E D Schomburg

Georg-August-Universität Göttingen, Göttingen, Lower Saxony, Germany

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Publications (86)220.9 Total impact

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    ABSTRACT: Chronic muscular limb pain requires the adoption of motor patterns distinct from the classic ipsilateral flexion, crossed extension and corresponding reciprocal inhibitions to acute exteroceptive stimulation. Using selective chemical activation of group III/IV afferents in gastrocnemius-soleus (GS) muscles we investigated bilaterally their reflex responses conditioned by a), acute 'myositis' induced either by intramuscular carrageenan; and b), sub-acute 'myositis' induced by infusion of complete Freund's adjuvant (CFA). Reflex transmission was detected by monosynaptic testing and c-Fos staining used to identify increased neuronal activity. In all control experiments with chemical stimulation of Group III/IV afferents, ipsilateral responses conformed to the flexor reflex pattern. However, the expected contralateral facilitation of GS motoneurones occurred in fewer than 50% trials while only 9% of trials induced contralateral inhibition of flexor posterior-biceps-semitendinosus (PBSt) motoneurones. During carrageenan acute myositis contralateral PBSt was transiently facilitated by selective activation of group III/IV afferents. During CFA-induced myositis, contralateral only inhibition of GS motoneurones occurred instead of any facilitation, while bidirectionally a crossed facilitation of PBST dominated. These reflex changes were mirrored in an enhanced number of neurones with enhanced c-fos expression. Muscle pain, particularly if chronically persistent, requires another behavioural response pattern than acute exteroceptive pain. Copyright © 2015. Published by Elsevier Ireland Ltd.
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    ABSTRACT: Investigation and interpretation of defective motor circuitries in transgenic mice required further basic results from wild-type mice. Therefore, we investigated the lumbar motor reflex pattern in anaesthetised mice using intracellular motoneuronal recording and monosynaptic reflex testing. Thresholds and latencies in mice were similar to those in cats: thresholds for monosynaptic (group I) EPSPs were slightly above 1T (T=threshold for the lowest threshold fibres), around 1.5T for group II EPSPs and above 10T for group III EPSPs; group I EPSPs were maximal with a stimulus strength around 2T, group Il EPSPs were maximal with 5-8T; latencies to the group I incoming volley were below 1ms for monosynaptic group I EPSPs, around 3ms for polysynaptic group II EPSPs and above 4ms for polysynaptic group III EPSPs. In contrast to reflex actions in the cat, monosynaptic gastrocnemius-soleus reflexes were facilitated by conditioning stimulation of the peroneal, sural and tibial nerves, i.e. by a variety of different, probably flexor reflex afferents. This facilitation persisted after high lumbar spinalisation indicating an independency to supraspinal influences. Nociceptive muscle afferents facilitated the peroneal monosynaptic reflex while nociceptive cutaneous afferents from the foot sole inhibited the ipsilateral but facilitated the contralateral peroneal reflex.
    Neuroscience Research 04/2013; DOI:10.1016/j.neures.2013.03.011 · 2.15 Impact Factor
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    ABSTRACT: Mutations in SOD1 cause hereditary variants of the fatal motor neuron disease amyotrophic lateral sclerosis (ALS). Pathophysiology of the disease is non-cell-autonomous, with toxicity deriving also from glia. In particular, microglia contribute to disease progression. Methylene blue (MB) inhibits the effect of nitric oxide, which mediates microglial responses to injury. In vivo 2P-LSM imaging was performed in ALS-linked transgenic SOD1(G93A) mice to investigate the effect of MB on microglia-mediated inflammation in the spinal cord. Local superfusion of the lateral spinal cord with MB inhibited the microglial reaction directed at a laser-induced axon transection in control and SOD1(G93A) mice. In vitro, MB at high concentrations inhibited cytokine and chemokine release from microglia of control and advanced clinical SOD1(G93A) mice. Systemic MB-treatment of SOD1(G93A) mice at early preclinical stages significantly delayed disease onset and motor dysfunction. However, an increase of MB dose had no additional effect on disease progression; this was unexpected in view of the local anti-inflammatory effects. Furthermore, in vivo imaging of systemically MB-treated mice also showed no alterations of microglia activity in response to local lesions. Thus although systemic MB treatment had no effect on microgliosis, instead, its use revealed an important influence on motor neuron survival as indicated by an increased number of lumbar anterior horn neurons present at the time of disease onset. Thus, potentially beneficial effects of locally applied MB on inflammatory events contributing to disease progression could not be reproduced in SOD1(G93A) mice via systemic administration, whereas systemic MB application delayed disease onset via neuroprotection.
