The Role of Beta-Adrenergic System on the Enhancement of Spatial Learning Caused by Glucose Injection in Young Male Rats
ABSTRACT This study was designed to evaluate the role of beta-adrenergic system on the enhancement of spatial learning caused by glucose injection in the Y-maze. Young male Wistar rats were given daily injections of glucose (500 mg kg-1, i.p.) 10 min before training, propranolol (20 mg kg-1, s.c.) 30 min before training and co-administration of glucose (500 mg kg-1) and propranolol (20 mg kg-1). Three sham groups were received saline at the same volume and conditions. Comparison between co-administration of glucose and propranolol and glucose groups, showed a significant differences at first (p<0.01), third (p<0.001), fourth (p<0.01) and fifth (p<0.001) days. Indeed, co-administration of glucose and propranolol caused impairment of spatial learning. There was no significant difference between propranolol and co-administered groups. These findings indicate that propranolol impairs improvement of spatial learning caused by glucose administration via blockade of beta-adrenergic receptors and thus it seems that glucose exerts its memory enhancing effects via beta-adrenergic receptors.
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ABSTRACT: One mechanism by which administration of glucose enhances cognitive functions may be by modulating central ATP-sensitive potassium (K-ATP) channels. K-ATP channels appear to couple glucose metabolism and neuronal excitability, with channel blockade increasing the likelihood of neurosecretion. The present experiment examined the effects of glucose and the direct K-ATP channel modulators glibenclamide and lemakalim on spontaneous alternation performance and hippocampal ACh release. Rats received either artificial CSF vehicle or vehicle plus drug for two consecutive 12 min periods via microdialysis probes (3 mm; flow rate of 2.1 microliter/min) implanted in the left hippocampus. During the second 12 min period, rats were tested for spontaneous alternation performance. Dialysate was simultaneously collected for later analysis of ACh content. Both glucose (6.6 mm) and glibenclamide (100 micrometer) significantly increased alternation scores compared with those of controls. Conversely, lemakalim (200 micrometer) significantly reduced alternation scores relative to those of controls. Simultaneous administration of lemakalim with either glucose or glibenclamide resulted in alternation scores not significantly different from control values. All drug treatments enhanced hippocampal ACh output relative to control values. The results demonstrate that K-ATP channel modulators influence behavior when administered directly into the hippocampus, with channel blockers enhancing and openers impairing spontaneous alternation performance, thus supporting the hypothesis that glucose enhances memory via action at central K-ATP channels. That lemakalim, as well as glibenclamide and glucose, increased hippocampal ACh output suggests a dissociation between the effects of K-ATP channel modulators on behavior and hippocampal ACh release.Journal of Neuroscience 02/2001; 21(2):609-14. · 6.91 Impact Factor
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ABSTRACT: Three experiments examined the effect of propranolol injected IP on a series of 16 extinction trials at 24-hour intertrial intervals after continuously rewarded running. In Experiment I, propranolol (1, 5 or 10 mg/kg) was injected, in different groups, shortly before or shortly after each extinction trial, but without effect. In Experiment II, the same doses were injected daily for 18 days preceding extinction, to allow longer for any long-term drug effect to accumulate. Propranolol (1 mg/kg) facilitated extinction. In Experiment III, a single dose (7.5 mg/kg) was injected before or after extinction trials as in Experiment I; the acute effect was to impair extinction. These results are consistent with previous findings in the Skinner box that propranolol has an acute disinhibitory effect on nonrewarded responses and a long-term inhibitory one. These effects have different dose-response relationships.Pharmacology Biochemistry and Behavior 07/1990; 36(2):249-53. · 2.61 Impact Factor
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ABSTRACT: Epinephrine, released from the adrenal medulla, enhances memory in young rats and mice and apparently does so, at least in part, by increasing blood glucose levels. Like epinephrine, administration of glucose enhances cognitive functions in humans and rodents, including reversing age-related impairments in learning and memory. Epinephrine responses to training are increased in aged rats but the subsequent increase in blood glucose levels is severely blunted. The absence of increases in blood glucose levels during training might contribute to age-related deficits in learning and memory. Also, extracellular glucose levels in the hippocampus are depleted during spontaneous alternation testing to a far greater extent in aged than in young rats. Importantly, systemic injections of glucose block the depletion in the hippocampus and also enhance performance on the alternation task. Thus, the extensive depletion of extracellular glucose during training in aged rats may be associated with age-related memory impairments, an effect that might be related to - or may exacerbate - the effects on learning and memory of an absence of the increases in blood glucose levels to training as seen in young rats. Together, these findings suggest that age-related changes in both peripheral and central glucose physiology contribute to age-related impairments in memory.Neurobiology of Aging 01/2006; 26 Suppl 1:60-4. · 6.17 Impact Factor