1,721,104 research outputs found
STEADY-STATE CONCENTRATIONS OF CHOLINE AND ACETYLCHOLINE IN RAT-BRAIN PARTS DURING A CONSTANT RATE INFUSION OF DEUTERATED CHOLINE
No full textAn intravenous infusion of deuterated choline at constant rate for 6 min (5 or 25 μmoles kg-1 min-1) significantly increases the concentration of choline in plasma, occipital cortex and striatum. Both 5 and 25 μmoles kg-1 min-1 increase the concentration of acetylcholine in cortex but only 25 μmoles kg-1 min-1 increases the acetylcholine content in striatum. In contrast, 1 μmole kg-1 min-1 does not change the choline or acetylcholine content in cortex or striatum. A single pulse injection of choline (200 μmoles kg-1) causes a significant increase in the concentration of choline in striatum 30 sec following injection. The choline content returns to normal values within 2 min. These studies show that when a pulse injection of a non-tracer dose of radioactive choline is used to measure brain acetylcholine turnover rate the maintenance of steady state must be verified within seconds after the pulse injection of radioactive choline. When constant infusion of deuterated choline is used to measure turnover rate of acetylcholine in the brain of rats, a dose of 1 μmole kg-1 min-1 appears to be a maximal infusion rate
CHOLINE ACETYLTRANSFERASE ACTIVITY AND MASS FRAGMENTOGRAPHIC MEASUREMENT OF ACETYLCHOLINE IN SPECIFIC NUCLEI AND TRACTS OF RAT BRAIN
No full textThe mass fragmentographic assay of acetylcholine (ACh) is the only available method to measure the acetylcholine content of rat brain nuclei. The ACh concentration and the choline acetyltransferase activity (ChA) of specific rat brain nuclei and tracts are reported. The highest ACh concentration (1.2 nmol mg protein) and ChA activity (576 nmol mg protein per hr) was in the nucleus interpeduncularis, which possessed twice as much ACh and ChA as the nucleus accumbens and nucleus caudatus. The midbrain nuclei: dorsalis raphes and linearis pars caudalis contained as much ACh as the nuclei accumbens and caudatus but the ChA activity was only a fraction of that of the accumbens and caudatus. The three pontine nuclei: locus eoeruleus, tegmenti dorsalis and dorsalis vagi contained slightly less ACh than the nuclei accumbens and caudatus but the ChA varied. It was low in the locus coeruleus but 10- fold higher in the dorsalis vagi. It is proposed that the ratio of ACh content to ChA activity may have some predictive value to determine whether most of the ACh measured in various brain nuclei is located in cell bodies or axon terminals. The data presented are compared with histochemical data on the location of acetylcholinesterase (Palkovits and Jacobowitz, 1974). This comparison suggests that when the ratio ACh/ChA × 100 is greater than 0.7 and the ACh content is 0.30 nmol mg protein or greater, the transmitter may be located in nerve terminals. When this ratio is smaller than 0.4 and the ChA activity is greater than 5.0 nmol mg protein per hr, the ACh measured may be located in cholinergic cell bodies or small cholinergic interneurones. This suggestion is supported by measurement of the ACh concentration and ChA activity in brain nuclei which are known to contain cholinergic cell bodies (e.g. motor nucleus of the vagus), small cholinergic interneurones (n. caudatus and n. accumbens) and cholinergic nerve terminals (n. locus coeruleus, dorsalis raphes)
CONSTANT RATE INFUSION OF DEUTERATED PHOSPHORYLCHOLINE TO MEASURE EFFECTS OF MORPHINE ON ACETYLCHOLINE TURNOVER RATE IN SPECIFIC NUCLEI OF RAT BRAIN
No full textBy using constant rate infusion of deuterated phosphorylcholine the turnover rate of acetylcholine in nucleus accumbens, n. septi, n. interpeduncularis, n. raphes dorsalis, substantia nigra, cortex, hippocampus (regio superior) and n. caudatus was measured. A dose of morphine which is the effective median dose for analgesia, failed to change the steady-state of choline and acetylcholine in the above-mentioned nuclei, but it lowered the turnover rate of acetylcholine in hippocampus, cortex and n. accumbens. The action of morphine on acetylcholine turnover rate could be antagonized by naltrexone, which per se failed to change the steady-state of acetylcholine and choline or of acetylcholine turnover rate. The possibility that opiate receptor activation in n. accumbens through inhibition of the turnover rate of acetylcholine triggers a series of events that cause analgesia and/or catatonia is discussed