    PLoS ONE 08/2012; 7(8):e43963. DOI:10.1371/journal.pone.0043963 · 3.53 Impact Factor
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    H Steffens, P Dibaj, E D Schomburg
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    ABSTRACT: Electrophysiological investigations in mice, particularly with altered myelination, require reference data of the nerve conduction velocity (CV). CVs of different fibre groups were determined in the hindlimb of anaesthetized adult mice. Differentiation between afferent and efferent fibres was performed by recording at dorsal roots and stimulating at ventral roots, respectively. Correspondingly, recording or stimulation was performed at peripheral hindlimb nerves. Stimulation was performed with graded strength to differentiate between fibre groups. CVs of the same fibre groups were different in different nerves of the hindlimb. CVs for motor fibres were for the tibial nerve (Tib) 38.5±4.0 m/s (Agamma: 16.7±3.0 m/s), the sural nerve (Sur) 39.3±3.1 m/s (12.0±0.8 m/s) and the common peroneal nerve (Per) 46.7±4.7 m/s (22.2±4.4 m/s). CVs for group I afferents were 47.4±3.1 m/s (Tib), 43.8±3.8 m/s (Sur), 55.2±6.1 m/s (Per) and 42.9±4.3 m/s for the posterior biceps (PB). CVs of higher threshold afferents, presumably muscle and cutaneous, cover a broad range and do not really exhibit nerve specific differences. Ranges are for group II 22-38 m/s, for group III 9-19 m/s, and for group IV 0.8-0.9 m/s. Incontrovertible evidence was found for the presence of motor fibres in the sural nerve. The results are useful as references for further electrophysiological investigations particularly in genetically modified mice with myelination changes.
    Physiological research / Academia Scientiarum Bohemoslovaca 01/2012; 61(2):203-14. · 1.49 Impact Factor
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    ABSTRACT: The contribution of activated nociceptive muscle afferents to pathologically increased muscle tone remains obscure. The aim of the present study was to investigate whether an acute myositis of the gastrocnemius-soleus (GS) influences spinal reflex activity and to test whether Aδ-fibre or C-fibre were mainly responsible for any effects. In high spinal cats monosynaptic reflexes (MRs) of flexors and extensors and transmission in reflex pathways from group III and IV muscle afferents (activated by intra-arterial KCl injection) were investigated. After infiltration of GS with carrageenan there was a distinct increase in the MRs of flexors and extensors, coupled with facilitation of the flexors, induced by chemically activated group III and IV afferents. The inhibition evoked in extensors by these afferents was also mainly enhanced but less consistently. The reflex effects of carrageenan started within 1h and reached their maximum after about 1.5h. After blocking the input of all myelinated A-fibres, including Aδ-fibres, from the inflamed muscle by TTX, only a small facilitatory effect on MRs remained and the facilitation of excitatory transmission in the excitatory pathway to the flexor PBSt was abolished. The results show that the action of carrageenan-induced inflammation on spinal reflex function derives mainly from Aδ-fibres.
