P01.145 Amyloid beta peptide 1–40 influences a recognition site of hemicholinium-3 sensitive choline carriers and their proteolytic degradation

Krištofiková, Zdeňka; Tejkalová, H.

doi:10.1016/s0924-9338(00)94552-8

Cited by 7 publications

(15 citation statements)

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“…The exact mechanism through which GKB modulates β-amyloid-suppressed ACh remains unknown. However, it is of interest to note that β-amyloid peptides have been shown to reduce high affinity choline uptake (Kristofikova et al, 2001), whereas ginkgo extract (EGb 761) has been reported to increase choline uptake in the hippocampal synaptosomes (Kristofikova and Klaschka, 1997). Therefore, GKB could have a direct effect in reversing the inhibitory effect of β-amyloid peptides by altering central cholinergic activities.…”

Section: Discussionmentioning

confidence: 99%

Effect of ginkgolides on β‐amyloid‐suppressed acetylocholine release from rat hippocampal slices

Lee

Chen²,

Wang

2004

Phytotherapy Research

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As Ginkgo has been shown to improve age-related memory de fi cits and beta-amyloid-related peptides have been suggested to play a signi fi cant role in memory degeneration in Alzheimer's disease, the present study was carried out to examine the effect of two major ginkgolides, A and B, on beta-amyloid peptide-modulated acetylcholine (ACh) release from hippocampal brain slices. Addition of beta-amyloid fragment(25-35) (0.01-1 micro M) in the superfusion medium suppressed the K(+)-evoked [(3)H]-ACh release from the rat hippocampal slices in a concentration-related manner; a 40% reduction in ACh out fl ow was observed with the highest amyloid concentration used (1 micro M). Inclusion of ginkgolide B (GKB, 0.01-10 micro M) caused a concentration-related reversion of the inhibitory effect elicited by the effective concentration of beta-amyloid (1 micro M). The reversal of the beta-amyloid-inhibited ACh release by GKB (1 micro M) was not blocked by tetrodotoxin (1 micro M) indicating a direct interaction of GKB on the cholinergic nerve terminals. In contrast, addition of the same concentration range of ginkgolide A (GKA, 0.01-10 micro M) had no effect on beta-amyloid-inhibited ACh release. These results suggest that GKB may elicit its anti-amnesic effect by minimizing the inhibitory effect of beta-amyloid peptides on cholinergic transmission.

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Section: Discussionmentioning

confidence: 99%

Effect of ginkgolides on β‐amyloid‐suppressed acetylocholine release from rat hippocampal slices

Lee

Chen²,

Wang

2004

Phytotherapy Research

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“…Causes could be as follows: (i) Ab is produced constitutively by brain cells including neurons and is present at pM-nM concentrations in the CSF of normal individuals, (ii) Ab, as well as APP, mediates both neurotrophic and neurotoxic effects, and finally (iii) Ab is secreted from healthy neurons in response to the neuronal activity, subsequently downregulates excitatory synaptic transmission and via this negative feedback can maintain physiological homeostatic mechanism [e.g., 12,13]. The neuromodulation actions of Ab are not restricted only to cholinergic system but hypofunction of basal forebrain cholinergic neurons mediated by low physiological concentrations seems to be the best documented so far [12][13][14][15][16][17][18].…”

Section: Introductionmentioning

confidence: 99%

“…It is surprising that actions of Ab have not been evaluated yet on hippocampal synaptosomes isolated from immature postnatal rats via measurements of a high-affinity choline uptake (HACU) values. It is well known that physiological pM-nM concentrations of Ab inhibit HACU transport that is directly associated with a synthesis of acetylcholine as a key regulatory step in the mature brain tissue [14][15][16]. It seems that the inhibition could occur by a direct interaction of Ab with hemicholinium-3 (HC-3) sensitive choline carriers [16].…”

Section: Introductionmentioning

confidence: 99%

“…It is well known that physiological pM-nM concentrations of Ab inhibit HACU transport that is directly associated with a synthesis of acetylcholine as a key regulatory step in the mature brain tissue [14][15][16]. It seems that the inhibition could occur by a direct interaction of Ab with hemicholinium-3 (HC-3) sensitive choline carriers [16]. Moreover, the carriers operating in the active transport are localized selectively on presynaptic cholinergic nerve terminals.…”

Section: Introductionmentioning

confidence: 99%

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Sex-dependent Actions of Amyloid Beta Peptides on Hippocampal Choline Carriers of Postnatal Rats

