Search PubMed⌕ Search

Biomedical subjects

R Tapia

Publications and source records attributed to R Tapia.

At least 91 records · Page 5Linked to original sources
PubMed1982

Effect of 4-aminopyridine on transmitter release in synaptosomes.

The effect of 4-aminopyridine (4-AP) on the release of labeled transmitters in mouse brain synaptosomes was studied in a superfusion system. 4-AP at microM concentrations notably stimulated the spontaneous release of labeled GABA and glutamate, and of acetylcholine (ACh) derived from tritiated choline. No effects on the release of labeled alpha-aminoisobutyric acid were observed. The stimulation of GABA and ACh release was dependent on the presence of Ca2+ in the superfusion media, whereas the effect on glutamate release was more variable and no clear Ca2+-dependence was observed. In contrast to these results, 4-AP did not have any effect on the release of the above transmitters stimulated by K+-depolarization in the presence of Ca2+. These results are discussed in terms of the possible participation of Ca2+ in the action of 4-AP on spontaneous transmitter release in isolated nerve endings.

4-Aminopyridine↗
PubMed1982

Antagonism of the ruthenium red-induced paralysis in mice by 4-aminopyridine, guanidine and lanthanum.

4-Aminopyridine and guanidine were administered intraperitoneally to mice during the complete flaccid paralysis induced by treatment with ruthenium red (RuR). At 1-8 min after 4-aminopyridine or guanidine the animals had recovered completely from the paralysis, whereas the control mice injected only with RuR remained paralytic for at least 60 min. Intraperitoneal injections of LaCl3 had no apparent effects on animal motility and did not reverse the paralysis produced by RuR. However, when La3 + was administered 30 min prior to RuR the occurrence of flaccid paralysis was totally prevented. The results obtained are discussed in terms of the possible antagonist effects of the compounds used on acetylcholine release at neuromuscular junctions.

4-Aminopyridine↗
PubMed1982

A procedure for detecting changes in the internal Ca2+ concentration in isolated nerve endings using the metallochromic dye arsenazo III.

A method for detecting changes in the internal concentration of Ca2+ in synaptosomes from mouse brain is described. Synaptosomes were fused with phosphatidylcholine-phosphatidylserine unilamellar liposomes previously loaded with the metalochromic, Ca2+ -sensitive dye arsenazo III, in order to introduce the dye into the synaptosomes. The fusion was promoted by La3+. Changes in the differential absorption between 660 and 690 nm, which indicate changes in Ca2+ concentration, were followed in a double beam spectrophotometer. It was found that both in the dye-loaded liposomes and in the fused synaptosomes, the addition of the Ca2+ ionophore A23187 to the medium containing Ca2+ produced a notable change in the differential absorbance 660-690 nm. When the depolarizing alkaloid veratridine was added, there was no response in the liposomes, whereas a change in the differential absorbance 660-690 nm was detected in the fused synaptosomes containing arsenazo but only when Na+ was present in the medium. These fused synaptosomes were able to release labeled gamma-aminobutyric acid as a response to veratridine, in a Na+ -dependent manner, similarly to control non-fused synaptosomes. These results demonstrate the feasibility of fusion to introduce Ca2+ -sensitive dyes into isolated nerve endings from the mammalian brain and therefore to detect changes in their internal Ca2+ concentration.

Animals↗
PubMed1982

Selective stimulation of neurotransmitter release from chick retina by kainic and glutamic acids.

The excitatory action of kainic and glutamic acids in chick whole retina was demonstrated as an immediate stimulation of the release of labeled gamma-aminobutyric acid (GABA) and glycine in a superfusion system. This stimulatory effect was 3-10 times greater than that produced by a depolarizing K+ concentration; in addition, it was independent of Ca2+ in the medium, but notably inhibited when Na+ was omitted from the medium. Under identical experimental conditions, neither kainic nor glutamic acid had any effect on the release of labeled dopamine or alpha-aminoisobutyric acid, thus indicating that their effect is not unspecific or due to cell damage. Similar although less marked stimulation of labeled GABA and glycine release by kainic acid was obtained in subcellular retinal fractions, particularly in fraction P1, which contained photoreceptor terminals and outer segments. This stimulation was also Ca2+ independent and greatly reduced when Na+ was omitted from the medium. It is suggested that the stimulation of GABA release by kainic and glutamic acids is probably due to a Na+-dependent, carrier-mediated mechanism that responds to the entry of Na+ produced by the interaction of glutamic and kainic acids with retinal membranes. In cortical or striatal slices from mouse brain, these acids had a negligible stimulatory effect on GABA and dopamine release.

