PubMed Health⌕ Search

Biomedical subjects

M Strupp

Publications and source records attributed to M Strupp.

80 records · Page 5Linked to original sources
PubMed1991

A chloride channel in rat and human axons.

Current recordings from single chloride channels were obtained from excised and cell-attached patches of rat and human axons. In rat axons the channels showed an outwardly rectifying current-voltage relationship with a slope conductance of 33 pS at negative membrane potentials and 65 pS at positive potentials (symmetrical 150 mM CsCl). They were measurably permeable for cations (PNa/PCs/PCl = 0.1/0.2/1). Channel currents were independent of cytoplasmatic calcium concentration. Inactivation was not observed and gating was weakly voltage dependent. Cl- channels in human axons showed similar gating behavior but had a lower conductance.

Animals↗
PubMed1991

Glucose availability and sensitivity to anoxia of isolated rat peroneal nerve.

The contrast between resistance to ischemia and ischemic lesions in peripheral nerves of diabetic patients was explored by in vitro experiments. Isolated and desheathed rat peroneal nerves were incubated in the following solutions with different glucose availability: 1) 25 mM glucose, 2) 2.5 mM glucose, and 3) 2.5 mM glucose plus 10 mM 2-deoxy-D-glucose. Additionally, the buffering power of all of these solutions was modified. Compound nerve action potential (CNAP), extracellular pH, and extracellular potassium activity (aKe) were measured simultaneously before, during, and after a period of 30 min of anoxia. An increase in glucose availability led to a slower decline in CNAP and to a smaller rise in aKe during anoxia. This resistance to anoxia was accompanied by an enhanced extracellular acidosis. Postanoxic recovery of CNAP was always complete in 25 mM HCO3(-)-buffered solutions. In 5 mM HCO3- and in HCO3(-)-free solutions, however, nerves incubated in 25 mM glucose did not recover functionally after anoxia, whereas nerves bathed in solutions 2 or 3 showed a complete restitution of CNAP. We conclude that high glucose availability and low PO2 in the combination with decreased buffering power and/or inhibition of HCO3(-)-dependent pH regulation mechanisms may damage peripheral mammalian nerves due to a pronounced intracellular acidosis.

Action Potentials↗
PubMed1990

Enhancement of K+ conductance improves in vitro the contraction force of skeletal muscle in hypokalemic periodic paralysis.

An abnormal ratio between Na+ and K+ conductances seems to be the cause for the depolarization and paralysis of skeletal muscle in primary hypokalemic periodic paralysis. Recently we have shown that the "K+ channel opener" cromakalim hyperpolarizes mammalian skeletal muscle fibers. Now we have studied the effects of this drug on the twitch force of muscle biopsies from normal and diseased human skeletal muscle. Cromakalim had little effect on the twitch force of normal muscle whereas it strongly improved the contraction force of fibers from patients suffering from hypokalemic periodic paralysis. Recordings of intracellular K+ and Cl- activities in human muscle and isolated rat soleus muscle support the view that cromakalim enhances the membrane K+ conductance (gK+). These data indicate that "K+ channel openers" may have a beneficial effect in primary hypokalemic periodic paralysis.

Benzopyrans↗
PubMed1990

Is resistance to ischaemia of motor axons in diabetic subjects due to membrane depolarization?

The reasons for the resistance to ischaemia of peripheral nerves in diabetics are not well understood. We have now explored whether axonal depolarization underlies this phenomenon, as has previously been proposed. Resistance to ischaemia was determined by the new method of "threshold tracking". This method revealed an increase in excitability of the peroneal nerve at the popliteal fossa during ischaemia, and a decrease in excitability in the post-ischaemic period. The extent of these alterations in 28 type 1 diabetics without peripheral neuropathy showed a strong correlation with the mean blood glucose concentrations during the last 24 h before examination. To test whether the ischaemic resistance was related to membrane potential, we also measured axonal superexcitability in 11 selected diabetics, since it has been shown that post-spike changes in excitability depend on membrane potential. Changes in excitability of the peroneal nerve were measured in the period between 10 and 30 msec following a conditioning supramaximal compound action potential. Under resting conditions, no differences in the post-spike superexcitability were found between controls and diabetics, despite striking differences in their responses to a 10-min pressure cuff. These observations indicate that membrane depolarization is not involved in the resistance to ischaemia of motor axons in diabetic subjects.

