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S Lindström

Publications and source records attributed to S Lindström.

88 records · Page 5Linked to original sources
PubMed1972

Morphology of interneurones mediating Ia reciprocal inhibition of motoneurones in the spinal cord of the cat.

1. Interneurones identified by physiological criteria (Hultborn, Jankowska & Lindström, 1971b) to mediate Ia reciprocal inhibition of motoneurones in the spinal cord of the cat were stained by intracellular injection of a fluorescent dye (Procion Yellow).2. The somas of the stained cells were found in Rexed's lamina VII, just dorsal or dorsomedial to the motor nuclei. Their size was about 30 x 20 mum. The cells had four to five slender, weakly branching dendrites. The total extension of their dendritic trees was about 600 mum dorsoventrally, 400 mum mediolaterally and 300 mum rostrocaudally.3. The axons originated from a separate axon hillock or from the base of a dendrite. They were myelinated with external diameter of about 6-14 mum and projected to either the ipsilateral ventral or lateral funiculi. Early collaterals were found only exceptionally. Some axons bifurcated into an ascending and a descending branch within the funiculi.4. The possibility of identifying the Ia inhibitory interneurones on purely morphological grounds is discussed.

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PubMed1971

Recurrent inhibition from motor axon collaterals of transmission in the Ia inhibitory pathway to motoneurones.

1. The effects of impulses in recurrent motor axon collaterals on reflex transmission from different types of primary afferents to motoneurones were investigated in the cat by conditioning of PSPs evoked in motoneurones.2. IPSPs evoked by volleys in large muscle spindle (Ia) afferents were effectively decreased when preceded by an antidromic stimulation of ventral roots. Some IPSPs from group II muscle afferents and low threshold cutaneous afferents were also slightly depressed, while other PSPs were unaffected.3. The depression of the IPSPs could be evoked by antidromic volleys, which produced neither conductance changes in the motoneurones nor depolarization of Ia afferent terminals.4. The effect on the Ia IPSPs is most likely due to post-synaptic inhibition of the Ia inhibitory interneurones, evoked through alpha-motor axon collaterals and Renshaw cells. The depression of some IPSPs from flexor reflex afferents is explained by a convergence of excitatory effects from these afferents on the Ia inhibitory interneurones.5. The results indicate a selective recurrent control from motor axon collaterals of the interneurones in the reciprocal Ia inhibitory pathway to motoneurones.

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PubMed1971

Recurrent inhibition of interneurones monosynaptically activated from group Ia afferents.

1. Interneurones monosynaptically excited from large muscle spindle (Ia) afferents and inhibited from motor axon collaterals were searched for in the lumbar spinal cord of the cat.2. Monosynaptic Ia excitation was found in sixty-seven of sixty-nine interneurones inhibited by antidromic volleys. These interneurones were excited from Ia afferents from one or a few muscles (mainly close synergists). Volleys in high threshold muscle and skin afferents (FRA) evoked polysynaptic excitation or inhibition. Weak inhibition from Ia afferents (from antagonists to those giving Ia excitation) was seen in a few cells. Monosynaptic excitation was evoked from the ventral quadrant of the spinal cord and polysynaptic excitation from the dorsal quadrant.3. Inhibition from motor axon collaterals was evoked with a latency (1.2-2.0 msec) suggesting a disynaptic linkage and had the same time course as in motoneurones. It prevented synaptic activation of 60% of interneurones and decreased the firing index and delayed generation of spikes in the remaining.4. The interneurones with convergence of monosynaptic Ia excitation and inhibition from motor axon collaterals were found in the ventral horn dorsomedial to motor nuclei. No inhibition by antidromic volleys could be detected in interneurones located in intermediate nucleus and activated monosynaptically from Ia, Ib, group I or cutaneous afferents.5. It was concluded that the ventral Ia interneurones inhibited by volleys in recurrent motor axon collaterals mediate the reciprocal Ia inhibition to motoneurones.

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PubMed1971

Relative contribution from different nerves to recurrent depression of Ia IPSPs in motoneurones.