Animals↗
PubMed1980

Mathematical models of synaptic plasticity: I. Posttetanic potentiation.

A mathematical model of post-tetanic potentiation is proposed. The model uses differential equations and is based upon physiological postulates of the electrical, metabolic, and neuroendocrine activities that are related to synaptic connectivity. These activities may modify some important parameters in synaptic function. In the proposed model these parameters are restricted to the presynapse in view of the physiological evidence indicating that posttetanic potentiation is probably due to presynaptic mechanisms. The model takes into consideration the size of the transmitter pool available for release, the mobilization of transmitter from and to this pool, and the fraction of transmitter released. Based upon the above postulates, we have simulated different phases of the phenomenon of posttetanic potentiation, and we have presented the results of several preparations in which this event has been studied. This work represents a successful attempt to reproduce the dynamics of posttetanic potentiation based upon physiological results with a mathematical model.

Calcium↗
PubMed1980

Mathematical model of synaptic plasticity: II. Habituation.

A mathematical model of the phenomenon of habituation as a homosynaptic depression of the amount of transmitter release is proposed. The model is based on the physiological studies of habituation in invertebrates and in the spinal cord of vertebrates, where a single synapse has been isolated and some of the physiological mechanisms of this process have been elucidated. The model simulates the following properties of habituation: (1) reduced amount of transmitter release attributed to a repetitive stimulus through changes in the membrane permeability to Ca2+ ions; (2) spontaneous recovery by rest; (3) the amplitude and frequency dependence of habituation; (4) modulation of habituation: sensitization, through an increase in membrane Ca2+ permeability, and presynaptic inhibition, through a reduced depolarization of the physiological stimulus; (5) long-term habituation attributed to repetitive trials of habituation and spontaneous recovery.

Animals↗
PubMed1980

Mathematical model of synaptic plasticity: III. Heterosynaptic changes.

A mathematical model, using differential equations, of heterosynaptic plasticity is proposed. The model is based on physiological studies of invertebrates in which nonspecific conditioning, such as sensitization and heterosynaptic inhibition, starts to be elucidated and behavioral studies of classical and instrumental conditioning, which we postulate to have the same mechanisms as those found in nonspecific conditioning. The model permits us to simulate the following heterosynaptic changes: sensitization, heterosynaptic inhibition, classical and instrumental conditioning--including short- and long-term memory--extinction and recuperation--spontaneously and by stimulation.

Animals↗
PubMed1979

Glutamate decarboxylase activity in chick brain and retina. Inhibition of the immature enzyme by Triton-X-100.

We have studied the effect of Triton-X-100 on glutamate decarboxylase (GAD) activity in brain and retina from chick embryos of 12 and 16 days' incubation and from chicks 4--6 weeks old. GAD activity was measured in five different homogenization media. Triton-X-100 inhibited the enzyme by about 60% in both brain and retina of 12-day embryos and by about 50% in 16-day embryos, independently of the homogenization medium. In chicks only about 20% inhibition by the detergent was observed in brain whereas no effect was found in retina. These results indicate that the evaluation of the experimental conditions of enzyme assays at different ages is essential for developmental studies of GAD activity in nervous tissue.

Aging↗
PubMed1979

Neurophysiological and neurochemical studies on the action of the anticonvulsant gamma-hydroxy, gamma-ethyl, gamma-phenyl-butyramide.

The effect of gamma-hydroxy, gamma-ethyl, gamma-phenyl-butyramide (HEPB) on afterdischarges produced by hippocampal stimulation in cats was studied. HEPB notably diminished the duration of afterdischarges and in some cats blocked their propagation into the substantia nigra and the amygdala. HEPB treatment also antagonized the enhancement of afterdischarge duration produced by subconvulsive doses of bicuculline, whereas treatment with diphenylhydantoin strongly potentiated this effect of bicuculline. The intracisternal injection of HEPB or gamma-aminobutyric acid (GABA) in mice resulted in a potentiation of strychnine-induced convulsions. On the other hand, neurochemical experiments in mouse brain cortex slices and in synaptosomes demonstrated that HEPB did not affect the high affinity uptake of [3H] GABA, its spontaneous or Ca2+ dependent release stimulated by depolarizing K+ concentrations, and its Na+ independent binding to synaptic plasma membranes.

Amygdala↗