Differential involvement of cortical receptor mechanisms in working, short-term and long-term memory

lzquierdo, I; Izquierdo, Luciana A.; Barros, Daniela M.; Souza, Tadéu Mello e; Souza, Márcia María de; Quevedo, João; Rodrigues, Carlos Ewerton Maia; Anna, Marcia K. Sant’; Vicente, Miguel Madruga; Medina, Jorge H.

doi:10.1097/00008877-199809000-00005

Cited by 89 publications

(60 citation statements)

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“…In addition, results obtained with the local administration of scopolamine suggest that its effects on aversive learning are mediated by limbic forebrain circuits involving entorhinal and parietal cortices, hippocampus, amygdala and septum (Izquierdo et al, 1992(Izquierdo et al, , 1998Nomura et al, 1994;Riekkinen et al, 1995). In this context, the ability of the 5-HT 1A receptor antagonists to attenuate the impairment of PA caused by systemic scopolamine administration in a manner similar to tacrine is both unexpected and intriguing.…”

Section: Discussionmentioning

confidence: 99%

Selective 5-HT1A Antagonists WAY 100635 and NAD-299 Attenuate the Impairment of Passive Avoidance Caused by Scopolamine in the Rat

Misane

Ögren

2003

Neuropsychopharmacol

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Systemic administration of the muscarinic-receptor antagonists atropine and scopolamine produces cognitive deficits in humans, nonhuman primates and rodents. In humans, these deficits resemble symptoms of dementia seen in Alzheimer's disease. The passive avoidance (PA) task has been one of the most frequently used animal models for studying cholinergic mechanisms in learning and memory. The present study examined the ability of two selective 5-HT 1A receptor antagonists WAY 100635 and NAD-299 (robalzotan) and two acetylcholinesterase (AChE) inhibitors tacrine and donepezil to attenuate the impairment of PA retention caused by the nonselective muscarinic receptor antagonist scopolamine in the rat. Although demonstrating differences in their temporal kinetics, both WAY 100635 and NAD-299 attenuated the impairment of PA caused by scopolamine (0.3 mg/kg s.c.). Donepezil did not block the PA deficit caused by the 0.3 mg/kg dose of scopolamine, but it prevented the inhibitory effects of the 0.2 mg/kg dose of scopolamine. In contrast, tacrine was effective vs both the 0.2 and 0.3 mg/kg doses of scopolamine. These results indicate that (1) a functional 5-HT 1A receptor antagonism can attenuate the anterograde amnesia produced by muscarinic-receptor blockade, and (2) the AChE inhibitors tacrine and donepezil differ in their ability to modify muscarinic-receptor-mediated function in vivo. These results suggest that 5-HT 1A receptor antagonists may have a potential in the treatment of cognitive symptoms in psychopathologies characterized by reduced ACh transmission such as Alzheimer's disease.

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Section: Discussionmentioning

confidence: 99%

Selective 5-HT1A Antagonists WAY 100635 and NAD-299 Attenuate the Impairment of Passive Avoidance Caused by Scopolamine in the Rat

Misane

Ögren

2003

Neuropsychopharmacol

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“…Through hippocampal GABAergic interneurons, serotonergic inputs modulate the activity of glutamate receptors, which is related to memory storage (36,37). Izquierdo et al (23) showed that hippocampal AMPA receptor-mediated glutamatergic transmission, which is susceptible to GABA inhibition, is necessary for working memory retrieval in the inhibitory avoidance task. Furthermore, Ohno et al (38) reported that intrahippocampal infusion of a competitive NMDA-receptor antagonist such as CPP impairs working memory performance of rats in a tree-panel runway task.…”

Section: Discussionmentioning

confidence: 99%

“…Animals received a bilateral 1-µl infusion of vehicle or scopolamine (2 or 4 µg/side) through the infusion cannula. The drug was used in a dose range previously shown to produce a marked working memory deficit in the inhibitory avoidance task (23). Infusion was performed with a pump (Cole Palmer, Model 210) at a rate of 0.5 µl/min.…”

