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  • 1
    Electronic Resource
    Electronic Resource
    Role of Phospholipase D Activation in Nervous System Physiology and Pathophysiology (1995)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 65 (1995), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1995.65041445.x
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  • 2
    Electronic Resource
    Electronic Resource
    Glutamate Activates Phospholipase D in Hippocampal Slices of Newborn and Adult Rats (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 61 (1993), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Phospholipase D (PLD) is activated by many neuro-transmitters in a novel signal transduction pathway. In the present work, PLD activity was studied comparatively in hippocampal slices of newborn and adult rats. Basal PLD activity in adult rats was almost three times higher than in newborn rats. In newborn rats, L-glutamate and 1S,3R-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) time- and concentrationdependently enhanced the formation of [3H]phosphatidylpropanol ([3H]PP) and of [3H]phosphatidic acid in the presence of 2% propanol. N-MethylD-aspartate and kainate (both 1 mM) caused small, but significant increases (∼50%). whereas α-amino-3-hydroxy-5-methylisoxazole-4-propionate (100 μM) was ineffective. Maximally effective concentrations of glutamate (1 mM) and of 1S,3R-ACPD (300 μM) increased the PLD activity to almost 300% of basal activity; the EC50 values were 199 and 47 μM, respectively. Glutamate receptor antagonists, such as DL-2-amino-3-phosphonopropionic acid (AP3). DL-2-aminc-5-phosphonovalenic acid, and kynurenate (all 1 mM) did not inhibit the glutamate-evoked increase of PP formation. In slices of adult rats, the response to 1S,3R-ACPD was significant, but small, whereas glutamate was effective only in the presence of the glutamate uptake inhibitor L-aspartate-β-hydroxarnate. It is concluded that glutamate activates PLD in rat hippocampus through an AP3-resistant metabotropic receptor. This effect is subject to ontogenetic development, with one important factor being glutamate uptake.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1993.tb13659.x
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  • 3
    Electronic Resource
    Electronic Resource
    Uptake and Storage of Choline by Rat Brain: Influence of Dietary Choline Supplementation (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 57 (1991), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In order to elucidate the regulation of the levels of free choline in the brain, we investigated the influence of chronic and acute choline administration on choline levels in blood, CSF, and brain of the rat and on net movements of choline into and out of the brain as calculated from the arteriovenous differences of choline across the brain. Dietary choline supplementation led to an increase in plasma choline levels of 50% and to an increase in the net release of choline from the brain as compared to a matched group of animals which were kept on a standard diet and exhibited identical arterial plasma levels. Moreover, the choline concentration in the CSF and brain tissue was doubled. In the same rats, the injection of 60 mg/kg choline chloride did not lead to an additional increase of the brain choline levels, whereas in control animals choline injection caused a significant increase; however, this increase in no case surpassed the levels caused by chronic choline supplementation. The net uptake of choline after acute choline administration was strongly reduced in the high-choline group (from 418 to 158 nmol/g). Both diet groups metabolized the bulk (〉96%) of newly taken up choline rapidly. The results indicate that choline supplementation markedly attenuates the rise of free choline in the brain that is observed after acute choline administration. The rapid metabolic choline clearance was not reduced by dietary choline load. We conclude that the brain is protected from excess choline by rapid metabolism, as well as by adaptive, diet-induced changes of the net uptake and release of choline.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1991.tb03762.x
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  • 4
    Electronic Resource
    Electronic Resource
