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L Brodin

Publications and source records attributed to L Brodin.

67 records · Page 4Linked to original sources
PubMed1988

Three-dimensional reconstruction of transmitter-identified central neurons by "en bloc" immunofluorescence histochemistry and confocal scanning microscopy.

A new method for three-dimensional reconstruction of transmitter-identified neurons is presented which involves "en bloc" immunofluorescence histochemistry and confocal scanning microscopy. The technique was applied to different types of neurons in the rat brain and lamprey spinal cord. Thick sections or tissue "blocs" (50-200 micron thick) were incubated with antisera against neuropeptides or monoaminergic markers, followed by fluorescent secondary antibodies. Three-dimensional reconstructions were obtained by scanning the preparations in sequential focal planes with a thin laser beam, while sampling the emitted light in each focal plane. The method is convenient and can be applied to a wide variety of neuron types. The reconstructions obtained are accurate since the "optical serial sections" of the specimen are perfectly aligned, and optic disturbances such as "halo" phenomena do not occur.

Animals↗
PubMed1987

Survey of neuropeptide-like immunoreactivity in the lamprey spinal cord.

The distribution of neural elements immunoreactive to several peptides with a possible messenger role was studied in the lamprey spinal cord by using an indirect immunofluorescence method. Different patterns of immunoreactive (IR) fibers were detected by antisera raised against cholecystokinin, metorphamide, bombesin, galanin, corticotropin-releasing factor, somatostatin, peptide YY, neurotensin, calcitonin and FMRFamide. Somatostatin-IR cell bodies were located around the central canal. All immunoreactivity could be abolished by preabsorption with the corresponding peptide. The results suggest that the lamprey spinal cord has several fiber systems containing peptides sharing immunogenic properties with mammalian neuropeptides.

Animals↗
PubMed1987

Reticulospinal neurones activate excitatory amino acid receptors.

Paired intracellular recordings were used to study the monosynaptic excitatory postsynaptic potentials (EPSP) in lamprey motoneurones evoked by stimulation of single reticulospinal Müller and Mauthner cells. The chemical component of the synaptic potentials was depressed by both application of the non-selective excitatory amino acid antagonists kynurenic acid and cis-2,3-piperidine dicarboxylate. The N-methyl-D-aspartate (NMDA) antagonists Mg2+ and 2-amino-5-phosphonovalerate caused a selective depression of a late component of the EPSP. Thus, fast-conducting reticulospinal neurones appear to release an excitatory amino acid acting at both NMDA and non-NMDA receptors.

2-Amino-5-phosphonovalerate↗
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↗
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↗
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

N-Methyl-D-aspartate (NMDA), kainate and quisqualate receptors and the generation of fictive locomotion in the lamprey spinal cord.

The motor pattern underlying swimming can be elicited in an in vitro preparation of the lamprey spinal cord by applying excitatory amino acids in the bath activating N-methyl-D-aspartate (NMDA) receptors and kainate receptors, but not quisqualate receptors. L-DOPA exerts a weak rythmogenic effect due to an action on kainate receptors. The kainate-induced rhythm is unchanged when a NMDA receptor antagonist is applied (2APV) and the N-methyl-aspartate-induced fictive locomotion can occur when kainate receptors are blocked (PDA). The burst frequency of the NMA-induced activity (dose range 30-5000 microM) is wide and ranges from 0.05-0.1 Hz up to 2.5-4 Hz, while the kainate-induced activity (dose range 7-30 microM) ranges from 0.5-1 Hz up to 4-8 Hz. This frequency range overlaps largely with that of the intact swimming animal. The findings further consolidate that NMDA receptors are efficient and demonstrates that kainate can also be effective in inducing fictive locomotion, and also that activation of either receptor type is sufficient. It has previously been shown that fictive locomotion elicited via sensory stimuli is depressed by NMDA and kainate receptor antagonists. It is suggested that these effects, presumably via aspartate and/or glutamate actions, are exerted on the input stage of interneuronal network.

Animals↗