PubMed Health⌕ Search

Biomedical subjects

J S Colton

Publications and source records attributed to J S Colton.

At least 19 recordsLinked to original sources
PubMed1995

Analysis of evoked and spontaneous quantal release at high pressure in crustacean excitatory synapses.

The cellular mechanisms underlying the effect of high pressure on synaptic transmission were studied in the opener muscle of the lobster walking leg. Excitatory postsynaptic currents (EPSCs) were recorded using a loose macropatch-clamp technique at normal pressure and 3.5, 6.9 MPa helium pressure. Responses of the single excitatory axon could be grouped into two types: low-yield (L) synapses exhibiting small EPSCs with a considerable number of failures, and high-yield (H) synapses having larger EPSCs with very few failures. High pressure reduced the average EPSC amplitude in all synapses and shifted their amplitude histograms to the left by decreasing the quantal content (m) without changing their quantum current (q). A binomial distribution fit of EPSC amplitudes revealed that high pressure greatly decreased n, the number of available active zones, but the effect on p, the probability of release for each zone, was not consistent. Many of the spontaneous miniature EPSCs (mEPSCs), observed only in L-type synapses, were "giant" (size = 2-5 q). High pressure increased the frequency of the giant mEPSCs but had little effect on their amplitude histogram. High pressure depressed evoked synaptic transmission by modulating the presynaptic quantal release parameters, but concomitantly enhanced spontaneous quantal release by an unknown mechanism.

Air Pressure↗
PubMed1995

Protection from oxidation enhances the survival of cultured mesencephalic neurons.

Oxidative stress has been linked to the destruction of dopaminergic neurons in the substantia nigra and may be a significant factor in both Parkinson's disease and MPTP toxicity. Using primary cultures of embryonic rat mesencephalon and standard immunocytochemical techniques, we have examined the survival of tyrosine hydroxylase-containing (TH+) neurons cultured in the presence of antioxidants and/or in an environment of low oxygen partial pressure. The number of TH+ neurons increased approximately twofold if superoxide dismutase, glutathione peroxidase (GP), or N-acetyl cysteine (NAC) were added to the culture media. Exposure of the neurons to a 5% oxygen environment (38 torr, i.e., 38 mm Hg) also increased the survival of TH+ neurons by about twofold. A dramatic enhancement of survival, however, was seen when NAC was used in combination with the 5% oxygen environment. In this case, the number of TH+ neurons increased fourfold from nontreated controls. Morphological changes were also noted. GP increased the average neurite length while NAC increased the average area of the cell body in the TH+ neuron. These results suggest that manipulation of oxidative conditions by changing the ambient O2 tension or the level of antioxidants promotes survival of TH+ neurons in culture and may have implications for transplantation therapies in Parkinson's disease.

Acetylcysteine↗
PubMed1993

Evaluation of a hyperbaric system to be used in conjunction with a fluorometer.

A high-pressure chamber that can be used inside the sample chamber of a spectrofluorometer is described and some performance characteristics are presented. The chamber body, constructed of 316 stainless steel, is temperature regulated using resistive heating elements and a microprocessor-based proportional integral derivative controller. The chamber holds a standard 1-cm2 cuvette that indexes with an electromagnetic stirrer. Injection of different solutions into the closed and pressurized (6.8 MPa) vessel is accomplished by computer-controlled, low-volume solenoids attached to separate microliter injection ports. Repetitive injections of fluids down to a volume of 7 microliters are possible in the pressurized chamber. Temperature stability of the chamber is +/- 0.2 degrees C at atmospheric or elevated pressure. However, during the initial phase (first 3 min) of pressurization, at a compression rate of 0.62 MPa/min, a 0.23 degrees C/min increase in temperature occurs. The chamber windows depress the relative intensity of the emitted light by approximately 20% for visible light and 40% for near UV; however, total sensitivity of the system is sufficient to accomplish most determinations while maintaining a good signal-to-noise ratio. This system can be used to evaluate the response of several molecular and cellular events during compression and at depth with the use of various fluorometric probes.

Atmosphere Exposure Chambers↗
PubMed1992

Oxygen dependency of synaptic transmission at the squid Loligo pealei giant synapse.