    Muscarinic Mobilization of Choline in Rat Brain In Vivo as Shown by the Cerebral Arterio-Venous Difference of Choline (1987)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 48 (1987), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: In anesthetized rats, the choline levels of cerebrospinal fluid and plasma obtained from blood collected from peripheral vessels (carotid artery, cardiac vessels) and from the transverse sinus were determined with a radioenzymatic assay. Cortical release of choline was studied using the “cup technique.” The plasma choline level of the peripheral blood (11.5 μmol/L) was lower than that of the sinus blood. The resulting cerebral arterio-venous difference of choline was negative (3.2 μmol/L) and reflected the net release of choline from the whole brain. The plasma choline levels were not different irrespective of whether the rats were anesthetized with ether, urethane, or pentobarbital. However, the choline level of the cerebrospinal fluid, which normally was lower than the plasma choline levels, was increased by urethane anesthesia to a level between the arterial and venous plasma concentrations of the brain. In old rats (24 months), the choline level of the cerebrospinal fluid was significantly lowered, when compared with the results obtained with younger rats (2–4 months). In rats kept on a low-choline diet for 2 weeks, the plasma choline level of the peripheral blood was reduced to 51% of the control. The effect on the choline level of the sinus blood was smaller; the cerebral arterio-venous difference of choline was not reduced (it was even slightly enhanced). Likewise, the cholinelevel of the cerebrospinal fluid and the cortical release of choline were not altered. Intraperitoneal administration of oxotremorine in pentobarbital-anesthetized rats kept on a low-choline diet increased the plasma levels of choline. The rise of the plasma level of the peripheral blood was blocked by atropine and by methylatropine. Atropine alone or in combination with oxotremorine reduced the arterio-venous difference to half the level obtained by oxotremorine or oxotremorine plus methylatropine. In conclusion, the net formation of choline in the whole brain is partially controlled by central cholinergic activity and is unaltered even at a considerably reduced supply of choline from the peripheral circulation. Moreover, the remarkable maintenance of a certain choline level of the cerebrospinal fluid at a reduced (low-choline diet) or elevated (oxotremorine) plasma level also suggests that the extracellular concentration of choline in the brain is held at a constant level eventually at the expense of cellular phospholipids.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1987.tb05689.x
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  • 5
    Electronic Resource
    Electronic Resource
    Uptake and Metabolism of Choline by Rat Brain After Acute Choline Administration (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 58 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The present study is concerned with the uptake and metabolism of choline by the rat brain. Intraperitoneal administration of choline chloride (4-60 mg/kg) caused a dose-dependent elevation of the plasma choline concentration from 11.8 to up to 165.2 μM within 10 min and the reversal of the negative arteriovenous difference (AVD) of choline across the brain to positive values at plasma choline levels of 〉23 μM. Net choline release and uptake were linearly dependent on the plasma choline level in the physiological range of 10-50 μM, whereas the CSF choline level was significantly increased only at plasma choline levels of 〉50 μM. The bolus injection of 60 mg/kg of [3H]choline chloride caused the net uptake of 〉 500 μMol/g of choline by the brain as calculated from the AVD, which was reflected in a minor increase of free choline level and a long-lasting increase of brain phosphorylcholine content, which paralleled the uptake curve. Loss of label from phosphorylcholine 30 min to 24 h after choline administration was accompanied by an increase of label in phosphatidylcholine, an indication of a delayed transfer of newly taken-up choline into membrane choline pools. In conclusion, homeostasis of brain choline is maintained by a complex system that interrelates choline net movements into and out of the brain and choline incorporation into and release from phospholipids.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb09337.x
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  • 6
    Electronic Resource
    Electronic Resource
    Small Rises in Plasma Choline Reverse the Negative Arteriovenous Difference of Brain Choline (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 55 (1990), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The concentrations of free choline in blood plasma from a peripheral artery and from the transverse sinus, in the CSF, and in total brain homogenate, have been measured in untreated rats and in rats after acute intraperitoneal administration of choline chloride. In untreated rats, the arteriovenous difference of brain choline was related to the arterial choline level. At low arterial blood levels (〈10 μM) as observed under fasting conditions, the arteriovenous difference was negative (about -2 μM), indicating a net release of choline from the brain of about 1.6 