Biogenic Amine Transport

Tissari, Anja H.; Bogdanski, Donald F.

doi:10.1159/000136194

Cited by 32 publications

(3 citation statements)

References 18 publications

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“…The present study shows that in the guinea pig brain, HA develops differently from that of the rat brain. The pattern of HA increase resembles that of known or suggested transmitter substances, the concentrations of which correlate with the development of respective neurones in several species (TISSARI, 1966;1973;ACRAWAL et al, 1968;CONNOR & NEFF, 1970;LOIZOU, 1972;TENNYSON et al, 1973, see also the ref. above).…”

Section: Discussionmentioning

confidence: 63%

ONTOGENESIS AND REGIONAL DISTRIBUTION OF HISTAMINE AND HISTAMINE‐N‐METHYLTRANSFERASE IN THE GUINEA PIG BRAIN¹

Tuomisto

1977

Journal of Neurochemistry

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Abstract— The ontogenetic development and the regional distribution of histamine (HA) and histamine‐N‐methyltransferase (HMT, EC 2.1.1.8) in guinea pig brain and pituitary gland were studied. The samples were taken every fourth day beginning on the 28th foetal day. The HA concentration in the brains of the youngest foetuses was almost undetectable. A significant increase in HA concentrations occurred between days 40 and 44, which coincides with the period of rapid growth of nerve cell processes in this species. After this, a steep increase continued to the end of gestation in the hypothalamus, and to a lesser degree in the medulla‐midbrain and in the forebrain. In all parts of the brain the adult HA levels were reached by the time of birth. The HMT activity increased 15‐fold from the 28th foetal day to the adult and reached ca. 80% of the adult activity by the time of birth. The HMT activity developed earlier in the midbrain than in the forebrain or in the cerebellum, but after the birth the regional distribution of HMT was fairly even. In the pituitary gland the HA concentration and HMT activity increased hundredfold and tenfold, respectively. The developmental patterns of HA and HMT in the guinea pig brain give support to the concept that HA might be a neurotransmitter in the brain.

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Section: Discussionmentioning

confidence: 63%

ONTOGENESIS AND REGIONAL DISTRIBUTION OF HISTAMINE AND HISTAMINE‐N‐METHYLTRANSFERASE IN THE GUINEA PIG BRAIN¹

Tuomisto

1977

Journal of Neurochemistry

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“…Early studies had shown that neurotransmitter transport was sensitive to ouabain (an inhibitor of the Na + K + -ATPase), and that the transport was impaired when the energy metabolism was compromised [115][116][117][118][119]. This led to the hypothesis that the electrochemical gradients, generated primarily by Na + K + -ATPase, also drive neurotransmitter uptake [115,116,120,121].…”

Section: Uncovering Of the Driving Forces Of Neurotransmitter Uptakementioning

confidence: 99%

Reconstitution of GABA, Glycine and Glutamate Transporters

2021

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In contrast to water soluble enzymes which can be purified and studied while in solution, studies of solute carrier (transporter) proteins require both that the protein of interest is situated in a phospholipid membrane and that this membrane forms a closed compartment. An additional challenge to the study of transporter proteins has been that the transport depends on the transmembrane electrochemical gradients. Baruch I. Kanner understood this early on and first developed techniques for studying plasma membrane vesicles. This advanced the field in that the experimenter could control the electrochemical gradients. Kanner, however, did not stop there, but started to solubilize the membranes so that the transporter proteins were taken out of their natural environment. In order to study them, Kanner then had to find a way to reconstitute them (reinsert them into phospholipid membranes). The scope of the present review is both to describe the reconstitution method in full detail as that has never been done, and also to reveal the scientific impact that this method has had. Kanner’s later work is not reviewed here although that also deserves a review because it too has had a huge impact.

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“…

AbstractThe uptake of guanethidine (3.3×10<SUP>-5</SUP> M), debrisoquin (8.4×10<SUP>-4</SUP> M), The uptake of noradrenaline (NA) by the adrenergic neuron is energy dependent (1, 2, 3) and sodium dependent (4,5,6, 7,8,9). Guanethidine utilises this NA uptake me chanism for transport across the membrane of neurons (10, 11) and of human platelets (12) which can serve as convenient model for the neuron (13).

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mentioning

confidence: 99%

Some Factors Affecting the Neuron Blocking Action of Guanethidine, Xylocholine, Bretylium and Debrisoquin

Prasad¹,

Shah²,

Gulati³

1973

Jpn.J.Pharmacol

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The uptake of guanethidine (3.3×10^-5 M), debrisoquin (8.4×10^-4 M), The uptake of noradrenaline (NA) by the adrenergic neuron is energy dependent (1, 2, 3) and sodium dependent (4,5,6, 7,8,9). Guanethidine utilises this NA uptake me chanism for transport across the membrane of neurons (10, 11) and of human platelets (12) which can serve as convenient model for the neuron (13). Support for this common transport mechanism for NA and guanethidine is derived from observations of the ability of NA to block the uptake of guanethidine, and the failure of uptake of guanethidine in sodium-deficient medium and under conditions of reduced energy supply as at low temp.(12). Gulati and Jaykar (14) showed that in the Finkleman preparation (15), the neuron blocking action of guanethidine was prevented by NA, sodium-deprivation and at low temp. and concluded that guanethidine shares the uptake mechanism for NA. Since the neuron blocking action of a neuron blocker is consequential upon the uptake by the neuron, the prevention of neuron block by various procedures and drugs affecting uptake of NA should provide information about the uptake of a neuron blocker. Thus the present cotn munication is concerned with the investigation of the influence of NA, low temp. and so dium-deprivation in modifying the adrenergic neuron blocking action on Hukovic pre paration (16) Of guanethidine, xylocholine, bretylitun and debrisoquin. In addition the mechanisms ol' the utitake Of these neuron bloekers into the adrenergic neurons are dis cussed.

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Biogenic Amine Transport

Cited by 32 publications

References 18 publications

ONTOGENESIS AND REGIONAL DISTRIBUTION OF HISTAMINE AND HISTAMINE‐N‐METHYLTRANSFERASE IN THE GUINEA PIG BRAIN¹

ONTOGENESIS AND REGIONAL DISTRIBUTION OF HISTAMINE AND HISTAMINE‐N‐METHYLTRANSFERASE IN THE GUINEA PIG BRAIN¹

Reconstitution of GABA, Glycine and Glutamate Transporters

Some Factors Affecting the Neuron Blocking Action of Guanethidine, Xylocholine, Bretylium and Debrisoquin

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Biogenic Amine Transport

Cited by 32 publications

References 18 publications

ONTOGENESIS AND REGIONAL DISTRIBUTION OF HISTAMINE AND HISTAMINE‐N‐METHYLTRANSFERASE IN THE GUINEA PIG BRAIN1

ONTOGENESIS AND REGIONAL DISTRIBUTION OF HISTAMINE AND HISTAMINE‐N‐METHYLTRANSFERASE IN THE GUINEA PIG BRAIN1

Reconstitution of GABA, Glycine and Glutamate Transporters

Some Factors Affecting the Neuron Blocking Action of Guanethidine, Xylocholine, Bretylium and Debrisoquin

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Product

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ONTOGENESIS AND REGIONAL DISTRIBUTION OF HISTAMINE AND HISTAMINE‐N‐METHYLTRANSFERASE IN THE GUINEA PIG BRAIN¹

ONTOGENESIS AND REGIONAL DISTRIBUTION OF HISTAMINE AND HISTAMINE‐N‐METHYLTRANSFERASE IN THE GUINEA PIG BRAIN¹