A TECHNIQUE FOR THE STUDY OF ACETYLCHOLINE TURNOVER IN MOUSE BRAIN <i>IN VIVO</i>

Schuberth, Jan; Sparf, Bengt; Sundwall, A.

doi:10.1111/j.1471-4159.1969.tb06447.x

Cited by 168 publications

(31 citation statements)

References 16 publications

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“…In the striatum, chlorpromazine induced an increased turnover and release of acetylcholine (Trabucchi et al, 1974;VanWoert et al, 1975) which is believed to be due to the blockade of the dopamine receptor (Stadler et al, 1973). When examining cholinergic turnover in the entire brain, however, chlorpromazine induced a decreased turnover (Jenden, 1975) similar to that induced by oxotremorine (Schuberth et al, 1969) suggesting a cholinergic agonist-like activity for chlorpromazine. There have also been indications that TRH at high doses had CNS actions not mediated via the pituitary (Plotnikoff et al, 1972(Plotnikoff et al, , 1974 and that at least in certain instances, cholinergic mechanisms were activated (Cott et al, \9lS\Breese et al, 1975).…”

Section: Discussionmentioning

confidence: 99%

Influence of Cholinergic Receptor Blockade on Drug-Induced Prolactin Release in the Monkey

Gala¹,

Subramanian²,

Peters³

et al. 1976

Horm Res

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The influence of varying doses of perphenazine, thyrotropin-releasing hormone (TRH) and serotonin on prolactin release was examined in two species of monkeys: rhesus (Macaco mulatta) and crab-eating (Macaca fascicularis). The intravenous administration of 0.33 mg/kg body weight of perphenazine or 1.0µg/kg body weight of TRH gave a greater release of prolactin than higher doses of perphenazine (1.0 mg/kg) or TRH (3.4µg/kg), respectively. Prolactin release induced by serotonin at doses of 1, 5 and 10 mg/kg was similar. Both atropine sulfate (Atr-S0₄) and atropine methyl nitrate (Atr-MN) at a similar base level potentiated the prolactin releasing action of the high dose of perphenazine suggesting that high doses of perphenazine activate a cholinergic inhibitory component present in the pituitary. Atropine sulfate had no potentiating action on the TRH-induced prolactin release, while Atr-MN appeared to prolong the response of TRH without potentiating it. Neither form of atropine had any influence on serotonin-induced prolactin release. The data indicated that the lower prolactin response to high doses of perphenazine and TRH were brought about by different mechanisms, and that the mechanism for perphenazine appeared to be mediated through a pituitary cholinergic system.

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Section: Discussionmentioning

confidence: 99%

Influence of Cholinergic Receptor Blockade on Drug-Induced Prolactin Release in the Monkey

Gala¹,

Subramanian²,

Peters³

et al. 1976

Horm Res

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“…The concentration of ACh in the synaptic cleft of an active neuromuscular junction is about 5 × 10 −4 M [2]. There are many methods for measuring the concentration of ACh: GC-MS [3] and HPLC with chemiluminescence assay [4,5], colorimetric assay [6], and radioimmunoassay [7,8]. Recently, electrochemical methods using ACh esterase-modified electrodes have been developed [9,10].…”

Section: Introductionmentioning

confidence: 99%

Near-Infrared Fluorescence Detection of Acetylcholine in Aqueous Solution Using a Complex of Rhodamine 800 and p-Sulfonato-calix[8]arene

Jin

2010

Sensors

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The complexing properties of p-sulfonatocalix[n]arenes (n = 4: S[4], n = 6: S[6], and n = 8: S[8]) for rhodamine 800 (Rh800) and indocyanine green (ICG) were examined to develop a near-infrared (NIR) fluorescence detection method for acetylcholine (ACh). We found that Rh800 (as a cation) forms an inclusion complex with S[n], while ICG (as a twitter ion) have no binding ability for S[n]. The binding ability of Rh800 to S[n] decreased in the order of S[8] > S[6] >> S[4]. By the formation of the complex between Rh800 and S[8], fluorescence intensity of the Rh800 was significantly decreased. From the fluorescence titration of Rh800 by S[8], stoichiometry of the Rh800-S[8] complex was determined to be 1:1 with a dissociation constant of 2.2 μM in PBS. The addition of ACh to the aqueous solution of the Rh800-S[8] complex caused a fluorescence increase of Rh800, resulting from a competitive replacement of Rh800 by ACh in the complex. From the fluorescence change by the competitive fluorophore replacement, stoichiometry of the Rh800-ACh complex was found to be 1:1 with a dissociation constant of 1.7 mM. The effects of other neurotransmitters on the fluorescence spectra of the Rh800-S[8] complex were examined for dopamine, GABA, glycine, and l-asparatic acid. Among the neurotransmitters examined, fluorescence response of the Rh800-S[8] complex was highly specific to ACh. Rh800-S[8] complexes can be used as a NIR fluorescent probe for the detection of ACh (5 × 10−4−10−3 M) in PBS buffer (pH = 7.2).

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“…Oxotremorine, which decreases acetylcholine turnover in the brain (Schuberth, Sparf, and Sundwall, 1969) and which exerts its main effects on the structures around the lateral ventricles (Bartolini, Bartolini, and Pepeu, 1970;Campbell and Jenden, 1970), caused a decrease of Ch in the CSF from the lateral ventricle of the dog, while the Ch concentration in the cisternal CSF remained unaltered (Aquilonius, Schuberth, and Sundwall, 1970). Also, from the results of the amphetamine effect on CSF Ch in man, there is some evidence for a correlation between the Ch concentration in CSF and ACh turnover in the central nervous system.…”

Section: Discussionmentioning

confidence: 99%