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Biomedical subjects

T J Turner

Publications and source records attributed to T J Turner.

16 recordsLinked to original sources
PubMed1995

Exocytotic Ca2+ channels in mammalian central neurons.

Intracellular Ca2+ initiates physiological events as diverse as gene transcription, muscle contraction, cell division and exocytosis. Predictably, the metabolic machinery that elicits and responds to changes in intracellular Ca2+ is correspondingly heterogeneous. This review focuses on one element of this complex web that is of particular importance to neurobiologists: identifying which members of the voltage-dependent Ca(2+)-channel superfamily are responsible for the Ca2+ that enters nerve terminals and elicits vesicular release of chemical transmitters.

Amino Acid Sequence↗
PubMed1992

Calcium channels coupled to glutamate release identified by omega-Aga-IVA.

Presynaptic calcium channels are crucial elements of neuronal excitation-secretion coupling. In mammalian brain, they have been difficult to characterize because most presynaptic terminals are too small to probe with electrodes, and available pharmacological tools such as dihydropyridines and omega-conotoxin are largely ineffective. Subsecond measurements of synaptosomal glutamate release have now been used to assess presynaptic calcium channel activity in order to study the action of peptide toxins from the venom of the funnel web spider Agelenopsis aperta, which is known to inhibit dihydropyridine and omega-conotoxin-resistant neuronal calcium currents. A presynaptic calcium channel important in glutamate release is shown to be omega-Aga-IVA sensitive and omega-conotoxin resistant.

Agatoxins↗
PubMed1992

Basic emotions: can conflicting criteria converge?

The authors discuss some of the key points raised by Ekman (1992), Izard (1992), and Panksepp (1992) in their critiques of Ortony and Turner's (1990) suggestion that there are and probably can be no objective and generally acceptable criteria for what is to count as a basic emotion. A number of studies are discussed that are relevant to the authors' contention that a more promising approach to understanding the huge diversity among emotions is to think in terms of emotions being assemblages of basic components rather than combinations of other basic emotions. The authors stress that their position does not deny that emotions are based on "hardwired" biological systems. On the other hand, the existence of such systems does not mean that some emotions (such as those that appear on lists of basic emotions) have a special status. Finally, the authors note that Ekman, Izard, and Panksepp, in adopting different starting points for their research, arrive at rather different conclusions as to what basic emotions are and which emotions are basic. It is concluded that converging resolutions of these questions are improbable.

Arousal↗
PubMed1991

Calcium as a coagonist of inositol 1,4,5-trisphosphate-induced calcium release.

Inositol 1,4,5-trisphosphate (IP3)-induced calcium release from intracellular stores is a regulator of cytosolic-free calcium levels. The subsecond kinetics and regulation of IP3-induced calcium-45 release from synaptosome-derived microsomal vesicles were resolved by rapid superfusion. Extravesicular calcium acted as a coagonist, potentiating the transient IP3-induced release of calcium-45. Thus, rapid elevation of cytosolic calcium levels may trigger IP3-induced calcium release in vivo. Extravesicular calcium also produced a more slowly developing, reversible inhibition of IP3-induced calcium-45 release. Sequential positive and negative feedback regulation by calcium of IP3-induced calcium release may contribute to transients and oscillations of cytosolic-free calcium in vivo.

Adenosine Triphosphate↗
PubMed1991

Validation of the crisis triage rating scale for psychiatric emergencies.

Using a sample of 500 emergency psychiatric patients at Victoria Hospital in London, Ontario, this study replicated part of the research on the Crisis Triage Rating Scale (CTRS) conducted by Bengelsdorf, Levy, Emerson and Barile in 1984. The relationship between the suggested CTRS cut-off score and the decision whether or not to hospitalize the patient was studied, independently of these scores. The relative contribution of each of the subscales (Dangerousness, Support System and Ability to Cooperate) to this decision was also determined. The results of this study suggest that using a cut-off score of 9, the easily administered Crisis Triage Rating Scale could be an additional assessment aid in determining whether patients require emergency hospital admission to a psychiatric unit.

