Biomedical subjects

Eike D Schomburg

Publications and source records attributed to Eike D Schomburg.

5 recordsLinked to original sources

PubMed2006

Acute muscle inflammation enhances the monosynaptic reflexes and c-fos expression in the feline spinal cord.

The aim of this research was to study the changes of the motor reflex activity (monosynaptic reflex (MSR) of the flexor and extensor muscles) and Fos immunoreactivity in lumbo-sacral spinal cord after acute induced myositis of m. gastrocnemius-soleus (GS). The experiments were carried out on ischaemic decerebrated, spinalized in C1 cats. After infiltration of the GS muscle with carrageenan (2%) MSRs of flexors and extensors showed a significant increase in amplitude +127+/-24.5% and +155+/-28.5%, respectively, p<0.05. The exposed effect was initiated within 30 min and achieved a maximum 2.8h after the intramuscular injections of carrageenan. After analysis of dynamics of the MSRs, animals were perfused and c-fos expression in the spinal segments L6-S1 was evaluated. In comparison to sham-operated animals, the number of Fos-immunoreactive (Fos-ir) cells was noticeably increased in the lumbar cord of cats with carrageenan-induced myositis. The labeled cells were concentrated in the ipsilateral laminae I/II, neck of the dorsal horn (V/VI) and intermediate zone (VII), however, clear predominance of their concentration was found in the deep laminae. The effect of muscle inflammation was also expressed as a significant decline in the number of NADPH-d-reactive cells (p<0.05) in ipsilateral laminae I/II of L6/L7. The results show that the input from acutely inflamed muscles may induce an increase of the reflex responsiveness of flexors and extensors which is not mediated via the gamma-spindle-loop and which coincides with a significant increase in c-fos expression in the deep laminae of the lumbar spinal cord.

Action Potentials↗

PubMed2006

Dopamine and the spinal cord in restless legs syndrome: does spinal cord physiology reveal a basis for augmentation?

The pathophysiology of restless legs syndrome (RLS) is incompletely understood. L-DOPA, as the precursor of dopamine, as well as dopamine agonists, plays an essential role in the treatment of RLS leading to the assumption of a key role of dopamine function in the pathophysiology of RLS. Periodic limb movements in sleep are a key feature of RLS. They are generated in the spinal cord. Here we review RLS phenomenology on the basis of known dopaminergic influence on spinal control, which has been studied a great deal in recent decades in animals. In particular, we propose that the differential effects of l-DOPA and opioids on early and late flexor reflexes may be linked to the phenomenon of augmentation.

Afferent Pathways↗

PubMed2004

Neuronal LRP1 functionally associates with postsynaptic proteins and is required for normal motor function in mice.

The LDL receptor-related protein 1 (LRP1) is a multifunctional cell surface receptor that is highly expressed on neurons. Neuronal LRP1 in vitro can mediate ligand endocytosis, as well as modulate signal transduction processes. However, little is known about its role in the intact nervous system. Here, we report that mice that lack LRP1 selectively in differentiated neurons develop severe behavioral and motor abnormalities, including hyperactivity, tremor, and dystonia. Since their central nervous systems appear histoanatomically normal, we suggest that this phenotype is likely attributable to abnormal neurotransmission. This conclusion is supported by studies of primary cultured neurons that show that LRP1 is present in close proximity to the N-methyl-D-aspartate (NMDA) receptor in dendritic synapses and can be coprecipitated with NMDA receptor subunits and the postsynaptic density protein PSD-95 from neuronal cell lysates. Moreover, treatment with NMDA, but not dopamine, reduces the interaction of LRP1 with PSD-95, indicating that LRP1 participates in transmitter-dependent postsynaptic responses. Together, these findings suggest that LRP1, like other ApoE receptors, can modulate synaptic transmission in the brain.

Animals↗

PubMed2002

Only minor spinal motor reflex effects from feline group IV muscle nociceptors.

The contribution of group III and IV muscle nociceptors activated by injection of KCl or bradykinin into the muscle artery (i.a.) of the gastrocnemius-soleus muscle to spinal motor reflex pathways was investigated in high spinal cats. Group I-III fibres were completely blocked by TTX, leaving group IV-fibre conduction intact. Thus, effects from i.a. KCl or bradykinin injection persisting after TTX were attributed to TTX resistant group IV fibres while the contribution of group III fibres was approximately defined by the difference between those effects and the control effects before TTX. Confirming former findings the chemical activation of group III and IV muscle afferents induced distinct reflex facilitation of the flexor posterior biceps semitendinosus and inhibition of the extensor quadriceps. After the block of all myelinated fibres by TTX the same stimuli induced only minor reflex effects mediated by the persistently conducting TTX resistant group IV afferents. It is concluded that the main functional meaning of group IV muscle afferents, which respond preferentially with a higher threshold to mechanical stimuli, is probably less related to reflex motor control than that of group III afferents.

Afferent Pathways↗

PubMed2000

Interaction between cutaneous and muscle afferent activity in polysynaptic reflex pathways: a human experimental study.

Interactions between the input from cutaneous and nociceptive muscle afferents in polysynaptic reflex pathways were investigated in man. Interaction was tested by evoking reflexes before, during, and after a period of muscle pain induced by intramuscular injection of hypertonic saline. Muscle pain was induced either in the ankle flexor (tibialis anterior, TA) or in the extensor (soleus, SOL) muscles by injection of 1 ml hypertonic saline. Electrical skin stimulation (1.1 x initial reflex threshold) at the dorsum of the foot over the tarsal joint was used to elicit cutaneo-muscular polysynaptic reflexes in the knee flexor semitendinosus (ST). The injected hypertonic saline evoked a robust muscle pain (the subjects made a continuous score of the muscle pain on a 0-10 cm VAS scale, and the mean VAS area was 1229+/-251 cm x s and lasting 390+/-30 s). In five of 12 subjects, the infusion of hypertonic saline into TA evoked referred pain to the dorsal aspect of the ankle. A significant inhibition (17+/-8.2%, P<0.05) of the ST-reflex by pain in SOL was observed. Pain in TA facilitated (92+/-36%, P<0.05) the short-latency part (50-70 ms post stimulation) of the reflex. The muscle pain did not modulate the perceived sensory intensity of the electrical stimuli. The findings indicate an interaction of input from thin muscle afferents and cutaneous group A-fibre afferents in polysynaptic segmental reflex pathways, which seems to depend on the location of the muscle pain.

Adult↗