Amnesic effect of cycloheximide in the mouse mediated by adrenocortical hormones.

Nakajima, Shinshu

doi:10.1037/h0076207

Cited by 56 publications

(13 citation statements)

References 24 publications

(22 reference statements)

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“…The administration of FLU causes a dose-dependent increase in corticosterone from 2.5 to 20 mg/kg (Fuller et al 1975;Fuller et al 1976;Fuller and Snoddy 1979). Since administration of corticosteroids improves memory retention (Flood et al 1978b) and is anti-amnestic (Barondes and Cohen 1968;Nakajima 1975;Flood et al 1978 b), it is possible that FLU improved memory retention by increasing plasma corticosterone. However, increased plasma corticosteroid levels are not necessarily associated with improved retention.…”

Section: Discussionmentioning

confidence: 93%

“…We and others have reported that amnesia caused by inhibitors of brain protein synthesis can be blocked by a variety of neurotransmitter agonists and hormones (Nakajima 1975;Flood et al 1977Flood et al , 1978aFlood et al , b, 1985Davis and Squire 1984;Food and Cherkin 1986). Recently, we found that ACTH4_ lo or drugs affecting six neurotransmitter systems blocked scopolamine-induced amnesia (Flood and Cherkin 1986).…”

Section: Experiments 8 Anti-amnestic Effect Of Fluoxetinementioning

confidence: 92%

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Fluoxetine enhances memory processing in mice

Flood

Cherkin

1987

Psychopharmacology

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Fluoxetine (FLU) increases brain concentrations of serotonin by blocking its uptake, without appreciably affecting the dopamine or norepinephrine systems. The present experiments provide evidence that a subcutaneous injection of FLU enhanced post-memory processing ("consolidation") and retrieval, but not acquisition in young adult mice. FLU (15 mg/kg) enhanced 1-week memory retention when injected 2 min post-training. Similar enhancement was obtained with intracerebroventricular injection (20 micrograms per mouse). FLU enhanced retention when administered prior to training (1-5 mg/kg). FLU (2.5 mg/kg) enhanced recall scores when injected 1 h before the 1-week retention test, indicating an enhancing effect on memory retrieval. Neither the pre-training nor pre-testing effects depended on improved acquisition, since FLU did not improve acquisition of T-maze foot-shock avoidance over the dose range 0.5-35 mg/kg. The sensitive period for post-training enhancement by FLU (15 mg/kg) was less than 90 min, as shown by the temporal gradient typical of memory-enhancing drugs. The amnesia induced by a protein synthesis inhibitor anisomycin, or by an anticholinergic drug scopolamine, was blocked by FLU (15 mg/kg) injected post-training. Finally, FLU (15 mg/kg) injected after one-trial passive avoidance training enhanced 1-week retention, demonstrating effectiveness in this task as well as in the active avoidance task.

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Section: Discussionmentioning

confidence: 93%

Section: Experiments 8 Anti-amnestic Effect Of Fluoxetinementioning

confidence: 92%

Fluoxetine enhances memory processing in mice

Flood

Cherkin

1987

Psychopharmacology

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“…With the experience obtained in puromycin studies, studies of amnesia and pharmacological reversals of amnesia soon appeared. Some examples include findings that anisomycin-, cycloheximide-and / or acetoxycycloheximide-induced amnesias can be attenuated by administration of amphetamine, strychnine, picrotoxin, corticosteroids, dexamethasone, caffeine, nicotine, and phenoxybenzamine (Flood et al, 1977(Flood et al, , 1978aSerota et al, 1972;Oliver et al, 1979;Barondes and Cohen, 1968;Nakajima, 1975;Gold and Sternberg, 1978). In one series of experiments (Flood et al, 1977(Flood et al, , 1978a, a wide range of stimulants, as above, blocked amnesia.…”

Section: B Pharmacological Rescue Of Memory Impaired By Protein Symentioning

confidence: 98%

Protein synthesis inhibition and memory: Formation vs amnesia

Gold

2008

Neurobiology of Learning and Memory

110

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Studies using protein synthesis inhibitors have provided key support for the prevalent view that memory formation requires the initiation of protein synthesis as a primary element of the molecular biology of memory. However, many other interpretations of the amnesia data have received far less attention. These include: (a) protein synthesis may play a constitutive role in memory formation, providing proteins prior to an experience that can be activated by training; (b) protein synthesis may be needed to replace proteins available prior to learning but 'consumed' by learning; (c) inhibition of protein synthesis impairs the well-being of neurons, leading to an inability to deliver resources needed for memory formation; and (d) inhibition of protein synthesis results in abnormal neural functions that interfere with memory. One of these, abnormal release of neurotransmitters after inhibition of protein synthesis, is detailed here, along with a review of many circumstances in which it appears that protein synthesis at the time of training is not required for the formation of new memories. Evidence of activation of cell signaling molecules and transcription factors is another form of support for a role of training-initiated protein synthesis in memory. However, recent findings suggest that many of these molecules are activated by training and remain activated for days after training, i.e. activated for times well beyond those typically invoked for memory consolidation processes. Reviewing these results, this paper suggests that the long-lasting molecular changes may be the basis of a form of intracellular memory, one responsible for up-regulating the probability that a neuron, once activated in this manner, will engage in future plasticity. This view melds ideas of modulation of memory with those of consolidation of memory.

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“…In this regard, arecent study (Nakajima, 1975) is relevant. It was found that the amnesie effect of cycloheximide in a passive avoidance situation is mediated by the adrenocortical hormones.…”

Section: Meehanisms Underlying the Amnesie Effectmentioning

confidence: 99%

The Hippocampus

1975

122

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Amnesic effect of cycloheximide in the mouse mediated by adrenocortical hormones.

Cited by 56 publications

References 24 publications

Fluoxetine enhances memory processing in mice

Fluoxetine enhances memory processing in mice

Protein synthesis inhibition and memory: Formation vs amnesia

The Hippocampus

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