Simultaneous determination of indole- and catecholamines in small brain regions in the rat using a weak cation exchange resin

Holman, R. Bruce; Angwin, Pamela; Barchas, Jack D.

doi:10.1016/0306-4522(76)90010-5

Cited by 70 publications

(10 citation statements)

References 3 publications

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“…Brains were rinsed in ice-cold saline, gently blotted, and either frozen in liquid nitrogen for whole brain assay or dissected into brain regions. Rat brain areas were dissected on a glass plate over Dry Ice into the following regions according to the method of Holman et al (1976): cerebellum, cortex, hypothalamus, hippocampus, caudate, midbrain, pons plus medulla, and septum. All brain tissues were kept at -70°C until assayed (up to 2 months).…”

Section: Synthesis Of Deuterated Dhpg and Mhpgmentioning

confidence: 99%

Rat Brain and Plasma Norepinephrine Glycol Metabolites Determined by Gas Chromatography‐Mass Fragmentography

Warsh

Godse

Cheung

et al. 1981

Journal of Neurochemistry

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A gas chromatographic-mass fragmentographic (GC-MF) procedure is described for the simultaneous quantitation of 3,4-dihydroxyphenylethyleneglycol (DHPG) and 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG) in brain tissue and plasma. DHPG and MHPG were assayed as their respective acetyl-trifluoroacyl esters, using [2H2]DHPG and [2H3]MHPG as internal standards. Assay sensitives of at least 1 ng per sample were attainable for the quantitation of free glycols, whereas for determination of total DHPG, assay sensitivity was 2.5 ng. Whole rat brain total (99.2 +/- 4.11 ng/g) and free (13.0 +/- 1.14 ng/g) DHPG concentrations were similar to respective total (86.0 +/- 3.70 ng/g) and free (12.3 +/- 0.41 ng/g) MHPG levels. Total DHPG concentrations exceeded total MHPG levels in hypothalamus (3.0:1), midbrain (1.4:1), pons plus medulla (1.3:1), and hippocampus (1.5:1), whereas in other brain regions the levels of these metabolites were similar. In plasma, however, total DHPG levels were only 20% as high as MHPG concentrations. In mouse brain, DHPG and MHPG occurred almost entirely in free form (greater than 90%), but total DHPG levels were only 50% as high as respective MHPG concentrations. These results emphasize the substantial formation of DHPG compared with MHPG in rat and mouse brain and suggest that DHPG formation and efflux may be of equal or greater importance than MHPG in the metabolic clearance of CNS norepinephrine in some species.

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Section: Synthesis Of Deuterated Dhpg and Mhpgmentioning

confidence: 99%

Rat Brain and Plasma Norepinephrine Glycol Metabolites Determined by Gas Chromatography‐Mass Fragmentography

Warsh

Godse

Cheung

et al. 1981

Journal of Neurochemistry

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“…Assay procedures for isolation, purification, and quantification of serotonin were as described in (12) and adapted for use for small brain regions (13). Determination of cyclic AMP was by radioimmunoassay as described in (14).…”

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confidence: 99%

Environmental Influences on Serotonin and Cyclic Nucleotides in Rat Cerebral Cortex

Diamond¹,

Connor²,

Orenberg³

et al. 1980

Science

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The response to different environmental conditions and negative air ions was investigated on cerebral cortical serotonin and cyclic nucleotides. The results indicated that negative air ions alter the weight of the cerebral cortex and that concentrations of serotonin and cyclic nucleotides can be altered both by different environments and by negative air ions. The data stress the importance of the role of the environment when studying the structure and chemistry of the cerebral cortex.

