SUEMARYThe electrical properties of Schwann cells and the effects of neuronal impulses on their membrane potential have been studied in the giant nerve fibre of the squid.1. The behaviour of the Schwann cell membrane to current injection into the cell was ohmic. No impulse-like responses were observed with displacements of 35 mV in the membrane potential. The resistance of the Schwann cell membrane was found to be approximately 103 Q2 cm2.2. A long-lasting hyperpolarization is observed in the Schwann cells following the conduction of impulse trains by the axon. Whereas the propagation of a single impulse had little effect, prolonged stimulation of the fibre at 250 impulses/sec was followed by a hyperpolarization of the Schwann cell that gradually declined over a period of several minutes.3. The prolonged effects of nerve impulse trains on the Schwann cell were similar to those produced by depolarizing current pulses applied to the axon by the voltage-clamp technique. Thus, a series of depolarizing pulses in the axon was followed by a long-lasting hyperpolarization of the Schwann cells. In contrast, the application of a series of hyperpolarizing 100 mV pulses at a frequency of 1/sec had no apparent effects.4. Changes in the external potassium concentration did not reproduce the long-lasting effects of nerve excitation.5. The hyperpolarizing effects of impulse trains were abolished by the incubation of the nerve fibre in a sea-water solution containing trypsin.6. These findings are discussed in relation to the possible mechanisms that might be responsible for the long-lasting hyperpolarizations of the Schwann cells.
SUMMARY1. The effects of a range of neuropeptides were investigated on the membrane potential of the Schwann cells of the giant nerve fibre of the tropical squid.2. Vasoactive intestinal peptide (VIP) produced a dose-dependent, long-lasting hyperpolarization of the Schwann-cell membrane potential. Among peptides structurally related to VIP, similar effects were produced by peptide histidine isoleucine (PHI) but not by secretin and glucagon. 4. VIP produces its effects on the Schwann-cell membrane potential via a receptor system that is independent from those described previously which mediate the effects of carbachol and DL-octopamine. However, VIP can potentiate the effects of the latter systems.5. The actions of VIP on the Schwann cell are unlikely to be mediated via changes in adenosine 3',5'-cyclic monophosphate (cyclic AMP) levels and are insensitive to changes in the level of extracellular calcium in the superfusate. The actions of VIP are, however, potentiated in the presence of low concentrations of lithium ions suggesting that the VIP receptor may mediate its effects by inducing the hydrolysis of polyphosphatidylinositols in the Schwann-cell membrane.6. Evidence is presented for the existence of an endogenous VIP-like component in the normal hyperpolarizing action ofgiant-axon activity on the membrane potential of the Schwann cell.
SUMMARYThe effects of eserine and D-tubocurarine on the axon and Schwann cell membrane potentials have been studied in the giant nerve fibre of the squid.1. The addition of eserine at concentrations of up to 10-4M to the external sea-water medium has no appreciable effects on either the Schwann cell electrical potential of unstimulated nerve fibres or on the resting and action potentials of the axon.2. However, eserine at a concentration of 10-9 M prolongs the longlasting Schwann cell hyperpolarizations which follow the conduction of impulse trains by the axon.3. Higher concentrations of eserine (10-7, 10-4M) decrease and block the long-lasting effects of nerve impulse train conduction.4. D-tubocurarine at concentrations of up to 10-5 M has no appreciable effect on the resting and action potentials of the axon.5. However, D-tubocurarine at a concentration of 10-9 M blocks completely the hyperpolarizing effects of nerve impulse trains on the Schwann cell electrical potential.6. In addition to its blocking action, D-tubocurarine induces transient hyperpolarizations in the Schwann cells of unstimulated nerve fibres both in intact fibres and in slitted preparations.7. These findings suggest that a cholinergic system, which may be located at the axon-Schwann cell boundary, is involved in the genesis of the long-lasting Schwann cell hyperpolarization caused by the conduction of nerve impulse trains by the axon. 7-2
SUMMARY1. The effects of -bungarotoxin, nicotine and muscarine on the Schwann cell membrane potential have been studied in the giant nerve fibre of the squid. The external application of ez-bungarotoxin (10-6, 10-8, 10-9 M) irreversibly blocks the long-lasting Schwann cell hyperpolarizations following the conduction of nerve impulse trains by the axon. It also blocks the Schwann cell hyperpolarizing response to the external application of carbamylcholine (10-6 M) to the resting nerve fibre.2. Externally applied D-tubocurarine (10-5 M) protects against the irreversible action of a-bungarotoxin (10-9 M) on the Schwann cell. Within 10 min of reimmersion in toxin-free sea water there is complete recovery of the Schwann cell hyperpolarizing response to carbamylcholine (10-6 M) which had been initially abolished.3. Nicotine (10-6 M) induces a prolonged hyperpolarization of the Schwann cells in the resting nerve fibre, whereas at the same concentration, muscarine has no appreciable effect on the Schwann cell membrane potential.4. None of these drugs, at the concentrations utilized in the present study, had any appreciable effect on the resting and action potentials of the axon.5. These findings show the presence of acetylcholine receptors of the nicotinic type in the Schwann cell membrane, and give further support to the hypothesis on the role of the acetylcholine system in the genesis of the long-lasting Schwann cell hyperpolarizations caused by the conduction of nerve impulse trains by the axon.
