Memory enhancement with posttraining intraventricular glucose injections in rats.

Abstract

Recent findings suggest that peripheral epinephrine enhancement of memory storage may be mediated in part by an increase in circulating glucose levels subsequent to epinephrine release or injection. Because glucose, unlike epinephrine, has ready access to the central nervous system, it is possible that glucose acts directly on central processes to enhance memory. To test this possibility, rats were trained on a one-trial inhibitory avoidance task and received immediate or delayed injections of glucose in artificial cerebrospinal fluid. On retention tests 24 hr after training, animals that received 3 or 5 micrograms glucose (in 1 microl cerebrospinal fluid over 3 min) had significantly enhanced performance of the learned response. These findings are consistent with the view that glucose can regulate the storage of new information by acting on central processes. Whether there are additional peripheral contributions to glucose effects on memory remains to be determined.

Pretest administration of glucose attenuates infantile amnesia for passive avoidance conditioning in rats

“…This is the first study demonstrating the memorymodulating effects of glucose on preweanling rats in an infantile amnesia paradigm. In this case, glucose presumably either directly (Gold, 1995;Lee, Graham, & Gold, 1988) or through some peripheral mechanism (Messier & White, 1987;White, 1991;Williams & Jensen, 1991) affected the activity of the neurological substrates in the brain to allow for enhanced retention of the prior learning episode.…”

Insulin in the Brain: Sources, Localization and Functions

“…In addition, it has been shown that the insulin-sensitive glucose transporter GLUT4 is present in several brain regions such as the hippocampus [182]. On the other hand, the administration of glucose both peripherally [183][184][185] and centrally [186] has been shown to enhance memory. In contrast to this view, Zhao et al [187] believe that improvement of memory by insulin cannot be due to a direct glucoregulatory effect because the brain mainly expresses the two insulin-insensitive glucose transporters, including GLUT1 and GLUT3.…”

Vagus nerve stimulation potentiates hippocampal LTP in freely-moving rats

“…Findings from a number of studies indicate that an epinephrine-induced increase in circulating glucose concentrations may mediate epinephrine's effects on memory [7] and considerable evidence supports the hypothesis that glucose modulates memory by direct brain action [8][9]. On the other hand, peripherally administered L-glucose, an isomer of glucose, that does not readily enter the brain, also facilitates retention performance [10].…”