Scopolamine and KCl injections into the caudate nucleus. Overtraining-induced protection against deficits of learning

Prado‐Alcalá, Roberto A.; Kaufmann, Patricia; Moscona, Renee

doi:10.1016/0091-3057(80)90364-0

Cited by 29 publications

(10 citation statements)

References 9 publications

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“…There are data that indicate, however, that treatments which normally induce amnesia become ineffective when infused into these structures in rats that have been subjected to enhanced IA training (Giordano and Prado-Alcalá, 1986; Pérez-Ruíz and Prado-Alcalá, 1989; Parent et al, 1992, 1994, 1995; Parent and McGaugh, 1994; Prado-Alcalá, 1995; Cobos-Zapiaín et al, 1996). This protective effect of enhanced training has also been observed in cats (Prado-Alcalá and Cobos-Zapiaín, 1977, 1979) and rats (Prado-Alcalá et al, 1980) trained to perform operant responses in order to obtain positive reinforcers.…”

Section: Introductionmentioning

confidence: 63%

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

Sanchez‐Alavez

Quírarte

et al. 2011

Front. Behav. Neurosci.

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Memory is markedly impaired when normal activity of any of a number of cerebral structures is disturbed after a learning experience. A growing body of evidence indicates, however, that such interference with neuronal function becomes negligible when the learning experience is significantly enhanced. We now report on the effects of enhanced training on retention after temporary inactivation of cerebral nuclei known to be involved in memory, namely the substantia nigra (SN), striatum (STR), and amygdala (AMY). When training was conducted with a relatively low intensity of footshock (1.0 mA), post-training infusion of lidocaine into the SN, STR, or AMY produced a marked memory deficit. Increasing the aversive stimulation to 2.0 mA protected memory from the amnesic effect of intranigral lidocaine, but there was still a deficit after its infusion into the STR and AMY. Administration of lidocaine into each of these nuclei, in the groups that had been trained with 3.0 mA, was completely ineffective in producing alterations in memory consolidation. Simultaneous infusion of lidocaine into STR + SN, AMY + SN, or AMY + STR was also ineffective in altering memory formation when the highest footshock intensity was used for training. To our knowledge, this is the first demonstration that an enhanced learning experience guards against memory deficits after simultaneous temporary interruption of neural activity of brain nuclei heretofore thought to be necessary for memory formation. These findings support the proposition that brain structures involved in memory processing are functionally connected in series during memory consolidation and that, after an enhanced learning experience, these structures become functionally connected in parallel.

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Section: Introductionmentioning

confidence: 63%

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

Sanchez‐Alavez

Quírarte

et al. 2011

Front. Behav. Neurosci.

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“…A few years later it was found, for the first time, that overtraining of the lever-pressing task (by giving twice as many training sessions as in the former study) prevented the amnesic effect of the intra-caudate atropine infusions (Prado-Alcal á and Cobos-Zapia í n, 1977). The generality of this effect was confirmed in a subsequent study where intra-striatal scopolamine, another muscarinic antagonist, produced amnesia in rats that had been trained for 5 or 15 sessions on the CRF lever-pressing task, but there were no deficiencies in those trained for 25 sessions (Prado-Alcal á et al, 1980). An equivalent protective effect of overtraining was found after injecting scopolamine into the STR of rats trained in a positively reinforced, spatial alternation task (Prado-Alcal á et al, 1978).…”

Section: Striatummentioning

confidence: 74%

Intense emotional experiences and enhanced training prevent memory loss induced by post-training amnesic treatments administered to the striatum, amygdala, hippocampus or substantia nigra

Prada-Alcala¹,

Medina²,

Lopez³

et al. 2012

Reviews in the Neurosciences

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Most of the work related to the neurobiological basis of memory has been guided by the memory consolidation theory, which was derived from the seminal work of Miiller and Pilzecker that was published over a century ago. This theory proposes that the transfer from short- to long-term memory is mediated by a process called consolidation,and while consolidation is taking place, the information to be stored is in a labile state. A great deal of experimentation has given strong support to this proposal,as it has been found repeatedly that interference with neural activity shortly after a learning experience impedes durable retention of that experience. A growing body of evidence, however, indicates that intense emotional experiences prevent memory loss induced by amnesic treatments,even when these treatments are administered intracerebrally shortly after the learning experience. This evidence implies that the memory consolidation theory cannot account for long-term memory formation when neural activity is disrupted while consolidation should be taking place, and it calls for new hypotheses to account for these findings.

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“…Thus, after additional training, an increase in mushroom spines in DLS would be induced by heightened activation of the cortical-striatal connections. Previous work from our laboratory, where cats and rats were trained to perform an instrumental lever-press response, showed that infusion of cholinergic blockers (65) or sodium channel blockers (7) into the caudate nucleus and dorsal striatum, respectively, produced amnesia when the animals were treated during the early phases of learning, but no deficits were seen after extended training (i.e., when the response had become habitual). We can hypothesize that this extended training should have induced enhanced spinogenesis and an increased ratio of mushroom spines in DLS, at least in the rat.…”

Section: Discussionmentioning

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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Scopolamine and KCl injections into the caudate nucleus. Overtraining-induced protection against deficits of learning

Cited by 29 publications

References 9 publications

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

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

Intense emotional experiences and enhanced training prevent memory loss induced by post-training amnesic treatments administered to the striatum, amygdala, hippocampus or substantia nigra

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

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