Author
R. Laverty
Bio: R. Laverty is an academic researcher from University of Otago. The author has an hindex of 1, co-authored 1 publications receiving 697 citations.
Papers
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TL;DR: A fluorometric hydroxyindole assay method for a wide range of catecholamines and related compounds has been developed based on iodine oxidation, alkaline rearrangement, and subsequent measurement of the fluorescence of the final solution at an acid pH.
698 citations
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TL;DR: Brain, NE, DA, and 5-HT can be assayed simultaneously from discrete samples by this method, which is based upon the alumina method described by Anton and Sayre, utilizing acid extraction of tissues and a single solvent step.
538 citations
TL;DR: By measuring dopamine receptors in the putamen and caudate of postmortem brains from Parkinson patients, evidence is reported in support of the theory of dopaminergic supersensitivity in Parkinson's disease.
Abstract: IN patients with Parkinson's disease, the concentration of dopamine in the basal ganglia of the brain is markedly reduced in accordance with the degeneration of the nigrostriatal dopamine-containing neurones1,2. This fact provided the basis for the successful clinical introduction of L-dopa (L-3,4-dihydroxyphenylalaline) for Parkinson's disease3,6. It has been suggested that one of the critical factors compensating for the loss of dopamine neurones may be the development of “denervation supersensitivity” in the striatum, as severe cases react more sensitively to L-dopa than milder cases or controls7–9. By measuring dopamine receptors in the putamen and caudate of postmortem brains from Parkinson patients, we report here evidence in support of the theory of dopaminergic supersensitivity in Parkinson's disease.
466 citations
TL;DR: It is proposed that systemically administered d-amphet-amine selectively depresses the firing rate of dopamine-containing cells in the substantia nigra zona compacta and adjacent ventral tegmental area of the rat midbrain and that these drugs also slow dopamine cells.
Abstract: WE have reported that systemically administered d-amphet-amine selectively depresses the firing rate of dopamine-containing cells in the substantia nigra zona compacta and adjacent ventral tegmental area of the rat midbrain1. d-Amphetamine is believed to act by releasing dopamine and blocking its re-uptake, leading to stimulation of dopamine receptors by increasing the availability of dopamine at postsynaptic receptor sites2–4. The increased receptor stimulation is then thought to initiate neuronal feedback inhibition of dopamine units5. Two other drugs are believed to stimulate dopamine receptors: L-dopa is converted to dopamine by an aromatic amino acid decarboxylase, increasing the amount of dopamine potentially available at receptor sites6–8, while apomorphine seems to stimulate the receptors directly9–11. Because of this alleged ability to stimulate dopamine receptors, it has been predicted that these drugs also slow dopamine cells10.
449 citations
TL;DR: With the use of the method described in this publication, the metabolism of (—)− 3 H-NE released spontaneously from the rat vas deferens was studied and it accounted for 70 per cent of the total radioactivity.
340 citations
TL;DR: The effects of isoprenaline and of propranolol on transmitter release are compatible with the view that in addition to the presynaptic negative feed‐ back mechanism for noradrenaline release by nerve stimulation mediated via α‐adrenoceptors a positive feed‐back mechanism exists in adrenergic nerve endings which is triggered through the activation of presynptic β‐ad Renoceptor.
Abstract: 1 The effects of isoprenaline, propranolol and phentolamine, were studied on tritiated noradrenaline overflow elicited by postganglionic nerve stimulation in guinea-pig isolated atria. 2 Isoprenaline (1.2 times 10-minus 8M) increased while propranolol (1.0 times 10-minus 7M) reduced the overflow of tritiated noradrenaline evoked by nerve stimulation. These effects were less than those of phentolamine (3.1 times 10-minus 6M), which increased by approximately three-fold the overflow of [3H]-noradrenaline elicited by nerve stimulation. 3 Neuronal accumulation of tritiated noradrenaline in guinea-pig atria was not affected by isoprenaline, propranolol or phentolamine at the concentration employed in this study. 4 Isoprenaline (1.2 times 10-minus 8M) induced a positive chronotropic effect of about 80 percent of the maximum. On the other hand, propranolol produced a shift to the right in the frequency-response curve to nerve stimulation and in the concentration-response curve to exogenous noradrenaline in guinea-pig atria. 5 In the isolated nictitating membrane of the cat, the frequency-response curve to nerve stimulation was not modified by propranolol, while in the presence of 3.9 times 10-minus 6M of N,-2-(2,6-dimethylphenoxy)propyl-N,N,N-trimethylammonium (beta-methyl-TM 10) there was a shift to the right and a depression of slope. Neither propranolol nor beta-methyl-TM 10 affected responses to exogenous noradrenaline. 6. The effects of isoprenaline and of propranolol on transmitter release are compatible with the view that in addition to the presynaptic negative feed-back mechanism for noradrenaline release by nerve stimulation mediated via alpha-adrenoceptors a positive feed-back mechanism exists in adrenergic nerve endings which is triggered through the activation of presynaptic beta-adrenoceptors.
332 citations