Activities of Daily Living↗
PubMed1991

Interleukin-1 augments gamma-aminobutyric acidA receptor function in brain.

Interleukin-1 (IL-1), a cytokine involved in the acute phase reaction to injury and infection, has multiple effects in the central nervous system, including induction of fever and sleep and the release of several neuropeptides. We evaluated effects of IL-1 beta on inhibitory postsynaptic function at the gamma-aminobutyric acidA (GABAA) receptor. IL-1 (100 pg/ml to 10 ng/ml) augmented GABAA receptor function in cortical synaptic preparations. This effect of IL-1 was largely prevented by incubation with a specific IL-1 receptor antagonist. The related cytokines interleukin-6 and tumor necrosis factor did not augment GABA-dependent chloride transport. Similar enhancement of GABAA receptor function was observed in tissue prepared from mice previously injected intraperitoneally with IL-1 (1 microgram). Electrophysiological studies in cultured primary cortical neurons demonstrated that IL-1 enhanced the GABA-mediated increase in chloride permeability, whereas IL-1 alone produced no alterations in resting conductance. Behavioral studies indicated that IL-1 is similarly active in vivo; mice treated with IL-1 showed a decrease in open-field activity and an increase in the threshold for pentylenetetrazol-induced seizures. The interaction of IL-1 with GABAA receptors might account for the somnogenic and motor-depressant effects of this cytokine.

Animals↗
PubMed1990

What's basic about basic emotions?

A widespread assumption in theories of emotion is that there exists a small set of basic emotions. From a biological perspective, this idea is manifested in the belief that there might be neurophysiological and anatomical substrates corresponding to the basic emotions. From a psychological perspective, basic emotions are often held to be the primitive building blocks of other, nonbasic emotions. The content of such claims is examined, and the results suggest that there is no coherent nontrivial notion of basic emotions as the elementary psychological primitives in terms of which other emotions can be explained. Thus, the view that there exist basic emotions out of which all other emotions are built, and in terms of which they can be explained, is questioned, raising the possibility that this position is an article of faith rather than an empirically or theoretically defensible basis for the conduct of emotion research. This suggests that perhaps the notion of basic emotions will not lead to significant progress in the field. An alternative approach to explaining the phenomena that appear to motivate the postulation of basic emotions is presented.

Biological Evolution↗
PubMed1989

Multiple components of synaptosomal [3H]-gamma-aminobutyric acid release resolved by a rapid superfusion system.

Release of [3H]-gamma-aminobutyric acid ([3H]GABA) from rat brain synaptosomes was studied with 60-ms time resolution, using a novel rapid superfusion method. Synaptosomes were prelabeled with [3H]GABA via an associated GABA uptake system. KCl depolarization stimulated at least three distinct components of GABA release: (1) a phasic Ca-dependent component, which develops rapidly and decays with a time constant of at most 60 ms; (2) a tonic Ca-dependent component that persists after KCl depolarization is ended; (3) a Ca-independent component. The three components of GABA release are pharmacologically distinct. The phasic component was selectively blocked by 50 microM Cd2+, while the tonic component was selectively blocked by 100 microM Ni2+. The Ca-independent component was selectively blocked by nipecotic acid (IC50 = 21 microM), a known inhibitor of Na+-dependent GABA uptake. The time course and amplitude of Ca-dependent GABA release evoked by the Ca2+ ionophore A23187 were nearly identical with Ca-dependent release evoked by depolarization. This result indicates that Ca-dependent GABA release depends primarily on Ca2+ entry into the nerve terminal, and not depolarization, per se. The properties of the phasic component suggest that it is normally initiated by a voltage-sensitive Ca2+ channel that is functionally and pharmacologically distinct from those previously described. The Ca-independent component of GABA release is probably mediated by reversal of the Na-dependent, electrogenic GABA uptake system. The ability to identify multiple components of GABA release on a physiologically relevant time scale may afford a more precise definition of the mechanism of action of drugs thought to affect neurotransmission in the brain.

