Glucose attenuation of atropine-induced deficits in paradoxical sleep and memory

Stone, William S.; Rudd, Rebecca J.; Gold, Paul E.

doi:10.1016/0006-8993(95)00810-d

Cited by 22 publications

(9 citation statements)

References 24 publications

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“…Previous studies indicate that glucose is remarkably effective at attenuating or reversing memory impairments produced by a variety of centrally-acting pharmacological agents, including mecamylamine, scopolamine, morphine, and muscimol (Blanchard and Duncan, 1997; Jafari et al, 2004; Kopf and Baratti, 1994; Krebs and Parent, 2005; Krebs-Kraft and Parent, 2008; Ragozzino and Gold, 1991; Ragozzino et al, 1994, 1992; Stone et al, 1995, 1991, 1988). Glucose also reverses age-related memory impairments in inhibitory avoidance, spontaneous alternation, and other tasks (McNay and Gold, 2001; Morris et al, 2010; Salinas and Gold, 2005).…”

Section: Discussionmentioning

confidence: 99%

“…The subtypes of these receptors have diverse functions and variable expression patterns throughout the brain. Previous work indicates that peripheral injections of general muscarinic and nicotinic antagonists impair performance in a number of behavioral memory paradigms, including inhibitory avoidance and spontaneous alternation tasks, and that co-administration of glucose attenuates these impairments (Blanchard and Duncan, 1997; Kopf and Baratti, 1994; Ragozzino and Gold, 1991; Ragozzino et al, 1994; Stone et al, 1995, 1991, 1988). These results imply a lack of regional and receptor specificity in glucose’s actions, suggesting that glucose could compensate for deficits in muscarinic receptors by promoting signaling through nicotinic receptors, and vice versa.…”

Section: Introductionmentioning

confidence: 99%

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Glucose attenuates impairments in memory and CREB activation produced by an α4β2 but not an α7 nicotinic receptor antagonist

Morris

Bui

et al. 2013

Neuropharmacology

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Glucose improves memory for a variety of tasks when administered to rats and mice near the time of training. Prior work indicates glucose may enhance memory by increasing the synthesis and release of the neurotransmitter acetylcholine in the brain. To investigate if specific acetylcholine receptor subtypes may mediate some of the memory-enhancing actions of glucose, we examined the effects of subtype-specific nicotinic acetylcholine receptor antagonists on memory in Fischer-344 rats and also examined the ability of glucose to reverse drug-induced impairments. Pre-training peripheral injections of methyllycaconitine (MLA) or dihydro-beta-erythroidine (DHβE), which are specific α7 and α4β2 nicotinic receptor antagonists, respectively, dose-dependently impaired retention latencies in an inhibitory avoidance task when tested 7-days but not 1 hour after training. Immediate post-training glucose injections attenuated the impairments, but were more effective in attenuating the DHβE-induced impairments. Likewise, peripheral or direct intrahippocampal injections of MLA or DHβE dosedependently impaired spatial working memory scores on a spontaneous alternation task. Concurrent administration of glucose reversed DHβE- but not MLA-induced impairments. CREB phosphorylation downstream of cholinergic signaling was assessed 30 minutes after spontaneous alternation testing and intrahippocampal drug infusions. Both MLA and DHβE impaired hippocampal CREB phosphorylation; glucose reversed DHβE but not MLA-induced deficits. The effectiveness of glucose in reversing DHβE- but not MLA- induced impairments in behavioral performance and CREB phosphorylation suggests that activation of α7 receptors may play an important role in memory enhancement by glucose.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Glucose attenuates impairments in memory and CREB activation produced by an α4β2 but not an α7 nicotinic receptor antagonist

Morris

Bui

et al. 2013

Neuropharmacology

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“…Rats tested in the Y-maze, where administration of exogenous glucose and other treatments do not improve performance unless that performance is impaired by amnestic drugs or age (28,(32)(33)(34)(35)(36)(37), show only a small (though statistically significant) decrease in ECF glucose during testing. Testing in the ϩ-maze, in which administration of glucose enhances performance, imposes a higher memory load with similar experimental conditions, including handling, introduction into a novel environment, and locomotor activity, and results in a large decrease in hippocampal ECF glucose.…”

Section: Discussionmentioning

confidence: 99%

Decreases in rat extracellular hippocampal glucose concentration associated with cognitive demand during a spatial task

McNay

Fries

Gold

2000

Proc. Natl. Acad. Sci. U.S.A.

