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Biomedical subjects

R N Adams

Publications and source records attributed to R N Adams.

At least 91 records · Page 5Linked to original sources
PubMed1978

[In vivo continuous electrochemical determination of dopamine release in rat neostriatum].

Polarographic micro-electrodes (carbon fiber, o. d. 8 micron) implanted in the Rat caudate nucleus, allowed a practically continuous in vivo monitoring (one measurement every 5 sec.) of the extra-cellular concentration of dopamine released by striatal dopaminergic terminals. Administration of amphetamine produced a reproducible increase of the oxidation current. This effect was suppressed after the selective degeneration of the striatal dopaminergic terminals following the injection of 6-OHDA into the substantia nigra or after inhibition of the synthesis of the amine by alpha methyl-p-tyrosin. After 5 hrs. this drug produced a 70% decrease of the oxidation current.

Animals↗
PubMed1978

Selective attention dysfunctions in adult rats neonatally treated with 6-hydoxydopamine.

Adult rats treated intracisternally with 6-hydroxydopamine during the perinatal period were trained on a black-white discrimination. Alterations in cue shape and cue location failed to selectively distinguish differences in response patterns for the treated animals. However, when irrelevant stimuli were added to the discriminative array, the 6-hydroxydopamine group evidenced marked impairment of performance throughout the period of distraction.

Animals↗
PubMed1978

Effect of myasthenic patients' immunoglobulin on acetylcholine receptor turnover: selectivity of degradation process.

Antibodies in the sera of patients with myasthenia gravis are believed to play an important role in the pathogenesis of the disorder. They have recently been shown to accelerate the degradation of acetylcholine receptors in cultured mammalian skeletal muscle and at intact neuromuscular junctions. To elucidate the mechanism of the antibody-accelerated degradation process, we have prepared cultures in which one set of acetylcholine receptors was exposed to myasthenic immunoglobulin while a second set of acetylcholine receptors, newly incorporated after exposure to the immunoglobulins, was not. The set of acetylcholine receptors with bound myasthenic immunoglobulin was degraded at 2 to 3 times the normal rate, while the second set of acetylcholine receptors without bound immunoglobulin was degraded at the control rate. This suggest that the binding of antibody from myasthenic patients alters the acetylcholine receptors in some way that causes them to be selected for preferential degradation by the muscle cells. New synthesis and incorporation of the acetyl-choline receptors into the surface membrane of cultured skeletal muscle was unaffected by exposure to myasthenic immunoglobulin.

Antigen-Antibody Reactions↗
PubMed1977

Isolation and identificaton of an in vivo reaction product of 6-hydroxydopamine.

The product of oxidized 6-OHDA and GSH reacted in vitro has been identified by a variety of chemical and physical methods to be 2,4,5-trihydroxy-6-S-(glutathionyl)phenethylamine. Its chemical properties show it easily undergoes a variety of oxidative condensations and polymerization. Its oxidized form, the p-quinone, can be identified in small quantities in rat brain and mouse brain 1-3 h after 6-OHDA injection. This is believed to be the first report of a chemically identified species resulting from the in vivo interaction of 6-OHDA with CNS tissue.

Animals↗
PubMed1976

Competitive oxidation of 6-hydroxydopamine by oxygen and hydrogen peroxide.

Simultaneous oxygen electrode and conventional polarographic measurements show the net concentration of hydrogen peroxide produced by air oxidation of 6-hydroxydopamine is considerably less than that predicted from the known stoichiometry of the reaction. This is due to competitive oxidation of 6-hydroxydopamine by the generated hydrogen peroxide. The presence of ascorbic acid in this reaction also results in significant decreases of hydrogen peroxide under most conditions. The implications of these results to the molecular mechanism of 6-hydroxydopamine neurotoxicity are discussed.

Ascorbic Acid↗
PubMed1976

The effect of 6-aminodopamine on electrical self-stimulation in rats.

The compound 6-aminodopamine is a powerful CNS catecholaminergic neurotoxin. Small dosages of 6-aminodopamine injected intraventricularly markedly depress electrical self-stimulation rates in rats. This 6-aminodopamine treatment produced whole brain lowering of norepinephrine to ca. 50% of normal while the dopamine content was unchanged. The possible use of 6-aminodopamine treatment to elucidate the relative roles of norepinephrine and dopamine pathways is discussed.

Animals↗
PubMed1976

Potential oxidative pathways of brain catecholamines.

The possibility that catecholamines can be oxidized via aberrant pathways in vivo is open to question, but in vitro oxidation via aerobic manipulations is established. Assuming oxidation does occur, we have examined quantitatively the fast chemical reactions of the initial oxidation products, the o-quinones. The nature and rates of these reactions were studies under the conditions simulating closely those which presumably exist in mammalian brain. The results are in close accord with existing literature and especially support oxidation pathways recently reported in [3H]-norepinephrine binding to particulate cell fractions.

Ascorbic Acid↗
PubMed1976

Intracyclization rates of 6-hydroxydopamine and 6-aminodopamine analogs under physiological conditions.

It is agreed that the neurotoxic action of 6-hydroxydopamine and 6-aminodopamine is related to their ease of oxidation. The initial oxidation products, the p-quinone and p-quinone imine, readily undergo 1,2-intracyclization. These reactions could represent an important loss of active neurotoxic agent available uptake. A variety of substituted 6-aminodopamine analogs was prepared and their formal potentials and cyclization rates were measured accurately. The effect of the balance of ease of oxidation vs. rate of cyclization on their neurotoxicity was examined. The results are in general accord with in vivo lifetimes for 6-hydroxydopamine and 6-aminodopamine in rat caudate nucleus.

Chemical Phenomena↗