    Neuroscience Research 10/2011; 72(2):155-62. DOI:10.1016/j.neures.2011.10.006 · 2.15 Impact Factor
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    ABSTRACT: Pathophysiology of the motoneuron disease amyotrophic lateral sclerosis (ALS) is non-cell-autonomous. In mouse models of familiar ALS, neurotoxicity is derived not only from mutant motor neurons but also from mutant neighbouring glial cells. In vivo imaging by two-photon laser-scanning microscopy was used to study rapid morphological reactions of astroglial cells towards laser-induced axonal transection in ALS-linked transgenic SOD1(G93A) mice. In the affected lateral spinal cord, mutated astroglial cells extended branches towards injured axons within a time frame of minutes to hours post lesion while in control animals astrocytes lack any rapid morphological alteration within the studied time frame. This suggests that astrocytes partially contribute to the rapid response of non-neuronal cells to acute axonal lesions in ALS mice.
    Neuroscience Letters 06/2011; 497(2):148-51. DOI:10.1016/j.neulet.2011.04.049 · 2.06 Impact Factor
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    E D Schomburg, P Dibaj, H Steffens
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    ABSTRACT: The role of L-DOPA in spinal nociceptive reflex activity has been re-evaluated. In high spinal cats, with supraspinal loops being excluded, the onset of reflex facilitation induced by noxious radiant heat is delayed after injection of L-DOPA by 4 to 10 s, i.e. the early component of nociceptive reflex facilitation is blocked, while the late component persisted. Further investigations have shown that the early component of reflex facilitation induced by noxious radiant heat is mediated by Adelta-fibres and the late component by C-fibres. Therefore, it can be assumed that L-DOPA, like opioids, preferentially blocks the transmission in nociceptive reflex pathways from Adelta-fibres.
    Physiological research / Academia Scientiarum Bohemoslovaca 05/2011; 60(4):701-3. · 1.49 Impact Factor
  • Heinz Steffens, Eike D Schomburg
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    ABSTRACT: For further evaluation of opioidergic spinal motor functions the action of the μ-opioid receptor agonist DAMGO was tested on transmission in different non-nociceptive and nociceptive spinal reflex pathways from flexor reflex afferents (FRA), and in non-FRA reflex pathways in spinal cats. The action of DAMGO was complex, not following a simple pattern with selective depression of nociceptive pathways compared to non-nociceptive ones. Monosynaptic reflexes of the flexor posterior biceps semitendinosus (PBSt) and transmission in nociceptive as well as non-nociceptive excitatory FRA pathways to PBSt were depressed, while the specific excitatory nociceptive non-FRA pathway from the central foot pad to foot extensors was mainly not depressed but rather facilitated by DAMGO. DAMGO caused a facilitation of monosynaptic reflexes to the extensor gastrocnemius soleus (GS) and partly a reversal of inhibitory to excitatory conditioning effects from cutaneous afferents to GS. FRA interneurones could show either an increase or a cessation of their spontaneous activity, but responsiveness to nociceptive and non-nociceptive afferent activation was blocked by DAMGO. The main DAMGO action is generated via interneuronal systems rather than on motoneurones themselves. The results indicate that opioidergic spinal functions are extensively involved in spinal motor control exceeding a mere suppression of nociceptive motor withdrawal reactions.
    Neuroscience Research 05/2011; 70(1):44-54. DOI:10.1016/j.neures.2011.01.011 · 2.15 Impact Factor
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    ABSTRACT: Mutations in the enzyme superoxide dismutase-1 (SOD1) cause hereditary variants of the fatal motor neuronal disease Amyotrophic lateral sclerosis (ALS). Pathophysiology of the disease is non-cell-autonomous: neurotoxicity is derived not only from mutant motor neurons but also from mutant neighbouring non-neuronal cells. In vivo imaging by two-photon laser-scanning microscopy was used to compare the role of microglia/macrophage-related neuroinflammation in the CNS and PNS using ALS-linked transgenic SOD1(G93A) mice. These mice contained labeled projection neurons and labeled microglia/macrophages. In the affected lateral spinal cord (in contrast to non-affected dorsal columns), different phases of microglia-mediated inflammation were observed: highly reactive microglial cells in preclinical stages (in 60-day-old mice the reaction to axonal transection was ∼180% of control) and morphologically transformed microglia that have lost their function of tissue surveillance and injury-directed response in clinical stages (reaction to axonal transection was lower than 50% of control). Furthermore, unlike CNS microglia, macrophages of the PNS lack any substantial morphological reaction while preclinical degeneration of peripheral motor axons and neuromuscular junctions was observed. We present in vivo evidence for a different inflammatory activity of microglia and macrophages: an aberrant neuroinflammatory response of microglia in the CNS and an apparently mainly neurodegenerative process in the PNS.