1. Synaptic transmission at the squid giant synapse was blocked in 45 min by exposure to 0.02 atm oxygen but was maintained for more than 90 min in air (0.21 atm oxygen) or pure oxygen (1 atm). 2. Excitatory post-synaptic potential amplitude decreased in 0.02 atm oxygen but did not change in either 1 or 0.21 atm oxygen. Fast facilitation was increased in 0.02 atm oxygen only. 3. Post-synaptic resting membrane potential (Vm) and input resistance (Ro) remained unchanged in 1 or 0.21 atm oxygen but Ro was increased in 0.02 atm oxygen. 4. Our results suggest that severe hypoxia decreased the release of transmitter from the pre-synaptic terminal.

Animals↗
PubMed1992

A system for saturating in vitro preparations with high pressure O2, He, H2, and mixtures.

Saturation of a liquid with gas before perfusing a tissue or cellular preparation under pressure can be achieved by bubbling the gas through the liquid. A container for this purpose that is housed in the pressure chamber with the preparation allows saturation of the liquid under hyperbaric conditions. Sealing the container allows saturation with a gas different from the gas used to compress the pressure chamber. If the pressure within the sealed container is maintained at a slightly higher level, the bubbling gas can also provide the driving force for the liquid to flow to the preparation. Based on this concept, an apparatus was built and tested to pressures of 6.8 MPa. This paper describes the saturator and the associated circuitry used to control bubbling gas pressure relative to the pressure vessel, gas flow through the saturator, and liquid flow to the preparation. A special application in the case of hydrogen gas is described, where this system has added safety advantages.

Equipment Design↗
PubMed1991

Interaction of Ca-channel blockers and high pressure at the crustacean neuromuscular junction.

Exposure to high pressure causes a significant depression of synaptic transmission. We examined the effects of various Ca-channel blockers and their interaction with high pressure on excitatory neuromuscular junction currents (EJCs) of lobster abdominal muscles. Reduced [Ca2+]o to half of normal concentration or exposure to 40-60 microM CdCl2, 10-20 microM NiCl2 and 1 microM omega-conotoxin decreased EJCs by 50%. Nifedipine, Nitrendipine and Bay K-8644 were ineffective. Either Ca-blockers or reduced [Ca2+]o, enhanced EJC suppression exerted by high pressure. The data suggest that high pressure primarily affects Ca2+ inflow at the presynaptic terminals through N-type voltage-gated Ca-channel.

Animals↗
PubMed1991

A 23187-stimulated calcium uptake and GABA release by cerebrocortical synaptosomes: effects of high pressure.

Guinea pig cerebrocortical synaptosome preparations were used to study the effect of compression to 62 ATA on 45Ca2+ uptake and [3H]GABA release using a calcium ionophore A 23187, which bypasses the voltage-sensitive calcium channel. Pressure was found to exert a suppressive effect on the A 23187-induced release of [3H]GABA, while having no significant effect on A 23187-stimulated 45Ca2+ uptake. On the other hand, both depolarization-induced 45Ca2+ uptake and [3H]GABA release were inhibited by pressure exposure. These results suggest that pressure may suppress GABA release by affecting pre-synaptic events subsequent to calcium influx.

Animals↗
PubMed1990

Effect of helium and heliox on glutamate decarboxylase activity.

The activity of glutamate decarboxylase (GAD) in pure helium at 6.8 MPa was significantly enhanced when compared to GAD activity in air at 0.1 MPa (906 vs. 602 nmol.h-1.mg-1 protein, respectively). No significant difference was found between GAD activities in heliox at 6.8 MPa (0.87% O2 at 6.8 MPa) and in air at 0.1 MPa. On the other hand, the activities in heliox at 0.1 MPa (0.87% O2 at 0.1 MPa) and air at 0.1 MPa were significantly different (655 and 446 nmol.h-1.mg-1 protein, respectively). These data indicate that pressures up to 6.8 MPa do not affect the GAD-catalyzed synthesis of gamma-aminobutyric acid, but that the enzyme, as previously reported, is sensitive to low levels of oxygen.

Animals↗
PubMed1989

Alterations in brain monoamine neurotransmitter release at high pressure.

