Abstract:A total of 182 young adult male Wistar rats were bilaterally implanted with cannulae into the CA1 region of the dorsal hippocampus and into the amygdaloid nucleus, the entorhinal cortex, and the posterior parietal cortex. After recovery, the animals were trained in a stepdown inhibitory avoidance task. At various times after training (0, 30, 60 or 90 min) the animals received a 0.5-µl microinfusion of vehicle (saline) or 0.5 µg of muscimol dissolved in the vehicle. A retention test was carried out 24 h after t… Show more
“…The findings establish an important advance in the ability to discover the temporal relationships between emotional arousal and the modulation of memory consolidation as well as set the stage for future experiments to use optogenetic inhibition in combination with other techniques. The data from the ArchT experiments are consistent with previous studies showing that BLA inactivation impairs retention for learning (33,34), although it should be noted that the CAG promoter is a general cellular promoter, limiting interpretation of the findings based on specific cell type. However, these previous studies were unable to determine the temporal window in which emotional arousal led to BLA activation and the subsequent modulation of memory consolidation, despite the need to determine the initiation time and duration of BLA activity for normal memory consolidation.…”
Memory consolidation studies, including those examining the role of the basolateral amygdala (BLA), have traditionally used techniques limited in their temporal and spatial precision. The development of optogenetics provides increased precision in the control of neuronal activity that can be used to address the temporal nature of the modulation of memory consolidation. The present experiments, therefore, investigated whether optogenetically stimulating and inhibiting BLA activity immediately after training on an inhibitory avoidance task enhances and impairs retention, respectively. The BLA of male Sprague-Dawley rats was transduced to express either ChR2(E123A) or archaerhodopsin-3 from the Halorubrum sodomense strain TP009 (ArchT). Immediately after inhibitory avoidance training, rats received optical stimulation or inhibition of the BLA, and 2 d later, rats' retention was tested. Stimulation of ChR2 (E123A)-expressing neurons in the BLA using trains of 40-Hz light pulses enhanced retention, consistent with recording studies suggesting the importance of BLA activity at this frequency. Light pulses alone given to control rats had no effect on retention. Inhibition of ArchT-expressing neurons in the BLA for 15 min, but not 1 min, significantly impaired retention. Again, illumination alone given to control rats had no effect on retention, and BLA inhibition 3 h after training had no effect. These findings provide critical evidence of the importance of specific frequency patterns of activity in the BLA during consolidation and indicate that optogenetic manipulations can be used to alter activity after a learning event to investigate the processes underlying memory consolidation.
“…The findings establish an important advance in the ability to discover the temporal relationships between emotional arousal and the modulation of memory consolidation as well as set the stage for future experiments to use optogenetic inhibition in combination with other techniques. The data from the ArchT experiments are consistent with previous studies showing that BLA inactivation impairs retention for learning (33,34), although it should be noted that the CAG promoter is a general cellular promoter, limiting interpretation of the findings based on specific cell type. However, these previous studies were unable to determine the temporal window in which emotional arousal led to BLA activation and the subsequent modulation of memory consolidation, despite the need to determine the initiation time and duration of BLA activity for normal memory consolidation.…”
Memory consolidation studies, including those examining the role of the basolateral amygdala (BLA), have traditionally used techniques limited in their temporal and spatial precision. The development of optogenetics provides increased precision in the control of neuronal activity that can be used to address the temporal nature of the modulation of memory consolidation. The present experiments, therefore, investigated whether optogenetically stimulating and inhibiting BLA activity immediately after training on an inhibitory avoidance task enhances and impairs retention, respectively. The BLA of male Sprague-Dawley rats was transduced to express either ChR2(E123A) or archaerhodopsin-3 from the Halorubrum sodomense strain TP009 (ArchT). Immediately after inhibitory avoidance training, rats received optical stimulation or inhibition of the BLA, and 2 d later, rats' retention was tested. Stimulation of ChR2 (E123A)-expressing neurons in the BLA using trains of 40-Hz light pulses enhanced retention, consistent with recording studies suggesting the importance of BLA activity at this frequency. Light pulses alone given to control rats had no effect on retention. Inhibition of ArchT-expressing neurons in the BLA for 15 min, but not 1 min, significantly impaired retention. Again, illumination alone given to control rats had no effect on retention, and BLA inhibition 3 h after training had no effect. These findings provide critical evidence of the importance of specific frequency patterns of activity in the BLA during consolidation and indicate that optogenetic manipulations can be used to alter activity after a learning event to investigate the processes underlying memory consolidation.