    PLoS ONE 03/2011; 6(3):e17910. DOI:10.1371/journal.pone.0017910 · 3.53 Impact Factor
  • Eike D Schomburg, Payam Dibaj, Heinz Steffens
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    ABSTRACT: The contribution of nociceptive Aδ-fibres and C-fibres of the central pad of the foot to nociceptive spinal flexor reflex pathways (FRA-type) and to nociceptive excitatory reflex pathways to foot extensors (non-FRA type) was investigated in high spinal cats. Persisting effects after complete blocking of A-fibres by tetrodotoxin (TTX) application were thus attributed to nociceptive C-fibres. The results revealed that both Aδ and C-fibre afferents contributed to nociceptive reflexes of a FRA-pattern and of a non-FRA pattern. Thereby, the effects of Aδ-fibres were evoked with a distinctly shorter delay than those of C-fibres. Furthermore, Aδ-fibres partly exerted a significant inhibitory influence on the C-fibre action in FRA and non-FRA pathways. Treatment with different opioid receptor agonists (DAMGO and DSLET) and subsequently with naloxone revealed that a distinct part of the opioid action on nociceptive reflex pathways of the FRA-type and of the non-FRA type was evidently exerted via Aδ-fibres.
    Neuroscience Research 03/2011; 69(3):241-5. DOI:10.1016/j.neures.2010.12.005 · 2.15 Impact Factor
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    ABSTRACT: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive loss of motor neurons. To analyze the progressive motor deficits during the course of this disease, we investigated fatigability and ability of recovery of spinal motor neurons by testing monosynaptic reflex transmission with increasing stimulus frequencies in the lumbar spinal cord of the SOD1(G93A) mouse model for ALS in a comparison with wild-type (WT) mice. Monosynaptic reflexes in WT and SOD1(G93A) mice without behavioral deficits showed no difference with respect to their resistance to increasing stimulus frequencies. During the progression of motor deficits in SOD1(G93A) mice, the vulnerability of monosynaptic reflexes to higher frequencies increased, the required time for reflex recovery was extended, and recovery was often incomplete. Fatigability and demand for recovery of spinal motor neurons in SOD1(G93A) mice rose with increasing motor deficits. This supports the assumption that impairment of the energy supply may contribute to the pathogenesis of ALS.
    Muscle & Nerve 02/2011; 43(2):230-6. DOI:10.1002/mus.21835 · 2.31 Impact Factor
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    ABSTRACT: Functional relevance of non-synaptic purinergic receptors on dorsal root ganglion cells was tested in vivo by the influence of ATP using 2P-LSM and Ca imaging. Within a few seconds after local application of ATP, neurones in dorsal root ganglion were activated indicated by an increase of their calcium signal. The signal reached its maximum within a few seconds and declined to control values after about 30 s. Purinergic action seems to include non-synaptic cell-to-cell communication within dorsal root ganglia.