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“…Comparison of the magnitude of the NA release in the two regions shows that the response was greater in the hippocampus (fivefold over basal) versus the frontal cortex (threefold over basal). Since ECS will release transmitters by depolarizing nerve terminals, the difference in the amounts of NA released in the two regions may be affected by: (1) differences in the flow of current, (2) changes in neuronal activity caused by the seizures, (3) the greater tissue concentration of NA in the hippocampus versus the cortex (Holman et al, 1976), or (4) the relative involvement of uptake and presynaptic inhibition in regulating extracellular NA levels. We have previously compared dose-response curves to uptake inhibition (desmethylimipramine, DMI, via the probe), M2-adrenoceptor inhibition (idazoxan) and to IDX (1.0 mg kg-') in the presence of increasing concentrations of DMI (via the probe) on extracellular NA content in the hippocampus and in the frontal cortex (Thomas & Holman, 1991b).…”

Section: Discussionmentioning

confidence: 99%

“…We have previously shown that in this anaesthetized rat preparation, the content of endogenous NA present in micro- (Holman et al, 1976), or (4) the relative involvement of uptake and presynaptic inhibition in regulating extracellular NA levels. We have previously compared dose-response curves to uptake inhibition (desmethylimipramine, DMI, via the probe), M2-adrenoceptor inhibition (idazoxan) and to IDX (1.0 mg kg-') in the presence of increasing concentrations of DMI (via the probe) on extracellular NA content in the hippocampus and in the frontal cortex (Thomas & Holman, 1991b).…”

Section: Discussionmentioning

confidence: 99%

Effects of acute and chronic electroconvulsive shock on noradrenaline release in the rat hippocampus and frontal cortex

Thomas

Nutt

Holman

1992

British J Pharmacology

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Changes in the extracellular content of endogenous noradrenaline (NA) in frontal cortex and hippocampus were determined by in vivo microdialysis following acute and chronic electroconvulsive shock (ECS) in rats anaesthetized with chloral hydrate. Basal release of NA in the frontal cortex (4.9 ± 0.3 pg/sample) did not differ significantly from that in the hippocampus (4.6 ± 0.2 pg/sample). A single ECS resulted in an increase of NA release in the hippocampus (21.1 ± 1.3 pg/sample) and in the frontal cortex (11.6 ± 1.2 pg/sample). In both brain regions extracellular NA had returned to basal values within 30 min. Animals were treated chronically with ECS (once per day for seven days). Twenty‐four h later (day 8), basal release of NA into dialysis samples from the frontal cortex was significantly increased (50%) as compared to chronic sham controls. Basal release in the hippocampus was not significantly different from the sham controls. In the chronic ECS animals the increase in NA released in both brain areas following an ECS on day 8 did not differ from either the chronic sham controls or from animals given acute ECS. Animals were challenged 24 h after eight ECS or sham control treatments (once per day) with the α2‐adrenoceptor antagonist, idazoxan (10 mg kg−1, s.c). Idazoxan increased NA release in the hippocampus in both groups. There was no difference in the magnitude of the response in ECS‐ and in sham‐treated rats. In the frontal cortex, idazoxan increased the extracellular NA content in the chronic sham controls, but the response to idazoxan was significantly attenuated in the chronic ECS animals. Chronic but not acute ECS was found to elicit a sustained (> 24 h) increase in the release of NA in the frontal cortex, but not in the hippocampus. The idazoxan data suggest that the increase may be due to a downregulation of presynaptic α2‐adrenoceptors in the frontal cortex. The difference in response of these two brain regions to chronic ECS is discussed in terms of differences in the regulation of extracellular NA content by uptake and autoreceptor activation.

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Simultaneous determination of indole- and catecholamines in small brain regions in the rat using a weak cation exchange resin

Cited by 70 publications

References 3 publications

Rat Brain and Plasma Norepinephrine Glycol Metabolites Determined by Gas Chromatography‐Mass Fragmentography

Rat Brain and Plasma Norepinephrine Glycol Metabolites Determined by Gas Chromatography‐Mass Fragmentography

Environmental Influences on Serotonin and Cyclic Nucleotides in Rat Cerebral Cortex

Effects of acute and chronic electroconvulsive shock on noradrenaline release in the rat hippocampus and frontal cortex

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