Action Potentials↗
PubMedDate not supplied

HSV-1 not only in human vestibular ganglia but also in the vestibular labyrinth.

Reactivation of herpes simplex virus type 1 (HSV-1) in the vestibular ganglion (VG) is the suspected cause of vestibular neuritis (VN). Recent studies reported the presence of HSV-1 DNA not only in human VGs but also in vestibular nuclei, a finding that indicates the possibility of viral migration to the human vestibular labyrinth. Distribution of HSV-1 DNA was determined in geniculate ganglia, VGs, semicircular canals, and macula organs of 21 randomly obtained human temporal bones by nested PCR. Viral DNA was detected in 48% of the labyrinths, 62% of the VGs, and 57% of the geniculate ganglia. The potential significance of this finding is twofold: (1) Inflammation in VN could also involve the labyrinth and thereby cause acute unilateral vestibular deafferentation. (2) As benign paroxysmal positional vertigo often occurs in patients who have had VN, it could also be a sequel of viral labyrinthitis.

Adult↗
PubMedDate not supplied

Episodic ataxia type 1 and 2 (familial periodic ataxia/vertigo).

Episodic ataxia (EA) is a rare, disabling condition of autosomal dominant inheritance, but it is not a distinct clinical entity. Synonyms are familial periodic ataxia or hereditary paroxysmal cerebellar ataxia. Family members have a similar clinical syndrome; however, the syndrome varies considerably from family to family. At least two groups of disorders have been separated clinically: (1) episodic ataxia type 1 (EA-1), which manifests without vertigo and is associated with 'interictal' myokymia, and (2) episodic ataxia type 2 (EA-2), which often manifests with vertigo and is associated with 'interictal' nystagmus. EA-1 and EA-2 have been identified as channelopathies. EA-1 is due to different heterozygous missense point mutations in a voltage-gated (delayed rectifier) potassium channel gene (KCNA1/Kv1.1) on chromosome 12p13, whereas EA-2 is caused by mutations of the cerebral P/Q-type calcium channel alpha 1 subunit gene CACNL1A4 localized on chromosome 19p, which is highly expressed in the cerebellum. The diagnosis of EA-1 and EA-2 is important, since they can be easily treated and are often mislabeled. As effective as acetazolamide is in preventing attacks, prospective studies still have to prove whether it can prevent progressive ataxia in EA-2 or even improve chronic cerebellar deficits.

Acetazolamide↗
PubMedDate not supplied

High resolution Gd-DTPA MR imaging of the inner ear in 60 patients with idiopathic vestibular neuritis: no evidence for contrast enhancement of the labyrinth or vestibular nerve.

Sixty patients with acute idiopathic vestibular neuritis (confirmed by clinical examination and caloric irrigation) were evaluated in a prospective study by high resolution magnetic resonance imaging (hr-MRI) between days 3 and 30 after onset of symptoms. We used a 1.5 Tesla imager with an axial and coronal T1-weighted 2D-fast low angle shot-, T2-weighted turbo spin echo-, and an axial T2-weighted 3D-constructive interference in steady-state sequence for MRI. None of the patients' MRIs exhibited contrast enhancement of the labyrinth, vestibulocochlear nerve, or vestibular ganglion, even when high doses of gadolinium (0.2 mmol/kg) were used. In contrast, several previous studies demonstrated contrast enhancement of the vestibulocochlear nerve/labyrinth in herpes zoster oticus, labyrinthitis, and Cogan's syndrome or of the facial nerve in Bell's palsy. On the basis of our MRI findings, we speculate that idiopathic vestibular neuritis is neither a viral infection directly affecting the nerve (such as herpes zoster) nor a labyrinthitis. An autoimmunological disease of the labyrinth, which should involve only the anterior and horizontal semicircular canals, is also unlikely. A subacute reactivation of a latent viral infection--as discussed for Bell's palsy--is compatible with our MRI findings. The observed differences between contrast enhancement of the facial nerve in Bell's palsy and the vestibulocochlear nerve in vestibular neuritis may be due to their dissimilar anatomy: contrary to the vestibular nerve, the facial nerve has very prominent circumneural arteriovenous structures. Hyperemia within these vascular structures may cause the contrast enhancement seen in Bell's palsy.

Acute Disease↗