    Neuroscience Letters 10/2010; 487(1):107-9. DOI:10.1016/j.neulet.2010.10.005 · 2.06 Impact Factor
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    ABSTRACT: To understand the pathomechanisms of spinal cord injuries will be a prerequisite to develop efficient therapies. By investigating acute lesions of spinal cord white matter in anesthetized mice with fluorescently labeled microglia and axons using in vivo two-photon laser-scanning microscopy (2P-LSM), we identified the messenger nitric oxide (NO) as a modulator of injury-activated microglia. Local tissue damages evoked by high-power laser pulses provoked an immediate attraction of microglial processes. Spinal superfusion with NO synthase and guanylate cyclase inhibitors blocked these extensions. Furthermore, local injection of the NO-donor spermine NONOate (SPNO) or the NO-dependent second messenger cGMP induced efficient migration of microglial cells toward the injection site. High-tissue levels of NO, achieved by uniform superfusion with SPNO and mimicking extended tissue damage, resulted in a fast conversion of the microglial shape from ramified to ameboid indicating cellular activation. When the spinal white matter was preconditioned by increased, ambient ATP (known as a microglial chemoattractant) levels, the attraction of microglial processes to local NO release was augmented, whereas it was abolished at low levels of tissue ATP. Because both signaling molecules, NO and ATP, mediate acute microglial reactions, coordinated pharmacological targeting of NO and purinergic pathways will be an effective mean to influence the innate immune processes after spinal cord injury.
    Glia 07/2010; 58(9):1133-44. DOI:10.1002/glia.20993 · 5.47 Impact Factor
  • Klinische Neurophysiologie 03/2010; 41(01). DOI:10.1055/s-0030-1250927 · 0.33 Impact Factor
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    ABSTRACT: As CNS macrophages, microglia show a high spontaneous motility of their processes, continuously surveying their microenvironment. Upon CNS injury, microglia react by immediate cellular polarization and process extension toward the lesion site as well as by subsequent amoeboid lesion-directed migration and phagocytosis. To determine the ability of microglia to fulfill their role within distinctively lesioned tissue in the absence of life support, we investigated microglial activity and responsiveness to laser-induced axonal injuries in the spinal dorsal columns in situ after cardiac and respiratory arrest, i.e., post-mortem, in the progressively degrading nervous tissue. For this purpose, we used time-lapse two-photon laser scanning microscopy in double transgenic mice expressing enhanced green fluorescent protein in microglia and enhanced yellow fluorescent protein in projection neurons. Depending on the premortal condition of the animal, microglial activity and responsiveness remain for up to5-10 hr post-mortem. Thereby, the continuously decreasing glial reaction is independent of oxygen and glucose supply but requires residual ATP, suggesting a parasitic form of energy, such as a transmembrane uptake of ATP released from injured nervous tissue. Even though initially microglia are able to detect axonal injury after disruption of the blood supply, the later aspects of glial reaction, for example amoeboid conversion and migration, are absent post- mortem, corresponding to the failure of microglia to prevent secondary damage after injury of nervous tissue.
    Journal of Neuroscience Research 01/2010; 88(11):2431-40. DOI:10.1002/jnr.22402 · 2.73 Impact Factor
  • Aktuelle Neurologie 09/2009; 36(S 02). DOI:10.1055/s-0029-1238906 · 0.32 Impact Factor
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    ABSTRACT: 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.
