Enhanced training protects memory against amnesia produced by concurrent inactivation of amygdala and striatum, amygdala and substantia nigra, or striatum and substantia nigra

Salado‐Castillo, Rigoberto; Sanchez‐Alavez, Manuel; Quírarte, Gina L.; García, María Isabel Martínez; Prado-Alcalá, Roberto A.

doi:10.3389/fnbeh.2011.00083

Cited by 15 publications

(12 citation statements)

References 42 publications

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“…These results allowed to operationally defining high, medium, and low level of training (Garín‐Aguilar et al, ). We further found that post‐training lidocaine infusion into the SN, STR, or AMY produced strong amnesia in animals trained in IA with 1.0 mA, but training with 2.0 mA protected memory in animals infused with lidocaine into the SN, but not in those infused into the STR, or AMY, and lidocaine was totally ineffective in altering memory when training was conducted with 3.0 mA, regardless of infusion site (Salado‐Castillo et al, ).…”

Section: Methodsmentioning

confidence: 88%

“…The recruitment of other brain systems appears to enable the storage of such information (Ambrogi Lorenzini et al, ). This interpretation may also provide an explanation of the finding that extensive training attenuates the amnestic effects of treatments administered shortly after training into the AMY, SN, and STR (Salado‐Castillo et al, ; Prado‐Alcalá et al, ).…”

Section: Introductionmentioning

confidence: 92%

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Intense aversive training protects memory from the amnestic effects of hippocampal inactivation

et al. 2013

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There is extensive evidence that amnestic treatments are less effective, or ineffective when administered to subjects that have been overtrained or subjected to high foot-shock intensities in aversively motivated learning. This protective effect has been found with a variety of learning tasks and with treatments that disrupt activity in several regions of the brain, including the hippocampus, amygdala, striatum, and substantia nigra. Such findings have been interpreted as suggesting that the brain regions disrupted are not critical sites for the memory processes induced by these types of training. In most experiments investigating this issue the amnestic treatments were administered after training. Thus, it might be less amnesia was induced because the training accelerated memory consolidation and, thus, the maximum effect of the amnestic treatment occurred after memory of the learning experience was consolidated. This study investigated this issue by inactivating the hippocampus of rats bilaterally with tetrodotoxin (TTX) (10 ng/side) 30 min before one-trial inhibitory avoidance training using relatively low (1.0 mA), medium (2.0 mA), or high (3.0 mA) foot-shock intensities. Retention of the task was measured 48 h after training. TTX produced a profound retention deficit, a mild deficit, and no deficit at all in the 1.0, 2.0, and 3.0 mA groups, respectively. These data confirm the protective effect of training with relatively high foot-shock intensity against experimentally induced amnesia, and suggests that this protection is not due to accelerated consolidation. Rather, the findings suggest that strong training activates brain systems other than those typically involved in mediating memory consolidation.

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Section: Methodsmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 92%

Intense aversive training protects memory from the amnestic effects of hippocampal inactivation

et al. 2013

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“…IA is by far the one in which more biochemical and pharmacological studies of memory consolidation in mammalian hippocampus in awake, behaving animals were carried out (70,72,73,105,116,183,208,264,265,267,271,272,400,401,403,405,413,563,657). Contextual and tone-conditioned fear and the LA or BLA come a distant second; Maren (379) commented on results of his own laboratory that suggest a specific role for the BLA in fear conditioning.…”

Section: Lessons From One-trial Inhibitory Avoidance Learningmentioning

confidence: 99%

Fear Memory

Izquierdo

Furini

Myskiw

2016

Physiological Reviews

373

259

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Fear memory is the best-studied form of memory. It was thoroughly investigated in the past 60 years mostly using two classical conditioning procedures (contextual fear conditioning and fear conditioning to a tone) and one instrumental procedure (one-trial inhibitory avoidance). Fear memory is formed in the hippocampus (contextual conditioning and inhibitory avoidance), in the basolateral amygdala (inhibitory avoidance), and in the lateral amygdala (conditioning to a tone). The circuitry involves, in addition, the pre-and infralimbic ventromedial prefrontal cortex, the central amygdala subnuclei, and the dentate gyrus. Fear learning models, notably inhibitory avoidance, have also been very useful for the analysis of the biochemical mechanisms of memory consolidation as a whole. These studies have capitalized on in vitro observations on long-term potentiation and other kinds of plasticity. The effect of a very large number of drugs on fear learning has been intensively studied, often as a prelude to the investigation of effects on anxiety. The extinction of fear learning involves to an extent a reversal of the flow of information in the mentioned structures and is used in the therapy of posttraumatic stress disorder and fear memories in general.

