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T Shimahara

Publications and source records attributed to T Shimahara.

48 records · Page 3Linked to original sources
PubMed1975

Multiple interneuronal afferents to the giant cells in Aplysia.

1. Several different types of presynaptic neurones to the giant cells of Aplysia have been found in the pleural ganglion. Some of these presynaptic neurones are common to the left giant cell in the pleural ganglion and to the right giant cell in the abdominal ganglion but others make contact only with one. 2. Interneurones of the left giant cell were studied in detail. They can be identified not only physiologically from the type of post-synapitc potential (p.s.p.) which they produce in the left giant cell, but also by their localization in the ganglion. 3. Direct stimulation of these presynaptic neurones produced not only the classical types of post-synaptic potentials known as e.p.s.p. or i.p.s.p. but also a slow e.p.s.p. and more complex post-synaptic potentials consisting of a rapid depolarizing or hyperpolarizing component (e for excitatory; i for inhibitory). According the p.s.p.s. which have been found were classified as being of eight different types: e.p.s.p., slow e.p.s.p., pseudo-slow e.p.s.p., e.i.p.s.p., i.e.p.s.p., i.i.p.s.p., to which is added the biphasic p.s.p. (b.p.s.p.) of electrical origin. 4. The monosynaptic nature of each of these p.s.p.s. was established by four criteria: (a) ability to follow one to one the presynaptic spike, (b) short and constant latency, (c) change of p.s.p. with the presynaptic spike when the duration is prolonged by iontophoretic injection of TEA, (d) sensitivity of the synaptic efficacy to presynaptic polarization. 5. For all p.s.p.s., the hyperpolarization of the interneurone was followed by a decrease in the corresponding amplitude; on the contrary depolarization produced an increase in p.s.p. amplitude. 6. The physiological role of these p.s.p.s. and their possible mechanism are discussed.

Action Potentials↗
PubMed1975

Heterosynaptic facilitation in the giant cell of Aplysia.

1. Heterosynaptic facilitation, defined as an increase of the efficacy of synaptic transmission between a test interneurone and a post-synaptic neurone, produced by the stimulation of a separate pathway, was studied in the left pleural ganglion. The experimental procedure consisted of detecting the effects of a brief tetanus, applied to tentacular and tegumentary nerves, on the amplitude of monosynaptic and unitary post-synaptic potentials (p.s.p.s) recorded in the left giant cell and generated by stimulating the test interneurone every 10 sec. The membrane potential of the test interneurone was simultaneously recorded. 2. Following heterosynaptic stimulation, the amplitude of the test p.s.p. increased, after a delay of about 30 sec, up to 250% of its original size; this increase subsided after 2-3 min or more. 3. Only the interneurones producing in the giant cell the e.i.p.s.p. (excitatory-inhibitory post-synaptic potential) were affected by hetero-synaptic facilitation. Other interneuronal types showed no changes in their synaptic transmission on the giant cell after heterosynaptic stimulation. 4. Heterosynaptic stimulation did not produce either orthodromic or antidromic spikes in the test interneurones clearly indicating that facilitation of test p.s.p. did not result from increased spike activity in the test interneurone. 5. Often heterosynaptic facilitation of the test p.s.p. was observed due to spontaneous activity in the heterosynaptic pathway, demonstrating the normal occurrence of the phenomenon. 6. Iontophoretic injection of 5-HT at critical, presumably synaptic, sites in the neuropil, evoked a facilitation of the test p.s.p. similar to heterosynaptic facilitation. Only the e.i.p.s.p.s. were so affected by 5-HT. On the contrary, other p.s.p. types were depressed by 5-HT as a result of conductance changes in the left giant cells. 7. Both heterosynaptic facilitation and 5-HT facilitation were suppressed by the presence in the bath of 5-HT (10(-5) M) and of LSD-25 (3 X 10(-4) M). The action of injected 5-HT on the membrane conductance of the left giant cell was also depressed in the pressence of 5-HT in the bath, but was unaffected by LSD-25 (3 X 10(-4) M). 8. From the parallelism of properties of heterosynaptic and 5-HT facilitation, it is suggested that 5-HT is the probable transmitter mediating heterosynaptic facilitation. It seems likely that 5HT is released from the heterosynaptic pathway at the level of the synaptic ending of the test interneurone on to the giant cell and that it increases the efficacy of this synapse, probably acting on the quantity of synaptic transmitter liberated.

Animals↗
PubMedDate not supplied

cAMP-dependent modulation of L-type calcium currents in mouse diaphragmatic cells.

The regulation of calcium channels by cAMP-dependent phosphorylation was investigated in the diaphragm muscle. Experiments were performed on dissociated costal diaphragmatic cells from 16- to 17-day-old fetal mice. The ionic current through calcium channels was measured using the whole cell clamp technique with barium as the charge carrier. A depolarizing pulse delivered from a holding potential of -80 mV elicited a low-threshold dihydropyridine (DHP)-insensitive T-type current and a high-threshold DHP-sensitive L-type current. Agents that either increase intracellular cAMP levels (forskolin, 10(-4) M, and dibutyryladenosine 3'-5' cyclic monophosphate, 10(-4) M) or inhibit cAMP degradation (theophylline, 10(-4) M) produced relative increases in L-type current amplitude of 24.4 +/- 13.8%, 13.4 +/- 4.6%, and 15.9 +/- 2.8% (p < 0.05), respectively. Current intensity increased after application of the beta-adrenergic agonist isoproterenol (10(-5) M, 16.5 +/- 3.6%, P < 0.005). None of these agents affected the T-type current. These results suggest that L-type calcium channel activities of the diaphragm muscle are regulated by cAMP-dependent phosphorylation.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMedDate not supplied

Restoration of dysgenic muscle contraction and calcium channel function by co-culture with normal spinal cord neurons.

Muscular dysgenesis (mdg) is a spontaneous recessive lethal mutation in the mouse. The disease is characterized by a total lack of excitation-contraction coupling in embryonic skeletal muscle. This developmental abnormality is associated with a drastic deficiency in the expression of voltage-sensitive Ca2+ channels in skeletal muscle without alteration of the properties of voltage-sensitive Na+ channels or of voltage-sensitive Ca2+ channels in cardiac and neuronal cells. Membrane couplings between sarcoplasmic reticulum and the transverse tubules, known as triads, were also found to be drastically altered in embryonic muscle of the homozygous mutant (mdg/mdg). Triads in the mdg/mdg muscle were less numerous, disorganized and lacked spaced densities. This paper shows that co-culture of mdg/mdg myotubes with normal spinal cord neurons re-establishes Ca2+ channel activity, contraction and normal triad organization. The decrease thus cannot be due to a mutation of the Ca2+ channel as previously suggested. Normal nerve cells may supply an essential factor to mutant muscle cells.

Animals↗