    European Journal of Pain 07/2007; 11(5):579-86. DOI:10.1016/j.ejpain.2006.09.004 · 3.22 Impact Factor
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    ABSTRACT: Effects of long-term (9 days) experimental unilateral inflammation in the mm. gastrocnemius-soleus (GS), induced by injection of Freund’s complete adjuvant, namely modulation of posterior biceps-semitendinosus (PBSt) monosynaptic reflexes (MSRs), which was induced by chemical activation of high-threshold (groups III and I) muscle afferents, and changes in c-fos expression and NADPH-diaphorase (d) reactivity in the lumbosacral spinal cord, were studied in anemically decapitated and highly (at the C1) spinalized cats. The mean amplitude of the MSRs on the pretreated side did not differ significantly from that on the opposite side. In adjuvant-injected cats, ipsilateral stimulation of nociceptive muscle afferents by KCl injection induced the bilateral enhancement of flexor reflexes. Significant bilateral increases in the mean number of Fos-immunoreactive (Fos-IR) neurons within the L6, L7, and S1 segments (157.5 ± 12.7, 201 ± 18.5, and 205 ± ± 18.6 per section; P < 0.05) were also found in adjuvant-injected cats. A lot of Fos-IR neurons was observed in the marginal zone (lamina I) and the neck of the dorsal horn (laminae V and VI); the highest number of labelled cells was detected in lamina VII. In adjuvant-injected cats, co-distribution of Fos-IR neurons and numerous Fos-IR glia-like cells in the dorsal and ventral horns was also found. Significant increases in the mean number of NADPH-d-reactive cells in lamina VII bilaterally and also in lamina I and in an area around the central canal (lamina X) contralaterally within the L6, L7, and S1 segments (P < 0.05) were also observed. In conclusion, activation of the nociceptive input during long-term inflammation of the GS muscles is associated with differential patterns of c-fos expression and NADPH-d reactivity and also with central neuronal hyperexcitability that contributes to bilateral facilitation of the PBSt MSRs.
    Neurophysiology 05/2007; 39(3):191-200. DOI:10.1007/s11062-007-0026-5 · 0.17 Impact Factor
  • Walter Paulus, Eike D Schomburg
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    ABSTRACT: 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.
    Sleep Medicine Reviews 07/2006; 10(3):185-96. DOI:10.1016/j.smrv.2006.01.004 · 9.14 Impact Factor
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    ABSTRACT: Neurotransmission at chemical synapses of the brain involves alpha-neurexins, neuron-specific cell-surface molecules that are encoded by three genes in mammals. Deletion of alpha-neurexins in mice previously demonstrated an essential function, leading to early postnatal death of many double-knockout mice and all triple mutants. Neurotransmitter release at central synapses of newborn knockouts was severely reduced, a function of alpha-neurexins that requires their extracellular sequences. Here, we investigated the role of alpha-neurexins at neuromuscular junctions, presynaptic terminals that lack a neuronal postsynaptic partner, addressing an important question because the function of neurexins was hypothesized to involve cell-adhesion complexes between neurons. Using systems physiology, morphological analyses and electrophysiological recordings, we show that quantal content, i.e. the number of acetylcholine quanta released per nerve impulse from motor nerve terminals, and frequency of spontaneous miniature endplate potentials at the slow-twitch soleus muscle are reduced in adult alpha-neurexin double-knockouts, consistent with earlier data on central synapses. However, the same parameters at diaphragm muscle neuromuscular junctions showed no difference in basal neurotransmission. To reconcile these observations, we tested the capability of control and alpha-neurexin-deficient diaphragm neuromuscular junctions to compensate for an experimental reduction of postsynaptic acetylcholine receptors by a compensatory increase of presynaptic release: Knockout neuromuscular junctions produced significantly less upregulation of quantal content than synapses from control mice. Our data suggest that alpha-neurexins are required for efficient neurotransmitter release at neuromuscular junctions, and that they may perform a role in the molecular mechanism of synaptic homeostasis at these peripheral synapses.
    Neuroscience 02/2006; 138(2):433-46. DOI:10.1016/j.neuroscience.2005.11.040 · 3.33 Impact Factor

Publication Stats

2k Citations
220.90 Total Impact Points


  • 1985–2013
    • Georg-August-Universität Göttingen
      • III. Physical Institute
      Göttingen, Lower Saxony, Germany
  • 1983–2001
    • Universitätsmedizin Göttingen
      • • Department of Neurosurgery
      • • Department of Neurology
      Göttingen, Lower Saxony, Germany
  • 1998
    • Johannes Gutenberg-Universität Mainz
      • Institut für Physiologie und Pathophysiologie
      Mainz, Rhineland-Palatinate, Germany
  • 1981
    • Christian-Albrechts-Universität zu Kiel
      • Institute of Physiology
      Kiel, Schleswig-Holstein, Germany