High pressure exposure produces neurological changes which manifest as tremors, EEG changes and convulsions. Since previous studies have implicated the involvement of the monoaminergic system in these symptoms, it was of interest to study monoamine release at high pressure. Synaptosomes isolated from guinea pig brain were used to follow monoamine efflux at 68 ATA. The major observation was a decrease in the initial calcium dependent release of all three monoamines in response to K+ induced depolarization. This response is similar to that previously observed for GABA, glycine and glutamate. This generalized pressure induced depression of initial transmitter release suggests a mechanism common to the release process for both excitatory and inhibitory neurotransmission.

Animals↗
PubMed1989

Pressure-dependent changes in the release of GABA by cerebrocortical synaptosomes.

Previous studies describe a depression in potassium-evoked, calcium-dependent transmitter release from guinea pig cerebrocortical synaptosomes in response to compression to 68 ATA with heliox. The study described in this paper was designed to evaluate whether a similar effect could be detected at lower pressures and to determine whether the effect had an abrupt onset with a fixed response or a progressive response varying over a range of pressures. A typical response to potassium-evoked depolarization was observed at all pressures studied. This consisted of an initial rising phase lasting 2 to 3 min followed by a falling phase. There was a pressure-dependent depression in the absolute amount of transmitter released as well as a depression in the rate of release in the first minute following stimulation. The mean depression in gamma-aminobutyric acid release during the first minute was an average of 15% at 19 ATA, 28% at 37 ATA, 38% at 50 ATA, and 54% at 62 ATA when compared to a 1 ATA control.

Animals↗
PubMed1988

Pressure suppresses serotonin release by guinea pig striatal synaptosomes.

Exposure to high pressure produces neurologic changes in humans which manifest as tremor, EEG changes, and convulsions. Since previous studies have implicated the involvement of the serotoninergic system in these symptoms, it was of interest to study serotonin release at high pressure. Synaptosomes isolated from guinea pig striatum were used to follow serotonin efflux at 68 ATA. The major observation was a decrease in [3H]serotonin release from depolarized striatal synaptosomes at 68 ATA. In view of the role of serotonin as an inhibitory neurotransmitter in this area, the observed decrease in synaptic release leads us to conclude that decreased serotoninergic activity in striatal neurons probably is contributing to the hyperexcitability associated with HPNS.

Animals↗
PubMed1988

Release of dopamine from striatal synaptosomes: high pressure effects.

Adverse neurological manifestations of exposure to high hydrostatic pressure include tremor and convulsions, suggesting an alteration in synaptic transmission, particularly with inhibitory pathways. Because striatal transmission has been implicated in the high pressure neurologic syndrome (HPNS), we investigated the effect of pressure exposure on the release of a major inhibitory neurotransmitter in this region. Synaptosomes isolated from the guinea pig striatum were used to study the effect of compression to 67.7 ATA on [3H]dopamine release. Pressure was found to have a suppressive effect on the initial release of [3H]dopamine by synaptosomes isolated from the striatum of guinea pigs. This finding suggests that decreased inhibitory regulation at the level of the striatum contributes to the hyperexcitability associated with compression to high pressure.

Animals↗
PubMed1987

Trigeminal responses to thermal stimulation of the oral cavity in rattlesnakes (Crotalus viridis) before and after bilateral anesthetization of the facial pit organs.

Multiunit neural responses from the superficial maxillary branch of the trigeminal nerve in prairie rattlesnakes were elicited by intraoral thermal stimulation. The responses to oral stimulation were shown to be independent of responses obtained by thermal stimulation of the loreal pits. Histological examination of the dorsal lip, palate, and fang sheath regions revealed dense ramifying neurons in the epidermal layers of the fang sheaths that were morphologically similar to suspected infrared sensitive neurons in the pit membranes.

Anesthesia, Local↗
PubMed1987

Effect of pressure on the release of radioactive glycine and gamma-aminobutyric acid from spinal cord synaptosomes.

Exposure to high hydrostatic pressure produces neurological changes referred to as the high-pressure nervous syndrome (HPNS). Manifestations of HPNS include tremor, EEG changes, and convulsions. These symptoms suggest an alteration in synaptic transmission, particularly with inhibitory neural pathways. Because spinal cord transmission has been implicated in HPNS, this study investigated inhibitory neurotransmitter function in the cord at high pressure. Guinea pig spinal cord synaptosome preparations were used to study the effect of compression to 67.7 atmospheres absolute on [3H]glycine and [3H]gamma-aminobutyric acid ([3H]GABA) release. Pressure was found to exert a significant suppressive effect on the depolarization-induced calcium-dependent release of glycine and GABA by these spinal cord presynaptic nerve terminals. This study suggests that decreased tonic inhibitory regulation at the level of the spinal cord contributes to the hyperexcitability observed in animals with compression to high pressure.

