Intra-amygdala injections of CREB antisense impair inhibitory avoidance memory: Role of norepinephrine and acetylcholine

Canal, Clinton E.; Chang, Qing; Gold, Paul E.

doi:10.1101/lm.904308

Cited by 23 publications

(19 citation statements)

References 93 publications

(110 reference statements)

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“…Studies by the groups of McGaugh, Izquierdo, and other authors suggest that the release of NA in the basolateral amygdala play a critical role in the memory consolidation of aversive tasks (McGaugh 2004;Canal et al 2008;Chamberlain et al 2006;Izquierdo et al 1992;Roozendaal et al 2008). Therefore, it is not surprising that, in the present study, the only significant alteration observed in the amygdala of the rats treated with NaF was a decrease in DHPG, a metabolite of NA.…”

Section: Daily Food Consumption (G)contrasting

confidence: 39%

Memory Impairment Induced by Sodium Fluoride is Associated with Changes in Brain Monoamine Levels

et al. 2009

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Previous studies suggest that sodium fluoride (NaF) can impair performance in some memory tasks, such as open-field habituation and two-way active avoidance. In the present study, we evaluated the effect of NaF intake (100 ppm in drinking water for 30 days) and its short-term (15 days) withdrawal on open-field habituation and brain monoamine level. Adult male rats were allocated to three groups: tap water (NaF 1.54 ppm) for 45 days (control group); 15 days of tap water followed by NaF for 30 days; and NaF for 30 days followed by 15 days of tap water. The results showed that NaF impairs open-field habituation and increases noradrenaline (NA) and serotonin (5-HT) in the striatum, hippocampus and neocortex. Dopamine (DA) increase was restricted to the striatum. Short-term NaF withdrawal did not reverse these NaF-induced changes, and both NaF treatments led to a mild fluorosis in rat incisors. No treatment effect was seen in body weight or fluid/water consumption. These results indicate that sodium fluoride induces memory impairment that outlasts short-term NaF withdrawal (2 weeks) and may be associated with NA and 5-HT increases in discrete brain regions.

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Section: Daily Food Consumption (G)contrasting

confidence: 39%

Memory Impairment Induced by Sodium Fluoride is Associated with Changes in Brain Monoamine Levels

et al. 2009

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“…The question arises, however, whether these treatments also have their actions on memory by their intended actions or by resulting in altered neurotransmitter functions that underlie the memory impairments. In a recent study, we found that CREB antisense treatment administered 6 h before training resulted in memory impairments assessed 48 h after training (Canal et al 2008). The antisense treatment also reduced training-initiated release of NE release; injections of clenbuterol, a b-adrenergic receptor agonist, at the time of training reversed the amnesia.…”

Section: Discussionmentioning

confidence: 99%

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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“…9 10 Acetylcholine and NE are excitatory neurotransmitters implicated in memory mechanisms. 11 Moreover, hippocampal activation of nAChRs stimulates NE release 12 and facilitates long-term potentiation. 13 As heterologously expressed neuronal nAChRs are highly sensitive to IAs at subanaesthetic concentrations, 14 15 we determined the effects of isoflurane on NE release as a potential neurochemical model for the amnesic effects of IAs.…”

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confidence: 99%

Nicotinic receptor-evoked hippocampal norepinephrine release is highly sensitive to inhibition by isoflurane

Westphalen

Gomez²,

Hemmings

2009

British Journal of Anaesthesia

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Background. Inhaled anaesthetics (IAs) produce multiple dose-dependent behavioural effects including amnesia, hypnosis, and immobility in response to painful stimuli that are mediated by distinct anatomical, cellular, and molecular mechanisms. Amnesia is produced at lower anaesthetic concentrations compared with hypnosis or immobility. Nicotinic acetylcholine receptors (nAChRs) modulate hippocampal neural network correlates of memory and are highly sensitive to IAs. Activation of hippocampal nAChRs stimulates the release of norepinephrine (NE), a neurotransmitter implicated in modulating hippocampal synaptic plasticity. We tested the hypothesis that IAs disrupt hippocampal synaptic mechanisms critical to memory by determining the effects of isoflurane on NE release from hippocampal nerve terminals.

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Intra-amygdala injections of CREB antisense impair inhibitory avoidance memory: Role of norepinephrine and acetylcholine

Cited by 23 publications

References 93 publications

Memory Impairment Induced by Sodium Fluoride is Associated with Changes in Brain Monoamine Levels

Memory Impairment Induced by Sodium Fluoride is Associated with Changes in Brain Monoamine Levels

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

Nicotinic receptor-evoked hippocampal norepinephrine release is highly sensitive to inhibition by isoflurane

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