nmol/g/min. In rats with spontaneously high arterial blood levels (〉 15 μM), the arteriovenous difference was positive, implying a marked net uptake of choline by the brain (3.1 nmol/g/min). The CSF choline concentration, which reflects changes in the extracellular choline concentration, also increased with increasing plasma levels and closely paralleled the gradually rising net uptake. Acute administration of 6, 20, or 60 mg of choline chloride/kg caused, in a dose-dependent manner, a sharp rise of the arterial blood levels and the CSF choline, and reversed the arteriovenous difference of choline to markedly positive values. The total free choline in the brain rose only initially and to a quantitatively negligible extent. Thus, the amount of choline taken up by the brain within 30 min was stored almost completely in a metabolized form and was sufficient to sustain the release of choline from the brain as long as the plasma level remained low. We conclude that the extracellular choline concentration of the brain closely parallels fluctuations in the plasma level of choline. Moreover, the often described release of choline from the brain as reflected by the negative arteriovenous difference of brain choline is not a steady-state phenomenon. Instead, the uptake of choline into and the release of choline from the brain seem to be in dynamic equilibrium that is closely related to the plasma choline level and, consequently, to nutritional choline uptake.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1990.tb03129.x
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  • 7
    Electronic Resource
    Electronic Resource
    Glutamatergic Activation of Hippocampal Phospholipase D: Postnatal Fading and Receptor Desensitization (1998)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 70 (1998), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Phospholipase D (PLD) activity was determined in rat hippocampal slices between postnatal days 3 and 35. After birth, basal PLD activity was low and, within 2 weeks, increased to reach a plateau that was maintained up to the adult age. Likewise the response to glutamate developed postnatally to reach a maximum at day 8, but then faded rapidly and was almost absent at day 35. Activation of PLD by 4β-phorbol 12β,13α-dibutyrate (PDB) was independent of age, whereas the effect of aluminum fluoride (AlF4−) increased to a plateau within the first week. At day 8, PLD stimulation by glutamate via metabotropic receptors involved protein kinase C activation, but was independent of Ca2+ influx; the time course of PLD activation by PDB or AlF4− was linear throughout the experiment, whereas the response to glutamate or 1-aminocyclopentane-1,3-dicarboxylic acid followed a biphasic pattern: the rapid “first phase activation” desensitized within a few minutes and disclosed a small, but maintained “second phase.” Pretreatment experiments confirmed desensitization of PLD activation by glutamate, but not by AlF4− or PDB. The biphasic pattern of glutamatergic PLD activation changed during development, i.e., the first phase activation faded and the second phase remained. These results were fully confirmed by the time courses of the PLD-mediated efflux of choline evoked by glutamate. In conclusion, postnatal glutamatergic activation of hippocampal PLD is composed of a pronounced and desensitizing first phase activation and a small, but nondesensitizing second phase. The first, but not the second, phase activation fades rapidly during development. The hypothesis is discussed that the glutamatergic activation of PLD occurs along different pathways in neonate and adult tissue.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1998.70041679.x
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  • 8
    Electronic Resource
    Electronic Resource
    A homeostatic mechanism counteracting K+-evoked choline release in adult brain (2002)
    Oxford, UK : Blackwell Science, Ltd
    Journal of neurochemistry 80 (2002), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Choline (Ch) is an essential nutrient as the biosynthetic precursor of acetylcholine (ACh) and phospholipids. Under resting conditions, the intracellular accumulation of Ch (above 10-fold), which is positively charged, is governed by the membrane potential and follows the Nernst equation. Accordingly, in synaptosomes from adult rats during depolarization, we observed a linear relationship between release of free cytoplasmic Ch and KCl concentration (2.7–120 mm). The K+-evoked Ch release was Ca2+-independent and did not originate from ACh or phospholipid hydrolysis. In superfused brain slices of adult rats, however, a K+-induced Ch efflux was absent. Also, under in vivo conditions, 30–60 mm KCl failed to increase the extracellular Ch level as shown by microdialysis in adult rat hippocampus. On the contrary, in brain slices from 1-week-old rats, high K+ as well as 4-aminopyridine evoked a marked Ch efflux in a concentration-dependent fashion. This phenomenon faded within 1 week. Hemicholinium-3 (HC-3, 1␣and 10 µm), a blocker of cellular choline uptake, caused a marked efflux of choline from adult rat slices but no or significantly less release from immature slices. We conclude that depolarization of synaptic endings causes a Ca2+-independent release of free cytoplasmic Ch into the extracellular space. In adult rat brain, this elevation of Ch is counteracted by a homeostatic mechanism such as uptake into brain cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.0022-3042.2001.00754.x