SUMMARY1. The effect of acetylcholine and carbamylcholine on the axon and Schwann cell membrane potential have been studied in the giant nerve fibre of the squid. The addition of carbamylcholine (10-6 M) to the external sea-water medium has no appreciable effects on the resting and action potentials of the axon. However, it induces a long-lasting hyperpolarization in the surrounding Schwann cells of the unstimulated intact or slit nerve fibres which is completely blocked by D-tubocurarine (10-9 M). Eserine (10-9 M) prolongs the Schwann cell hyperpolarizations induced by a 1 min exposure of the unstimulated nerve fibres to acetylcholine (10-7 M).2. The addition of carbamylcholine (10-6 M) to the external medium increases the relative permeability of the Schwann cell membrane to the potassium ion in slit nerve fibres. Yet, a hundredfold reduction in external sodium concentration has no appreciable effect on the hyperpolarization of the Schwann cells of the slit nerve fibre under similar conditions.3. Tetrodotoxin at a concentration of 5 x 10-8 M has no appreciable effects on either the Schwann cell electrical potential or on the hyperpolarizing action of carbamylcholine on the Schwann cells of the unstimulated intact nerve fibres.4. These findings indicate the presence of acetylcholine receptors in the plasma membrane of the Schwann cell in these nerve fibres and give further support to the hypothesis on the role of the cholinergic system in the genesis of the long-lasting Schwann cell hyperpolarizations caused by the conduction of nerve impulse trains by the axon.
ABST R ACT Sodium, potassium, a n d c h l o r i d e c o n c e n t r a t i o n s w e r e d e t e r m i n e d in the sheath cells and axoplasm of the nerve fiber of the squid Sepioteuthis sepioidea. The sheaths were obtained by slitting the nerve fiber, the extracellular electrolytes were washed out in isotonic sucrose solution, and the concentrations in the cells were determined after different soaking times in the sucrose solution.Values for the Schwann cell were calculated by extrapolation to zero time from the plots of the logarithms of the concentrations in the cells as a function of soaking time in sucrose solution. The Schwann cells made up 84 per cent of the sheath's total cellular volume. The Schwann cell concentrations in millimols per liter, are: 312 (404-241) for sodium, 220 (308-157) for potassium, and 167 (208-138) for chloride. The concentrations in the axoplasm (mean -4-sE), in miUimols per liter are: 52 4-l0 for sodium, 335 4-25 for potassium, and 135 4-14 for chloride. The possibility that some fraction of the Schwann cell electrolytes, especially of sodium, is bound, cannot be discarded.The present work deals with the determination of sodium, potassium, and chloride in the Schwann cell and axoplasm of the nerve fiber of the squid Sepioteuthis sepioidea.For the Schwann cell (Del Rio Hortega's peripheral glial cell) of the squid fiber, Schmitt and Geschwind (1) suggested that the sodium and potassium concentrations should be essentially similar to those of the axon, that is, low sodium and high potassium. On the contrary, Sj6strand (2) proposed that the Schwann cell should have, as the blood and interstitial fluid of the squid, high sodium and low potassium concentrations. Subsequent work of Coelho, Goodman, and Bowers (3) presented direct evidence of the high potassium concentration in the Schwann cell of the squid fiber. No determinations of sodium and chloride have been made in this cell. The concentrations of these electrolytes are needed to obtain further knowledge on the nature of the
SUMMARY1. The role of cyclic nucleotides in mediating the effects of nicotinic cholinergic receptors has been investigated in Schwann cells of the giant nerve fibre of the squid.2. Elevation of cyclic AMP levels in this preparation by means of the phosphodiesterase inhibitor, theophylline, by the diterpene adenylate cyclase activator, forskolin, and by cyclic nucleotide analogues mimics the action of activating the nicotinic cholinergic receptors in producing a long-lasting hyperpolarization of the membrane potential of the Schwann cell. Theophylline and forskolin also potentiate the effects of carbachol and of neural stimulation on the Schwann cell.3. The results suggest that the nicotinic receptor of the squid Schwann cell is likely to mediate its effects via a mechanism that activates adenylate cyclase.4. The results are discussed in terms of the role of cyclic AMP in the complex multistep interaction between the giant axon of the squid and its surrounding Schwann-cell layer.
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