Animals↗
PubMed1989

A superfusion system designed to measure release of radiolabeled neurotransmitters on a subsecond time scale.

A new method for subsecond measurement of release of neurotransmitters from nerve terminal preparations (e.g., synaptosomes) in vitro is described. Synaptosomes were prelabeled with [3H]GABA via a Na-dependent GABA uptake system. The prelabeled nerve terminals are retained on small glass fiber filters in a superfusion chamber accessed by three high speed, solenoid-driven valves. Microcomputer-programmed circuitry controls the timing of valve operation. Each valve controls the delivery of a separate solution to the chamber, permitting rapid and independent control of membrane potential, [Ca2+]e, and drug delivery. The minimal dead volume of the chamber and the relatively high solution flow rate afford time resolution for release of at least 60 ms. This time resolution was necessary to observe the most rapid of at least three components of GABA release.

Animals↗
PubMed1985

Calcium channels in rat brain synaptosomes: identification and pharmacological characterization. High affinity blockade by organic Ca2+ channel blockers.

Rat brain synaptosomes are shown to contain functional voltage-sensitive Ca2+ channels that are inhibited by organic Ca2+ channel blockers. Depolarization of synaptosomes with high K+ stimulates uptake of 45Ca2+ which is biphasic in its time course. Replacement of external Na+ with choline eliminates the slower phase of depolarization-stimulated Ca2+ uptake, leaving only a rapid uptake process which terminates within 1 sec. This rapid, tetrodotoxin-insensitive Ca2+ uptake can be inactivated by prior depolarization of the synaptosomes. Depolarization has no effect on the rate of synatptosomal 22Na+ efflux. These results are interpreted as ruling out Na+/Ca2+ exchange as a mediator of the rapid phase of depolarization-stimulated Ca2+ uptake. A portion (30 to 50%) of the rapid phase of depolarization-stimulated Ca2+ uptake is inhibited by nitrendipine, as is depolarization-stimulated [3H]norepinephrine release from synaptosomes. In external Na+, the inhibition constant (Kapp) for nitrendipine inhibition of Ca2+ uptake is 56 nM. The potency of nitrendipine is increased in the absence of external Na+ (Kapp = 1.7 nM), such that inhibition correlates more closely with the equilibrium dissociation constant for [3H] nitrendipine binding to synaptosomes (Kd = 0.35 nM). Other organic channel blockers (nifedipine, verapamil, D600, and dilitiazem) inhibit the rapid Ca2+ uptake. The potencies of all Ca2+ channel blockers tested by us are in reasonable agreement with their potencies, observed in other laboratories, as blockers of Ca2+ channels in smooth and cardiac muscle. These data demonstrate the existence of active voltage-sensitive Ca2+ channels in synaptosomes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1980

Obesity in children and adolescents.

The literature regarding etiology and consequences of childhood and juvenile obesity is briefly surveyed with special reference to recent trends in behavioral research. Major emphasis is focused on issues of differential diagnosis, and treatment. The objective is to offer a logical and coherent plan for approaching and managing obesity in childhood and adolescence. The importance of an awareness and understanding of both the patient's and therapist's attitudes toward the problem of obesity is addressed. Furthermore, the necessity for a cooperative approach, utilizing nonmedical professionals, in developing a coordinated treatment plan for obese young people is discussed.

Adipose Tissue↗
PubMed1976

Amylase: creatinine clearance ratio and urinary excretion of lysozyme in acute pancreatitis and acute duodenal perforation.

The amylase:creatinine clearance ratio in patients suffering from acute pancreatitis or acute duodenal perforation was higher than normal in both groups of patients. These findings cast doubt on the value of this parameter as a specific index of acute pancreatitis. The mechanism or mechanisms underlying the increased amylase excretion have not been determined. However, the markedly elevated urinary excretion of lysozyme observed in some patients suggests, by analogy, that diminished tubular reabsorption of amylase may contribute towards the elevated amylase:creatinine ratio.

Acute Disease↗