High Level of Footshock during Inhibitory Avoidance Training Prevents Amnesia Induced by Intranigral Injection of GABA Antagonists

Cobos-Zapiaı́n, Gillermo; Salado‐Castillo, Rigoberto; Sanchez‐Alavez, Manuel; Quírarte, Gina L.; Roldán-Roldán, Gabriel; Guante, Miguel A. Diaz Del; Prado-Alcalá, Roberto A.

doi:10.1006/nlme.1996.0024

Cited by 18 publications

(9 citation statements)

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“…Previous reports had shown, independently, that relatively high intensity of footshock during IA training prevented the effect of a number of amnesic treatments administered to the SN (Cobos-Zapiaín et al, 1996), STR (Giordano and Prado-Alcalá, 1986; Pérez-Ruíz and Prado-Alcalá, 1989; Prado-Alcalá, 1995), and AMY (Thatcher and Kimble, 1966; Parent et al, 1992, 1994, 1995; Parent and McGaugh, 1994). However, there are no direct comparisons among these structures of the effect of interference with their neural activity, using different levels of aversive stimulation in training.…”

Section: Discussionmentioning

confidence: 98%

“…As stated above, post-training interference with activity of STR, SN, or AMY produces marked retention deficits of IA, but enhanced training protects against these deficits (Thatcher and Kimble, 1966; 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). It is not known, however, whether these structures are equally important for retention of IA.…”

Section: Methodsmentioning

confidence: 96%

“…It has been shown, for example, that interference with the activity of the amygdala (AMY) (Liang et al, 1982; Power et al, 2000; Roesler et al, 2000; McGaugh, 2002; Roozendaal et al, 2009), striatum (STR) (Prado-Alcalá et al, 1972, 1973; Sanberg et al, 1978; Prado-Alcalá, 1995; Salado-Castillo et al, 1996; Ambrogi-Lorenzini et al, 1999; Packard and Knowlton, 2002; White and McDonald, 2002; Izquierdo et al, 2006; White, 2009; Miyoshi et al, 2012), and substantia nigra (SN) (Routtenberg and Holzman, 1973; Kim and Routtenberg, 1976; Ambrogi-Lorenzini et al, 1994; Da Cunha et al, 2001, 2003; Díaz del Guante et al, 2004) causes significant deficiencies in retention of inhibitory avoidance (IA). 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: 99%

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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

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: Discussionmentioning

confidence: 98%

Section: Methodsmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

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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

Salado‐Castillo

Sanchez‐Alavez

Quírarte

et al. 2011

Front. Behav. Neurosci.

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“…Rats were trained using relatively low-or high-intensity footshocks, and then injected with picrotoxin or bicuculline into the SN. Only the group that had been trained with the low-intensity footshocks showed amnesia (Cobos-Zapia í n et al, 1996).…”

Section: Substantia Nigramentioning

confidence: 99%

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, generalized interference with cholinergic or serotonergic central activity produces amnesia of inhibitory avoidance (IA) trained with relatively low levels of foot-shock, but memory remains intact when higher levels of stimulation are used during training (e.g., Duran-Arevalo et al, 1990; Galindo et al, 2008). Similarly, long-term memory deficits of IA are produced by hindrance of synaptic activity of the striatum, amygdala, and substantia nigra; in contrast, under this circumstance memory is spared after enhanced IA training (Giordano and Prado-Alcalá, 1986; Pérez-Ruíz and Prado-Alcalá, 1989; Parent et al, 1992, 1995; Parent and McGaugh, 1994; Prado-Alcalá, 1995; Cobos-Zapiaín et al, 1996; Salado-Castillo et al, 2011). Recently, it was found that enhanced IA training prevented the typical amnesic effects of cycloheximide, a protein synthesis inhibitor (Díaz-Trujillo et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Extinction procedure induces pruning of dendritic spines in CA1 hippocampal field depending on strength of training in rats

Garín-Aguilar¹,

Dı́az-Cintra²,

Quírarte³

et al. 2012

Front. Behav. Neurosci.

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Numerous reports indicate that learning and memory of conditioned responses are accompanied by genesis of dendritic spines in the hippocampus, although there is a conspicuous lack of information regarding spine modifications after behavioral extinction. There is ample evidence that treatments that typically produce amnesia become innocuous when animals are submitted to a procedure of enhanced training. We now report that extinction of inhibitory avoidance (IA), trained with relatively low foot-shock intensities, induces pruning of dendritic spines along the length of the apical dendrites of hippocampal CA1 neurons. When animals are trained with a relatively high foot-shock there is a high resistance to extinction, and pruning in the proximal and medial segments of the apical dendrite are seen, while spine count in the distal dendrite remains normal. These results indicate that pruning is involved in behavioral extinction, while maintenance of spines is a probable mechanism that mediates the protecting effect against amnesic treatments produced by enhanced training.

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High Level of Footshock during Inhibitory Avoidance Training Prevents Amnesia Induced by Intranigral Injection of GABA Antagonists

Cited by 18 publications

References 0 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

Extinction procedure induces pruning of dendritic spines in CA1 hippocampal field depending on strength of training in rats

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