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  • 9
    Electronic Resource
    Electronic Resource
    Compensatory mechanisms enhance hippocampal acetylcholine release in transgenic mice expressing human acetylcholinesterase (2001)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 77 (2001), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Central cholinergic neurotransmission was studied in learning-impaired transgenic mice expressing human acetylcholinesterase (hAChE-Tg). Total catalytic activity of AChE was approximately twofold higher in synaptosomes from hippocampus, striatum and cortex of hAChE-Tg mice as compared with controls (FVB/N mice). Extracellular acetylcholine (ACh) levels in the hippocampus, monitored by microdialysis in the absence or presence of 10−8−10−3m neostigmine in the perfusion fluid, were indistinguishable in freely moving control and hAChE-Tg mice. Muscarinic receptor functions were unchanged as indicated by similar effects of scopolamine on ACh release and of carbachol on inositol phosphate formation. However, when the mice were anaesthetized with halothane (0.8 vol. %), hippocampal ACh reached significantly lower levels in AChE-Tg mice as compared with controls. Also, the high-affinity choline uptake (HACU) in hippocampal synaptosomes from awake hAChE-Tg mice was accelerated but was reduced by halothane anaesthesia. Moreover, hAChE-Tg mice displayed increased motor activity in novel but not in familiar environment and presented reduced anxiety in the elevated plus-maze test. Systemic application of a low dose of physostigmine (100 µg/kg i.p.) normalized all of the enhanced parameters in hAChE-Tg mice: spontaneous motor activity, hippocampal ACh efflux and hippocampal HACU, attributing these parameters to the hypocholinergic state due to excessive AChE activity. We conclude that, in hAChE-Tg mice, hippocampal ACh release is up-regulated in response to external stimuli thereby facilitating cholinergic neurotransmission. Such compensatory phenomena most likely play important roles in counteracting functional deficits in mammals with central cholinergic dysfunctions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2001.00287.x
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  • 10
    Electronic Resource
    Electronic Resource
    Stimulatory and inhibitory effects of ethanol on hippocampal acetylcholine release (1998)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 357 (1998), S. 640-647 
    Details
    ISSN: 1432-1912
    Keywords: Key words Ethanol ; Acetylcholine ; Scopolamine ; Hippocampus ; Microdialysis ; HPLC
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Using the microdialysis technique and sensitive HPLC procedures for the determination of acetylcholine (ACh) and ethanol, we investigated the release of ACh in rat hippocampus after acute ethanol administration. Systemic administration of ethanol (0.8 and 2.4 g/kg i.p.) led to peak ethanol concentrations of 21 and 42 mM in the hippocampus, respectively. The high dose caused a long-lasting inhibition of basal ACh release by up to 33%. Local infusion of scopolamine (1 µM) enhanced hippocampal ACh release up to eightfold in the presence of neostigmine (10 µM), and this stimulated release was also inhibited after systemic ethanol administration (by up to 45%). The low dose of ethanol (0.8 g/kg) led to a delayed stimulation of hippocampal ACh release. A stimulatory effect on ACh release was also observed when ethanol (50–100 mM) was infused directly into the hippocampus or into the septal area, i.e. to the origin of the cholinergic septohippocampal pathway; thus, the stimulatory effect may be mediated by a direct effect on cholinergic fibres. We conclude that ethanol exerts dual modulatory effects on the activity of the septohippocampal cholinergic fibres, depending on the dose and the site of administration. It is suggested that the inhibition of hippocampal ACh release by intoxicating doses of ethanol may contribute to the well-known cognitive and amnesic effects of ethanol intake.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00005219
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