Reversal of cycloheximide-induced amnesia by adrenergic receptor stimulation

Quartermain, David; Freedman, Lewis S.; Botwinick, Chaim Y.; Gutwein, Baruch M.

doi:10.1016/0091-3057(77)90143-5

Cited by 46 publications

(14 citation statements)

References 22 publications

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“…The present results are consistent with those we have seen before (Canal et al , 2007); c-Fos immunoreactivity decreased after anisomycin injections into the amygdala but propranolol, which attenuated the amnesia, did not block the decrease in c-Fos immunoreactivity. Similar uncoupling of attenuating effects of neurotransmitter-related drugs on memory and on protein synthesis inhibition has been shown many times before (e.g., Barondes & Cohen, 1968; Serota et al , 1972; Hall et al , 1976; Quartermain et al , 1977; Flood et al , 1977, 1978; Lundgren & Carr, 1978; Sershen et al , 1982). The finding in the lidocaine + anisomycin group of substantial inhibition of expression of c-Fos while memory remains evident is not consistent with the view (Lamprecht & Dudai, 1996) that the transient expression of c-Fos in the amygdala is required for the formation of memory for amygdala-dependent tasks.…”

Section: Discussionsupporting

confidence: 78%

Lidocaine attenuates anisomycin-induced amnesia and release of norepinephrine in the amygdala

Sadowski

Canal

Gold

2011

Neurobiology of Learning and Memory

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When administered near the time of training, protein synthesis inhibitors such as anisomycin impair later memory. A common interpretation of these findings is that memory consolidation requires new protein synthesis initiated by training. However, recent findings support an alternative interpretation that abnormally large increases in neurotransmitter release after injections of anisomycin may be responsible for producing amnesia. In the present study, a local anesthetic was administered prior to anisomycin injections in an attempt to mitigate neurotransmitter actions and thereby attenuate the resulting amnesia. Rats received lidocaine and anisomycin injections into the amygdala 130 and 120 min, respectively, prior to inhibitory avoidance training. Memory tests 48 hr later revealed that lidocaine attenuated anisomycin-induced amnesia. In other rats, in vivo microdialysis was performed at the site of amygdala infusion of lidocaine and anisomycin. As seen previously, anisomycin injections produced large increases in release of norepinephrine in the amygdala. Lidocaine attenuated the anisomycin-induced increase in release of norepinephrine but did not reverse anisomycin inhibition of protein synthesis, as assessed by c-Fos immunohistochemistry. These findings are consistent with past evidence suggesting that anisomycin causes amnesia by initiating abnormal release of neurotransmitters in response to the inhibition of protein synthesis.

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Section: Discussionsupporting

confidence: 78%

Lidocaine attenuates anisomycin-induced amnesia and release of norepinephrine in the amygdala

Sadowski

Canal

Gold

2011

Neurobiology of Learning and Memory

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“…This possibility was suggested in early studies (e.g., Flexner and Goodman 1975;Quartermain et al 1977) and has recently been supported by studies of neurotransmitter release at the site of intra-amygdala injections of anisomycin ). In addition to impairing later memory after inhibitory avoidance training, pretraining injections of anisomycin into the amygdala produced rapid and dramatic increases in release of norepinephrine (NE), dopamine (DA), and serotonin (5-HT) at the sites of injection.…”

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confidence: 72%

Intrahippocampal infusions of anisomycin produce amnesia: Contribution of increased release of norepinephrine, dopamine, and acetylcholine

Qi¹,

Gold²

2009

Learn. Mem.

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Intra-amygdala injections of anisomycin produce large increases in the release of norepinephrine (NE), dopamine (DA), and serotonin in the amygdala. Pretreatment with intra-amygdala injections of the b-adrenergic receptor antagonist propranolol attenuates anisomycin-induced amnesia without reversing the inhibition of protein synthesis, and injections of NE alone produce amnesia. These findings suggest that abnormal neurotransmitter responses may be the basis for amnesia produced by inhibition of protein synthesis. The present experiment extends these findings to the hippocampus and adds acetylcholine (ACh) to the list of neurotransmitters affected by anisomycin. Using in vivo microdialysis at the site of injection, release of NE, DA, and ACh was measured before and after injections of anisomycin into the hippocampus. Anisomycin impaired inhibitory avoidance memory when rats were tested 48 h after training and also produced substantial increases in local release of NE, DA, and ACh. In an additional experiment, pretreatment with intrahippocampal injections of propranolol prior to anisomycin and training significantly attenuated anisomycininduced amnesia. The disruption of neurotransmitter release patterns at the site of injection appears to contribute significantly to the mechanisms underlying amnesia produced by protein synthesis inhibitors, calling into question the dominant interpretation that the amnesia reflects loss of training-initiated protein synthesis necessary for memory formation. Instead, the findings suggest that proteins needed for memory formation are available prior to an experience, and that post-translational modifications of these proteins may be sufficient to enable the formation of new memories.A dominant view of the molecular basis for memory is that the formation of long-term memory for an experience depends on de novo protein synthesis initiated by that experience (Davis and Squire

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“…(2) pretesting administration of pharmacological agents that increase catecholamine (CA) activity can alleviate experimentally induced amnesias (Freedman, Bachman, & Quartermain, 1979;Quartermain & Botwinick, 1975b; Quartermain, Freedman, Botwinick, & Gutwein, 1977) and retard normal forgetting (Quartermain, 1982b;Quartermain & Botwinick, 1975a). These findings suggest that release of central CAs may be involved in the neural processes that underlie retrieval.…”

Section: Facilitation Of Retrieval By D-amphetaminementioning

confidence: 99%

Facilitation of retrieval by d-amphetamine following anisomycin-induced amnesia

Quartermain

Altman

1982

Psychobiology

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A durable amnesia for an inhibitory avoidance response was induced in mice by an immediate posttraining injection of the protein-synthesis inhibitor anisomycin. Different groups were injected, immediately after training or 30 min prior to testing, with various doses of d-amphetamine in an attempt to alleviate the amnesia. Results indicated that, while immediate posttraining treatments were ineffective, substantial recovery of memory occurred when d-amphetamine (.5, 1.0,and 2.0 mg/kg) was administered before testing. Additional experiments showed: (1) that amphetamine-induced facilitation of avoidance was specific for the situation in which training occurred and thus could not beattributed to nonspecific effects of acute amphetamine treatment and (2) that enhanced avoidance could not be produced by pentylenetetrazol, strychnine, or noncontingent footshock. Amnesia could also be reversed by pretest treatment with methylphenidate (15 and 20 mg/kg). Administration of the amphetamine analog 4-hydroxyamphetamine, which principally releases peripheral catecholamines, failed to reverse the amnesia. These findings add to the growing body of evidence that suggests that catecholamines are involved in memory retrieval processes.

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Reversal of cycloheximide-induced amnesia by adrenergic receptor stimulation

Cited by 46 publications

References 22 publications

Lidocaine attenuates anisomycin-induced amnesia and release of norepinephrine in the amygdala

Lidocaine attenuates anisomycin-induced amnesia and release of norepinephrine in the amygdala

Intrahippocampal infusions of anisomycin produce amnesia: Contribution of increased release of norepinephrine, dopamine, and acetylcholine

Facilitation of retrieval by d-amphetamine following anisomycin-induced amnesia

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