Animals↗
PubMed1986

The action of oxygen and oxygen at high pressure on inhibitory transmission.

The effect of 100% oxygen at ambient pressure, 100% oxygen at 1.7 Atmospheres Absolute (ATA), 100% oxygen at 5.1 ATA, helium at 1.7 ATA and helium at 5.1 ATA on inhibitory synaptic transmission was studied using the lobster walking leg neuromuscular preparation. Exposure to 100% oxygen at ambient pressure, at 1.7 ATA or at 5.1 ATA produced a decrease in inhibitory transmission manifest as a fall in inhibitory synaptic conductance (Ginh). The largest decrease in Ginh was seen in 100% oxygen at ambient pressure, while a progressively smaller decrease was seen in 100% oxygen at 1.7 ATA and 5.1 ATA, respectively. Also associated with 100% oxygen at ambient pressure was the disappearance of inhibitory junction potentials. Pressurization with helium produced a fall in Ginh at 5.1 ATA but no change or a slight increase at 1.7 ATA. The action of either 100% oxygen at ambient and at 1.7 or 5.1 ATA or helium at 1.7 or 5.1 ATA was shown to be on presynaptic parameters since the percent decrease in Ro induced by exogenous application of gamma-aminobutyric acid (GABA), the inhibitory transmitter, was the same in either 100% oxygen at ambient pressure, 100% oxygen or helium at 1.7 ATA and 5.1 ATA. The similarity in action of oxygen to the action of isoniazid, a known glutamic acid decarboxylase (the enzyme that catalyzes the production of GABA) inhibitor in the same preparation suggests that one possible site of oxygen action is on GABA production.

Animals↗
PubMed1986

Changes in synaptic transmission produced by hydrogen peroxide.

The effect of hydrogen peroxide (H2O2) on excitatory and inhibitory synaptic transmission was studied at the lobster neuromuscular junction. H2O2 produced a dose dependent decrease in the amplitude of the junction potential (Vejp). This decrease was due to changes in both presynaptic transmitter release and the postsynaptic response to the neurotransmitter. Observed presynaptic changes due to exposure to H2O2 were a decrease in the amount of transmitter released, that is, quantal content, as well as a decrease in the fast facilitation, that is, the amplitude increase of successive excitatory junction potentials at a rate of 3 Hz. To discern postsynaptic changes, glutamate, the putative excitatory neurotransmitter for this preparation was applied directly to the bathing medium in order to bypass the presynaptic release process. H2O2 produced a decreased response of the glutamate receptor/ionophore. The action of H2O2 was not selective to excitatory (glutamate-mediated) transmission because inhibitory (GABA-mediated) transmission was also depressed by H2O2. This effect was primarily presynaptic since H2O2 produced no change in the postsynaptic response to applied GABA.

Animals↗
PubMed1986

Effect of pressure on [3H]GABA release by synaptosomes isolated from cerebral cortex.

High hydrostatic pressure has been shown to produce neurological changes in humans which manifest, in part, as tremor, myoclonic jerks, electroencephalographic changes, and convulsions. This clinical pattern has been termed high-pressure nervous syndrome (HPNS). These symptoms may represent an alteration in synaptic transmission in the central nervous system with the inhibitory neural pathways being affected in particular. Since gamma-aminobutyric acid (GABA) transmission has been implicated in other seizure disorders, it was of interest to study GABAergic function at high pressure. Isolated synaptosomes were used to follow GABA release at 67.7 ATA of pressure. The major observation was a 33% depression in total [3H]GABA efflux from depolarized cerebrocortical synaptosomes at 67.7 ATA. The Ca2+-dependent component of release was found to be completely blocked during the 1st min of [3H]GABA efflux with a slow rise over the subsequent 3 min. These findings lead us to conclude that high pressure interferes with the intraterminal cascade for Ca2+-dependent release of GABA.

Animals↗