Section: Drug and Intrahippocampal Infusionmentioning

confidence: 99%

“…It is believed that tasks assessing working memory should be able to distinguish the non-mnemonic changes from mnemonic processes within one session (10,20) and also distinguish the formation and storage of immediate memory lasting seconds or a few minutes (8,21). The immediate memory in a single-trial inhibitory avoidance test is now identified as working memory (21)(22)(23).…”

Section: Introductionmentioning

confidence: 99%

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Excitotoxic median raphe lesions aggravate working memory storage performance deficits caused by scopolamine infusion into the dentate gyrus of the hippocampus in the inhibitory avoidance task in rats

Babar

Melik

Özgünen

2002

Braz J Med Biol Res

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The interactions between the median raphe nucleus (MRN) serotonergic system and the septohippocampal muscarinic cholinergic system in the modulation of immediate working memory storage performance were investigated. Rats with sham or ibotenic acid lesions of the MRN were bilaterally implanted with cannulae in the dentate gyrus of the hippocampus and tested in a light/dark step-through inhibitory avoidance task in which response latency to enter the dark compartment immediately after the shock served as a measure of immediate working memory storage. MRN lesion per se did not alter response latency. Post-training intrahippocampal scopolamine infusion (2 and 4 µg/ side) produced a more marked reduction in response latencies in the lesioned animals compared to the sham-lesioned rats. Results suggest that the immediate working memory storage performance is modulated by synergistic interactions between serotonergic projections of the MRN and the muscarinic cholinergic system of the hippocampus. Correspondence

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“…As such optimal levels of endogenous mBDNF and BDNF-mediated events are required for the long-term extinction per se, but Zif268-mediated mechanisms may negatively regulate extinction at least in the short term. In analogy to the distinct molecular mechanisms that underlie the expression of memory during the consolidation of LTM (McGaugh 1966(McGaugh , 2000Davis and Squire 1984;Emptage and Carew 1993;Izquierdo et al 1998Izquierdo et al , 2002Stough et al 2006), this may reflect that the expression of the extinction memory may be supported by different, and potentially independent, molecular mechanisms shortly after training compared to those required for persistent extinction.…”

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confidence: 99%

The exclusive induction of extinction is gated by BDNF

Kirtley¹,

Thomas²

2010

Learn. Mem.

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We have previously reported that the reconsolidation and extinction of hippocampal-dependent contextual fear memory can be initiated by a single context conditioned stimulus (CS) presentation of either short or long duration, and that both processes require protein synthesis in this brain region. Furthermore, reconsolidation depends on Zif268 activity in this region. Here we show that by infusing a recombinant brain-derived neurotrophic factor (rBDNF) directly into the brain of rats, that high levels of mature BDNF in the hippocampus at retrieval constrain the extinction of the fear memory after prolonged memory recall. We also show after a short CS exposure that reconsolidation was impaired using antisense oligonucleotides targeting Zif268, and that, similarly, reductions in conditioned behavior were observed after prolonged CS presentation when extinction is constrained by high levels of BDNF. This is direct evidence that in the mammalian brain extinction proceeds exclusively after prolonged CS exposure. In addition, that BDNF activity in the hippocampus contributes to a molecular switch for the extinction of hippocampal-dependent memory.

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Differential involvement of cortical receptor mechanisms in working, short-term and long-term memory

Cited by 89 publications

References 0 publications

Selective 5-HT1A Antagonists WAY 100635 and NAD-299 Attenuate the Impairment of Passive Avoidance Caused by Scopolamine in the Rat

Selective 5-HT1A Antagonists WAY 100635 and NAD-299 Attenuate the Impairment of Passive Avoidance Caused by Scopolamine in the Rat

Excitotoxic median raphe lesions aggravate working memory storage performance deficits caused by scopolamine infusion into the dentate gyrus of the hippocampus in the inhibitory avoidance task in rats

The exclusive induction of extinction is gated by BDNF

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