts in vertebrates are discussed. Particular consideration is given to the control of locomotion in both mammals and lower vertebrates. One in vitro model of the lamprey central nervous system has been developed. It can be maintained in vitro for several days and the motor pattern underlying locomotion can be elicited in isolated sections of the spinal cord. These findings now allow a detailed analysis of the underlying neural mechanisms. The hypothesis that different parts of the network controlling locomotion can be used in a variety of other motor acts, including learned ones, is reviewed.

Animals↗