Glucose plus choline improve passive avoidance behaviour and increase hippocampal acetylcholine release in mice

Kopf, Silvia R.; Buchholzer, Marie-Luise; Hilgert, Michael; Löffelholz, K.; Klein, Jochen

doi:10.1016/s0306-4522(01)00007-0

Cited by 85 publications

(51 citation statements)

References 45 publications

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“…Exposure to a novel environment has been shown to transiently increase cholinergic neurotransmission in the hippocampus. [35][36][37][38][39] In M2-KOs and much more in M2/M4-KOs, the increase in hippocampal acetylcholine triggered by exposure to a novel environment was more pronounced both in amplitude and duration as compared to WT mice. This enhancement in the acetylcholine response in the KO mice could be a consequence of a number of distinct phenomena, including an increase in acetylcholine synthesis or a reduction in catabolism.…”

Section: Discussionmentioning

confidence: 91%

“…It should be noted that agents that acutely increase acetylcholine synthesis cause a larger increase in hippocampal acetylcholine levels upon exposure to the novel environment, but do not affect the response of the animals upon return to their home cage. 35 Taken together, the observed differences in acetylcholine responses between the KO and the WT mice can be attributed to impaired autoreceptor function, involving particularly M2 receptors. The data obtained with the M2/M4 double KO mice suggest that M4 receptors that control tonic acetylcholine release may play a secondary role in mediating autoinhibition of acetylcholine release.…”

Section: Discussionmentioning

confidence: 95%

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Dysregulated hippocampal acetylcholine neurotransmission and impaired cognition in M2, M4 and M2/M4 muscarinic receptor knockout mice

et al. 2003

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Among the five different muscarinic receptors that have been cloned and characterized, M2 and M4 receptors are localized both post-and presynaptically and are believed to have a pronounced autoreceptor role. The functional importance of these receptors in the regulation of acetylcholine release in the hippocampus and in cognitive processes was investigated by using M2 and M4 receptor single knockout (KO) as well as M2/M4 receptor double KO mice. We found profound alterations in acetylcholine homeostasis in the hippocampus of both M2-and M4-KO mice as well as of the combined M2/M4-KOs, as assessed by in vivo microdialysis. Basal acetylcholine efflux in the hippocampus was significantly increased in M4-KO and was elevated further in M2/M4-KOs. The increase in hippocampal acetylcholine induced by local administration of scopolamine was markedly reduced in M2-KO and completely abolished in M2/M4-KOs. In M2-KO and much more in M2/M4-KOs, the increase in hippocampal acetylcholine triggered by exposure to a novel environment was more pronounced both in amplitude and duration, with a similar trend observed for M4-KOs. Dysregulation of cholinergic function in the hippocampus, as it could result from perturbed autoreceptor function, may be associated with cognitive deficits. Importantly, M2-and M2/M4-KO, but not M4-KO, animals showed an impaired performance in the passive avoidance test. Together these results suggest a crucial role for muscarinic M2 and M4 receptors in the tonic and phasic regulation of acetylcholine efflux in the hippocampus as well as in cognitive processes.

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Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 95%

Dysregulated hippocampal acetylcholine neurotransmission and impaired cognition in M2, M4 and M2/M4 muscarinic receptor knockout mice

et al. 2003

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“…These results are in part supported by other studies that demonstrate that stressful situations increase ACh levels in the hippocampus (eg . In addition, numerous other studies have implicated the hippocampus in memory formation and have attributed an increase in hippocampal ACh efflux to an enhancement of overall memory performance (see eg Fadda et al, 2000;Kopf et al, 2001;Stancampiano et al 1999). The increase in hippocampal ACh efflux observed during the training and retention sessions were abolished by a single systemic injection of fluoxetine 1 h prior to the training session, even though basal hippocampal ACh levels were not affected.…”