Action of opiates, antipsychotics, amphetamine and apomorphine on dopamine receptors in rat striatum: in vivo changes of 3′,5′-cyclic amp content and acetylcholine turnover rate
No full textIN VIVO ACTIONS OF CLOZAPINE AND HALOPERIDOL ON TURNOVER RATE OF ACETYLCHOLINE IN RAT STRIATUM
No full textThe authors have measured acetylcholine (ACh) content and turnover rate (TRach) in striatum and cortex of rats receiving haloperidol and clozapine i.p. Both clozapine (30 μmol/kg) and haloperidol (10 μmol/kg) reverse the decrease in striatal TRach elicited by apomorphine (11 μmol/kg) while each antipsychotic affects the steady state and the TRach in striatum differently. Haloperidol fails to change striatal ACh content but increases the TRach; clozapine (15 and 30 μmol/kg) neither decreases the content of ACh nor changes the TRach in striatum. Moreover, 60 or 90 μmol/kg of clozapine causes a 40% decrease in ACh content without affecting the TRach. Clozapine, but not haloperidol, antagonizes the increase in ACh content and the decrease in TRach elicited by arecoline (64 μmol/kg) and oxotremorine (9 μmol/kg) in striatum. Clozapine resembles trihexylphenidyl (14 μmol/kg) and benztropine (12 μmol/kg) because it decreases the ACh content of striatum without changing the TRach. Moreover, clozapine and benztropine reverse the increase in striatal TRach elicited by haloperidol. The increase in striatal TRach elicited by haloperidol could be of value to explain the extrapyramidal action of this drug. The anticholinergic action of clozapine could explain the absence of extrapyramidal side effects observed with this drug
CORRELATION BETWEEN ANALGESIA AND DECREASE OF ACETYLCHOLINE TURNOVER RATE IN CORTEX AND HIPPOCAMPUS ELICITED BY MORPHINE, MEPERIDINE, VIMINOL-R2 AND AZIDOMORPHINE
No full textIn rats, an ED50 for analgesia of morphine, meperidine, viminol R2 or azidomorphine decreases the turnover rate of acetylcholine (TR(ACh)) in cortex and hippocampus. These four analgetics fail to change the TR (ACh) in striatum when given in a dose range from ED30 for analgesia up to a cataleptic dose. Viminol S2, a nonanalgesic stereoisomer of viminol R2, fails to decrease the TR(ACh) in cortex and hippocampus. Naltrexone, an opiate antagonist, also fails to change the cortical and hippocampal TR (ACh) but it antagonizes the decrease in cortical and hippocampal TR(ACh) elicited by the four analgetics. Since the ED50 of these four analgetics fails to change the TR(ACh) in striatum which contains a high density of opiate receptors and intrinsic cholinergic neurons, but decreases the TR(ACh) in hippocampus and cortex which contain a low density of opiate receptors, it can be inferred that opiate receptors are not exclusively involved in the regulation of TR(ACh). However, the results suggest that certain cholinergic pathways participate in the mediation of analgesia
PENTOBARBITAL AND IN VIVO TURNOVER RATE OF ACETYLCHOLINE IN MOUSE-BRAIN AND IN REGIONS OF RAT BRAIN
No full textThe in vivo turnover rate of acetylcholine was measured in total brain of mice and brain parts of rats after treatment with Napentobarbital, para-chlorophenylalanine and following REM sleep deprivation for 96 hours. Na-pentobarbital decreased the turnover rate of acetylcholine both in total brain of mice and in cortex of rats, but no significant changes were detected in the striatum. Subchronic treatment with parachlorophenylalanine decreased the cortical content of acetylcholine and choline and partially reversed the decrease of turnover rate of acetylcholine elicited by Na-pentobarbital. In REM sleep deprivated rats, the turnover rate of acetylcholine in the cortex was increased
IN VIVO INHIBITION OF STRIATAL ACETYLCHOLINE TURNOVER BY L-DOPA, APOMORPHINE AND (+)-AMPHETAMINE
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