Krištofíková¹,

Říčný

Kozmiková³

et al. 2006

Neurochem Res

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It is suggested that amyloid beta peptides (Abeta) play a role in the pathogenesis of Alzheimer disease but their physiological function is still unknown. However, low pM-nM concentrations mediate a hypofunction of a basal forebrain cholinergic system without marked signs of neurotoxicity. In this study, we compared in vitro effects of soluble nonaggregated human Abeta 1-40 and 1-42 either on synaptosomal hemicholinium-3 sensitive choline carriers or on membrane fluidity in hippocampi of male and female Wistar rats aged 7 and 14 days or 2-3 months. The results indicate age- and sex-dependent effects mediated by peptides at nM concentrations but no significant differences between both fragments. Namely, opposite actions were observed in 14-day (the increase in the choline uptake and membrane fluidity) when compared to 7-day old and adult males (the mild drops). Lineweaver-Burk plot analysis revealed that the enhancement of the high-affinity choline transport in 14-day old males occurs via alterations in K (M )and the change was accompanied by a mild increase in the specific binding of [3H]hemicholinium-3. On the other hand, no age-dependent differences were found in females. Rat Abeta 1-40 mediated similar effects on 14-day old rats as the corresponding human fragment. Moreover, higher levels of soluble peptides were detected in immature when compared to mature male brains by means of competitive ELISA. Our study indicates that Abeta could play a role in postnatal sexual differentiation of hippocampal cholinergic system.

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“…The resulting floating particulate layer (synaptosomal fraction) was collected by decantation, washed with the homogenizing medium, and gently resuspended in the same medium. After the protein content of the preparations was determined (14), freshly prepared synaptosomes were immediately used in either assays of acetylcholine release (15) or assays of choline uptake (16).…”

Section: Acetylcholine (Ach) Which Is Synthesized From Choline (Ch)mentioning

confidence: 99%

Acetylcholine Release and Choline Uptake by Cuttlefish (Sepia officinalis) Optic Lobe Synaptosomes

Nunes

Santos

Cordeiro

et al. 2008

The Biological Bulletin

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Acetylcholine (ACh), which is synthesized from choline (Ch), is believed to hold a central place in signaling mechanisms within the central nervous system (CNS) of cuttlefish (Sepia officinalis) and other coleoid cephalopods. Although the main elements required for cholinergic functionCuttlefish, like other coleoid cephalopods, has been the subject of many neurobiological studies. Although the functional anatomy of the cuttlefish nervous system has been well illustrated, including investigation by electrical stimulation (1, 2), much less information is available on signaling mechanisms within the neural networks of cephalopods (3).The CNS of cuttlefish consists of distinct but interconnected lobes, of which the paired optic lobes correspond to more than half (4). The cuttlefish optic lobe comprises an outer granule cell layer, a neurophil layer, an inner granule cell layer (the outer cortex), and numerous clusters of cell bodies separated by areas of nerve fibers and synaptic areas (the central medulla) (5). The optic lobes contain a repertoire of neuronal circuits, which integrate the central visual processing, visuomotor, learning and memory systems (6). ACh has been suggested to mediate neuronal signaling at the CNS of cuttlefish, given that the Koelle-Friedenwald stain revealed a neuropilar localization of the reaction of cholinesterases (7). Moreover, it has been shown that ACh catabolism increases in the optic lobes as a response to memory formation with a long-term retention delay (8). Additionally, the optic lobes, in which nicotinic-like receptors are widely present (9), are among the cuttlefish CNS regions with the highest levels of enzyme activity responsible for the synthesis (choline acetyltransferase) and degradation (acetylcholinesterase) of ACh (10). Furthermore, recent work on cuttlefish optic lobe slices (11) has shown that mecamylamine hydrochloride, a nicotinic receptor antagonist, blocks excitatory postsynaptic currents, which are due to spontaneously released ACh. As far as we know, our recent paper (12) was the first to provide a brief insight into the release of ACh and the uptake of its precursor (Ch) in cuttlefish optic lobe. The present study further characterizes

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P01.145 Amyloid beta peptide 1–40 influences a recognition site of hemicholinium-3 sensitive choline carriers and their proteolytic degradation

Abstract: adequate psychosocial support, and better coordination between infectious-diseases and substance-use clinic teams.

Cited by 7 publications

References 0 publications

Effect of ginkgolides on β‐amyloid‐suppressed acetylocholine release from rat hippocampal slices

Effect of ginkgolides on β‐amyloid‐suppressed acetylocholine release from rat hippocampal slices

Sex-dependent Actions of Amyloid Beta Peptides on Hippocampal Choline Carriers of Postnatal Rats

Acetylcholine Release and Choline Uptake by Cuttlefish (Sepia officinalis) Optic Lobe Synaptosomes

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