Section: Discussionmentioning

confidence: 97%

Fluoxetine Disrupts the Integration of Anxiety and Aversive Memories

Degroot

Nomikos

2004

Neuropsychopharmacol

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Anxiety disorders may result from an overexpression of aversive memories. Evidence suggests that the hippocampal cholinergic system could be the point of convergence of anxiety and memory. We propose that clinically effective anxiolytics may exert their effect by interfering with this integration mechanism. To assess anxiety and aversive memory, we used the shock-probe burying test. A reduction in anxiety in this test is indicated by decreased burying, whereas impaired cognition is reflected by an increased number of probe-contacts and/or reduced retention latency. Both an aversive stimulus and the memory of that stimulus significantly increased hippocampal acetylcholine (ACh) levels (Experiment 1). In fact, the memory of the event seemed to be more important than the event itself since the aversive memory induced a greater increase in hippocampal ACh. Injections (i.p.) of fluoxetine (Prozac s ) reduced burying behavior, while not affecting probe contacts or retention latency (Experiment 2). Although injections of fluoxetine did not affect basal hippocampal ACh efflux (Experiment 3), fluoxetine abolished the increase in ACh induced by the aversive stimulus and the memory of that stimulus (Experiment 4), emphasizing the significance of aversive memories in anxiety disorders. These actions may be mediated by a decrease in the event-related enhancement in cholinergic neurotransmission through M1 cholinergic receptors (Experiment 5). Therefore, anxiety disorders may stem from an unopposed formation of aversive memories and clinically effective anxiolytics hinder the association between emotional and cognitive processing. This reduces the emotional impact of aversive memories, thereby opposing consequent anxiety.

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“…The most robust of these theories in terms of empirical evidence is the hypothesis that glucose enhances memory via its effects on ACh synthesis (Kopf et al, 2001;Ragozzino et al, 1998;Ragozzino et al, 1996). In addition, it has been reported that glucose administration replenishes the extracellular glucose levels of the rat hippocampus, 34 which become depleted during performance of demanding tasks (McNay and Gold, 2002).…”

Section: Discussionmentioning

confidence: 99%

“…In order to further develop an understanding of the relationship between hippocampal ACh output, glucose and memory, Kopf and colleagues (Kopf et al, 2001) investigated the effect of 28 glucose and choline (which are precursor metabolites of ACh) on memory performance in a maze task. First, it was observed that 30 mg/kg glucose injected into the mouse hippocampus enhanced task performance, relative to injection of saline.…”

Section: Ach Synthesismentioning

confidence: 99%

Glucose enhancement of human memory: A comprehensive research review of the glucose memory facilitation effect

Smith

Riby

Eekelen

et al. 2011

Neuroscience & Biobehavioral Reviews

127

123

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The brain relies upon glucose as its primary fuel. In recent years, a rich literature has developed from both human and animal studies indicating that increases in circulating blood glucose can facilitate cognitive functioning. This phenomenon has been termed the 'glucose memory facilitation effect'. The purpose of this review is to discuss a number of salient studies which have investigated the influence of glucose ingestion on neurocognitive performance in individuals with a) compromised neurocognitive capacity, as well as b) normally functioning individuals (with a focus on research conducted with human participants). The proposed neurocognitive mechanisms purported to underlie the modulatory effect of glucose on neurocognitive performance will also be considered. Many theories have focussed upon the hippocampus, given that this brain region is heavily implicated in learning and memory. Further, it will be suggested that glucose is a possible mechanism underlying the phenomenon that enhanced memory performance is typically observed for emotionally laden stimuli.

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Glucose plus choline improve passive avoidance behaviour and increase hippocampal acetylcholine release in mice

Cited by 85 publications

References 45 publications

Dysregulated hippocampal acetylcholine neurotransmission and impaired cognition in M2, M4 and M2/M4 muscarinic receptor knockout mice

Dysregulated hippocampal acetylcholine neurotransmission and impaired cognition in M2, M4 and M2/M4 muscarinic receptor knockout mice

Fluoxetine Disrupts the Integration of Anxiety and Aversive Memories

Glucose enhancement of human memory: A comprehensive research review of the glucose memory facilitation effect

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