329

274

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Using in vivo microdialysis, we measured hippocampal extracellular glucose concentrations in rats while they performed spontaneous alternation tests of spatial working memory in one of two mazes. Extracellular glucose levels in the hippocampus decreased by 32% below baseline during the test period on the more complex maze, but by a maximum of 11% on the less complex maze. Comparable decreases were not observed in samples taken from rats tested on the more complex maze but with probes located near but outside of the hippocampus. Systemic glucose fully blocked any decrease in extracellular glucose and enhanced alternation on the more complex maze. These findings suggest that cognitive activity can deplete extracellular glucose in the hippocampus and that exogenous glucose administration reverses the depletion while enhancing task performance.T raditional models of the distribution of glucose through the brain make two key statements: first, that the level of glucose is the same throughout the brain, which is viewed as a single compartment with respect to glucose; and second, that this level is invariant, with transport capacity always exceeding demand (1-3). Such models pose significant problems for interpretation of the large body of data showing that administration of glucose, either peripherally or directly into the brain, produces dosedependent effects on cognition, including enhancement of memory in a range of tasks (4-11). Most potential mechanisms for glucose effects on cognition, such as provision of additional energy, provision of additional substrate for neurotransmitters, and modulation of transmitter release, require that glucose administration lead to increased extracellular glucose availability in the brain. Moreover, because neuronal enzymes involved in the metabolism of glucose already are maximally active in the absence of exogenous glucose administration (12), it seemed perhaps likely that administration of glucose would act to reverse a reduction in available glucose caused by increased demand rather than to elevate the baseline extracellular concentration.Previous work has shown that the level of glucose in the brain's extracellular fluid (ECF) increases in line with increases in blood glucose (13)(14)(15)(16) and that the level of glucose in the ECF is lower than that predicted by traditional models (17,18). However, such findings do not address the question of whether provision of glucose to the brain is always sufficient to meet demand. To investigate this issue, we measured the levels of glucose in the hippocampus of freely moving rats before, during, and after tests of spontaneous alternation, a task requiring spatial working memory and which is sensitive to lesions and drug manipulations of the hippocampus (refs. 19-28; for a review of the underlying behavioral significance of performance in this task, see ref. 29).To determine further the effects of variation in cognitive demand on ECF glucose, two mazes of differing cognitive demand were used. We also assessed the effects on both perfor...

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“…For example, glucose attenuates spontaneous alternation deficits produced by cholinergic antagonists on a Y-maze, although glucose administration does not itself enhance performance on this task (18,19). Glucose also reduces hyperactivity and paradoxical sleep deficits produced by muscarinic cholinergic antagonists (20,21). Conversely, glucose increases the onset and severity of physostigmine-induced tremors, although glucose itself does not induce tremors (22).…”

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confidence: 99%

Hippocampal acetylcholine release during memory testing in rats: augmentation by glucose.

Ragozzino

Unick

Gold

1996

Proc. Natl. Acad. Sci. U.S.A.

291

190

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Several lines of evidence indicate that a modest increase in circulating glucose levels enhances memory. One mechanism underlying glucose effects on memory may be an increase in acetylcholine (ACh) release. The present experiment determined whether enhancement of spontaneous alternation performance by systemic glucose treatment is related to an increase in hippocampal ACh output. Samples of extracellular ACh were assessed at 12-min intervals using in vivo microdialysis with HPLC-EC. Twenty-four minutes after an intraperitoneal injection of saline or glucose (100, 250, or 1000 mg/kg), rats were tested in a four-arm cross maze for spontaneous alternation behavior combined with microdialysis collection. Glucose at 250 mg/kg, but not 100 or 1000 mg/kg, produced an increase in spontaneous alternation scores (69.5%) and ACh output (121.5% versus baseline) compared to alternation scores (44.7%) and ACh output (58.9%o versus baseline) of saline controls. The glucose-induced increase in alternation scores and ACh output was not secondary to changes in locomotor activity. Saline and glucose (100-1000 mg/kg) treatment had no effect on hippocampal ACh output when rats remained in the holding chamber. These findings suggest that glucose may enhance memory by directly or indirectly increasing the release ofACh. The results also indicate that hippocampal ACh release is increased in rats performing a spatial task. Moreover, because glucose enhanced ACh output only during behavioral testing, circulating glucose may modulate ACh release only under conditions in which cholinergic cells are activated.

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Glucose attenuation of atropine-induced deficits in paradoxical sleep and memory

Cited by 22 publications

References 24 publications

Glucose attenuates impairments in memory and CREB activation produced by an α4β2 but not an α7 nicotinic receptor antagonist

Glucose attenuates impairments in memory and CREB activation produced by an α4β2 but not an α7 nicotinic receptor antagonist

Decreases in rat extracellular hippocampal glucose concentration associated with cognitive demand during a spatial task

Hippocampal acetylcholine release during memory testing in rats: augmentation by glucose.

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