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“…If such spinogenesis occurred, then it might represent the basis of the protective effects of intense training against amnestic treatments that are administered to the dorsal striatum, as is the case with the administration of cholinergic and sodium channel blockers (8)(9)(10), which impede the activation of acetylcholine receptors and the production of action potentials, respectively, therefore inhibiting synaptic transmission. Thus, increased mushroom spine production could constitute a mechanism to store and relay information derived from the enhanced learning experience; by contrast, low or moderate levels of training would induce a limited increase of mushroom spines, which would not be sufficient to overcome the amnestic effects of treatments that interfere with neuronal activity of the dorsal striatum.…”

Section: Significancementioning

confidence: 99%

“…Interference with cholinergic activity of the dorsal striatum and reversible inactivation of this structure induced after moderate training impair memory consolidation. However, notably, these treatments are ineffective in impairing memory when animals are overtrained (6)(7)(8)(9)(10). Such findings suggest that intense training may induce functional changes within the dorsal striatum that prevent the impairment of memory.…”

mentioning

confidence: 99%

Mushroom spine dynamics in medium spiny neurons of dorsal striatum associated with memory of moderate and intense training

Bello-Medina

Flores

Quírarte

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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A growing body of evidence indicates that treatments that typically impair memory consolidation become ineffective when animals are given intense training. This effect has been obtained by treatments interfering with the neural activity of several brain structures, including the dorsal striatum. The mechanisms that mediate this phenomenon are unknown. One possibility is that intense training promotes the transfer of information derived from the enhanced training to a wider neuronal network. We now report that inhibitory avoidance (IA) induces mushroom spinogenesis in the medium spiny neurons (MSNs) of the dorsal striatum in rats, which is dependent upon the intensity of the foot-shock used for training; that is, the effect is seen only when high-intensity foot-shock is used in training. We also found that the relative density of thin spines was reduced. These changes were evident at 6 h after training and persisted for at least 24 h afterward. Importantly, foot-shock alone did not increase spinogenesis. Spine density in MSNs in the accumbens was also increased, but the increase did not correlate with the associative process involved in IA; rather, it resulted from the administration of the aversive stimulation alone. These findings suggest that mushroom spines of MSNs of the dorsal striatum receive afferent information that is involved in the integrative activity necessary for memory consolidation, and that intense training facilitates transfer of information from the dorsal striatum to other brain regions through augmented spinogenesis. A growing body of evidence indicates that treatments that commonly produce amnesia become ineffective when animals are given enhanced training (i.e., a high number of training sessions or relatively high levels of aversive stimulation). This protective effect against amnesia induced by interference with normal activity of brain nuclei has been found in a wide variety of learning tasks (1). Extensive evidence indicates that the dorsal striatum is intimately involved in the acquisition, consolidation, and retrieval memory for many kinds of training experiences (2-5). Interference with cholinergic activity of the dorsal striatum and reversible inactivation of this structure induced after moderate training impair memory consolidation. However, notably, these treatments are ineffective in impairing memory when animals are overtrained (6-10). Such findings suggest that intense training may induce functional changes within the dorsal striatum that prevent the impairment of memory. Although the dorsal striatum seems histologically homogeneous, there is a functional differentiation along its medial-lateral axis related to memory consolidation (11). Prior studies have shown that the dorsomedial striatum (DMS) is predominantly involved in spatial/contextual learning, influencing goal-directed behaviors (12, 13). In contrast, the dorsolateral striatum (DLS) enables the formation of procedural learning (4,14).Previous research suggests that memory consolidation may involve changes in the den...

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Enhanced training protects memory against amnesia produced by concurrent inactivation of amygdala and striatum, amygdala and substantia nigra, or striatum and substantia nigra

Cited by 15 publications

References 42 publications

Intense aversive training protects memory from the amnestic effects of hippocampal inactivation

Intense aversive training protects memory from the amnestic effects of hippocampal inactivation

Fear Memory

Mushroom spine dynamics in medium spiny neurons of dorsal striatum associated with memory of moderate and intense training

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