“…The Kruskal-Wallis ANOVA on the difference scores showed a significant effect of group [H (df ϭ 3; n ϭ 47) ϭ 9.76; p Ͻ 0.05] with a significant difference between the highest dose group and vehicle controls ( p Ͻ 0.01) and between the highest dose group and the lowest dose group ( p Ͻ 0.05). Consistent with previous work Izquierdo et al, 1997;Zanatta et al, 1997), post-training inactivation of the amygdala with muscimol dose-dependently impaired inhibitory avoidance learning. However, unlike the results of Brioni et al (1989), who found effects only at low doses, our results are more consistent with other inhibitory avoidance studies in the literature that found effects using our higher dose Zanatta et al, 1997).…”
Section: Post-training Functional Inactivation Of the Amygdala Impairsupporting
confidence: 91%
“…It is thus likely that the ability to affect one kind of learning and not the other with post-training manipulations of the amygdala reflects differences in the relative complexity of the neural network underlying each type of learning. Indeed, a number of lesion studies have implicated the entorhinal and parietal cortex in late memory phases of inhibitory avoidance learning Zanatta et al, 1997), whereas, for example, Pavlovian fear conditioning is spared after entorhinal cortex lesions (Phillips and LeDoux, 1995). Furthermore, although lesion studies have consistently implicated the amygdala in Pavlovian fear conditioning (LeDoux et al, 1990;Maren et al, 1996a;Maren, 1998), lesions of the amygdala appear to have less clear-cut effects on inhibitory avoidance learning, especially if given after training (Liang et al, 1982;Parent et al, 1995).…”
Section: Discussionmentioning
confidence: 99%
“…We next evaluated whether post-training functional inactivation of LBA with muscimol would affect single-trial auditory fear conditioning similarly to inhibitory avoidance learning Izquierdo et al, 1997;Zanatta et al, 1997). Rats were trained as before with one-trial auditory conditioning and given immediate post-training infusion of either ACSF or one of three doses of muscimol used in the first experiment (4.4, 0.44, or 0.001 nmol), including the dose (4.4 nmol) that clearly disrupted conditioning in the first experiment and the dose (0.001 nmol) that has been shown to impair inhibitory avoidance when infused after training .…”
Section: Post-training Functional Inactivation Of the Amygdala Does Nmentioning
Although the lateral and basal nuclei of the amygdala are believed to be essential for the acquisition of Pavlovian fear conditioning, studies using post-training manipulations of the amygdala in the inhibitory avoidance learning paradigm have recently called this view into question. We used the GABA A agonist muscimol to functionally inactivate these nuclei immediately after single-trial Pavlovian fear conditioning or single-trial inhibitory avoidance learning. Immediate post-training infusions of muscimol had no effect on Pavlovian conditioning but produced a dose-dependent effect on inhibitory avoidance. However, pretraining infusions dose-dependently disrupted Pavlovian conditioning. These findings indicate that the amygdala plays an essential role in the acquisition of Pavlovian fear conditioning and contributes to the modulation of memory consolidation of inhibitory avoidance but not of Pavlovian fear conditioning.
“…Moreover, it should be kept in mind that, as seen for memory consolidation (Dudai 2004), the systems and cellular processes underlying reconsolidation are likely to differ among different learning paradigms. For example, IA differs from auditory and contextual fear conditioning in the involvement of amygdala and cortical areas during both acquisition and consolidation (Phillips and LeDoux 1995;Izquierdo et al 1997;Zanatta et al 1997;Wilensky et al 2000). These differences likely reflect distinctions in the neuronal networks underlying each type of learning.…”
Section: The Temporally Limited Requirement Of Protein Synthesis and mentioning
Following learning, a memory is fragile and undergoes a protein synthesis-dependent consolidation process in order to become stable. Established memories can again become transiently sensitive to disruption if reactivated and require another protein synthesis-dependent process, known as reconsolidation, in order to persist. Here, we show that, in the basolateral amygdala (BLA), protein synthesis is necessary for both consolidation and reconsolidation of inhibitory avoidance (IA) memory, while the expression of the transcription factor CCAAT enhancer binding protein  (C/EBP) is essential only for the reconsolidation process. Moreover, the critical roles of both protein synthesis and C/EBP following IA reactivation are temporally restricted, as they are necessary only for recent but not old IA memories. These results, together with previous findings showing that in the hippocampus both protein synthesis and C/EBP expression are required for consolidation but not reconsolidation of IA indicate that the stabilization process that takes place either after training or memory retrieval engages distinct neural circuits. Within these circuits, the C/EBP-dependent molecular pathway appears to be differentially recruited.
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