1. The pattern of depression of Ia IPSPs by volleys in recurrent motor axon collaterals was investigated in motoneurones supplying hind-limb muscles in the cat. The test IPSPs were evoked by stimulation of dorsal roots and the conditioning antidromic volleys by stimulation of motor fibres in different peripheral muscle nerves.2. In all motor nuclei investigated the strongest depression of Ia IPSPs is evoked from motor fibres to muscles whose Ia afferents produce the IPSPs. For example, the Ia IPSP from the knee extensor recorded in motoneurones to a knee flexor is most effectively depressed by antidromic stimulation of motor fibres to the knee extensor.3. The origin of recurrent inhibition of alpha-motoneurones and of Ia inhibitory interneurones with the same Ia input display a striking similarity. This suggests that the same population of Renshaw cells mediates effects to motoneurones and to Ia inhibitory interneurones.4. The functional significance of impulses in motor axon collaterals was discussed and it was suggested that they have an important role in the control of the excitatory as well as inhibitory Ia actions to motoneurones. The recurrent inhibition may limit the Ia effects to excitation of homonymous motoneurones, which would provide optimal conditions for control of individual muscles via the gamma-loop.

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PubMed1971

Neuronal pathway of the recurrent facilitation of motoneurones.

1. The recurrent facilitation of motoneurones is a disinhibition, i.e. a release of the motoneurones from a sustained hyperpolarization evoked by tonically active inhibitory interneurones. Only two groups of interneurones are known to receive recurrent inhibition from motor axon collaterals via Renshaw cells; the interneurones mediating the reciprocal Ia inhibition and the Renshaw cells themselves. The properties of these two groups of neurones were studied to determine if they could produce the tonic inhibition of motoneurones removed during recurrent facilitation.2. It was found that the tonic firing of Ia inhibitory interneurones is sensitive to anaesthetics to the same degree as is recurrent facilitation. The range of frequencies of tonic discharges of Renshaw cells appeared to be similarly low in unanaesthetized and anaesthetized preparations although in individual cells the discharge rates were decreased by anaesthesia.3. The recurrent inhibition of Ia interneurones inhibiting a given group of motoneurones and the recurrent facilitation of the same group of motoneurones were, as a rule, evoked from the same nerves, although in some cats the origin of the recurrent facilitation was somewhat wider. In contrast no evidence could be found that the Renshaw cells which inhibit a functional group of motoneurones are inhibited by volleys in the nerves from which recurrent facilitation is regularly evoked.4. It was concluded that the recurrent facilitation is caused mainly by inhibition of the tonic activity of Ia inhibitory interneurones and that it is thus a manifestation of the recurrent control of Ia reciprocal inhibition of motoneurones.

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PubMedDate not supplied

A new injectable carbamazepine solution--antiepileptic effects and pharmaceutical properties.

Carbamazepine (CBZ) could be dissolved in Glycofurol (polyethylene glycol monotetra-hydrofurfuryl ether) with concentrations up to 100 mg/ml, and the solutions were stable for at least 14 days. Ethanol or benzyl alcohol was added without loss in solubility, while water, human serum albumin or Intralipid always led to immediate precipitation. The effect of a CBZ/Glycofurol solution on focal seizure threshold in the visual cortex in cats was investigated using a cerveau isolé preparation. Fourteen experiments were performed using i.v. injections of CBZ with concentrations ranging from 0.2 to 20 mg/kg. In all experiments with doses greater than 1 mg/kg the CBZ/Glycofurol injections exerted a pronounced and immediate effect on the seizure threshold, while Glycofurol alone was ineffective. On average, seizure threshold increased more than 5-fold with doses in the range of 5-20 mg/kg. Investigating the effect of CBZ/Glycofurol on picrotoxin-induced seizure activity in cats, 2 injections of 5 mg/ml of CBZ immediately stopped the seizure activity as evaluated by electrocorticography, while interictal activity remained.

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PubMedDate not supplied

Triiodothyronine and brain excitability.

We investigated mechanisms involved in thyroid hormone action on brain excitability. The effect of acute exposure of triiodothyronine (T3) to rat hippocampal slices in vitro was studied. No significant changes could be detected in prevolley, field excitatory postsynaptic potentials (fEPSP) and population spike amplitude, while there was a minor, nonsignificant trend toward shortening of the population spike latency time. T3 had no effect on penicillin-induced epileptiform activity. There was, however, an active accumulation of radioactively labeled T3 in the slices. A rat cervaux-isolé preparation was used to determine focal seizure thresholds in the visual cortex, and no acute (2-4 h) effects were demonstrated. No significant acute effects of T3 on brain excitability in the hippocampus and visual cortex was observed, despite an active accumulation of T3. Thus, the effect of T3 on brain excitability most likely is due to delayed effects.

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