Amnesia after Diazepam Infusion into Basolateral But Not Central Amygdala of Rattus norvegicus

Ma, Silva; Tomaz, Carlos

doi:10.1159/000119209

Cited by 48 publications

(4 citation statements)

References 36 publications

(56 reference statements)

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“…Therefore, this facilitation of avoidance conditioning could be interpreted as an improvement of memory, although the possibility of an enhancement of anxiety levels in learned fear situations cannot be ruled out. Several reports have suggested that intra-amygdala BRL 46470A [4] as well as peripheral administration of 5-HT3 receptor antagonists ondansetron [1] and granisetron [24] tend to improve memory, while the injection of BZDs had amnesic effects, particularly when injected into the basolateral amygdala [25], Thus, our results are in close agreement with these studies.…”

Section: Discussionsupporting

confidence: 92%

Effects on Anxiety and Memory of Systemic and Intra-Amygdala Injection of 5-HT<sub>3</sub> Receptor Antagonist BRL 46470A

et al. 1996

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This study deals with the effects of the 5-HT₃ receptor antagonist, BRL 46470A, on memory and anxiety, using the elevated T-maze. This method is useful for investigating the effects of anxiolytic drugs on memory, and the relationships between neural subsystems involved in emotionally related behaviors and in processes underlying learning. After the drug was either injected peripherally or microinjected into the amygdala, the animals were tested on the elevated T-maze (30 or 15 min later, respectively). Two kinds of aversively motivated behaviors, inhibitory avoidance and one-way escape, were recorded. These behaviors may reflect different types of fear/anxiety, namely, anticipatory anxiety and innate fear. Three days later, memory for these tasks was assessed by reexposing the subjects to the maze. The compound had an anxiolytic effect on the inhibitory avoidance response when given systemically, but an anxiogenic effect when injected into the amygdala. It had an anxiolytic action on the escape response when given either systemically or into the amygdala. The compound had no adverse effects on memory for either task. These results suggest that this new 5-HT₃ antagonist may be useful in the treatment of certain types of anxiety disorders, especially those related to unconditioned fear, e.g. phobic or panic disorders, with the likelihood of having no side effects on memory processes. The contrasting results obtained with different measures of anxiety may also account for the inconsistencies found in the experimental literature dealing with compounds of this nature.

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Section: Discussionsupporting

confidence: 92%

Effects on Anxiety and Memory of Systemic and Intra-Amygdala Injection of 5-HT<sub>3</sub> Receptor Antagonist BRL 46470A

et al. 1996

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“…As we found with glucocorticoids, the basolateral nucleus appears to be the critical region of the amygdala for BZD influences on memory. Infusions of midazolam into the basolateral nucleus impair memory, whereas infusions administered into the central nucleus are ineffective (75).…”

Section: Interactions With Other Neuromodulatory Systemsmentioning

confidence: 99%

Involvement of the amygdala in memory storage: Interaction with other brain systems

McGaugh

Cahill

Roozendaal

1996

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

662

348

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There is extensive evidence that the amygdala is involved in affectively inf luenced memory. The central hypothesis guiding the research reviewed in this paper is that emotional arousal activates the amygdala and that such activation results in the modulation of memory storage occurring in other brain regions. Several lines of evidence support this view. First, the effects of stress-related hormones (epinephrine and glucocorticoids) are mediated by inf luences involving the amygdala. In rats, lesions of the amygdala and the stria terminalis block the effects of posttraining administration of epinephrine and glucocorticoids on memory. Furthermore, memory is enhanced by posttraining intraamygdala infusions of drugs that activate ␤-adrenergic and glucocorticoid receptors. Additionally, infusion of ␤-adrenergic blockers into the amygdala blocks the memory-modulating effects of epinephrine and glucocorticoids, as well as those of drugs affecting opiate and GABAergic systems. Second, an intact amygdala is not required for expression of retention. Inactivation of the amygdala prior to retention testing (by posttraining lesions or drug infusions) does not block retention performance. Third, findings of studies using human subjects are consistent with those of animal experiments. ␤-Blockers and amygdala lesions attenuate the effects of emotional arousal on memory. Additionally, 3-week recall of emotional material is highly correlated with positronemission tomography activation (cerebral glucose metabolism) of the right amygdala during encoding. These findings provide strong evidence supporting the hypothesis that the amygdala is involved in modulating long-term memory storage.For decades there has been controversy over the question of whether the amygdala is involved in memory (1-4). Extensive evidence from many laboratories has now resolved this general controversy. Studies of the effects of lesions of the amygdala in animals and humans leave little doubt that the amygdala is involved in mediating affectively influenced memory (5-8). However, there remains considerable controversy concerning the specific role (or roles) of the amygdala in affectively influenced memory. The findings of lesion studies suggest that the amygdala may enable the formation of stimulus-reward associations (1, 9-11) and may be a site of neuroplasticity mediating aversive learning (12-15). Research from our laboratory using a variety of experimental methods provides extensive additional evidence that the amygdala is involved in memory. However, our findings suggest a somewhat different view of the role of the amygdala in affectively influenced memory. Our findings suggest that the amygdala regulates the storage or consolidation of information in other brain regions (16). The central hypothesis guiding our research is that emotional arousal activates the amygdala and that such activation results in modulation of memory storage processes occurring in brain regions influenced by the amygdala. According to this view, the amygdala is part of a...

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“…The first series of experiments demonstrating a selective involvement of the BLA in memory storage showed that lesions of the BLA, but not of the central nucleus of the amygdala, block the memory impairment induced by systemic injection of benzodiazepines [112]. Furthermore, benzodiazepines infused into the BLA impair retention [113], whereas infusion of a benzodiazepine antagonist into the BLA enhances memory [114]. The findings of subsequent experiments suggested a selective involvement of the BLA in mediating noradrenergic influences on memory for many kinds of tasks [115,116].…”

Section: Different Adrenoceptors In the Basolateral Amygdala Are Invomentioning

confidence: 99%

Role of Norepinephrine in Modulating Inhibitory Avoidance Memory Storage: Critical Involvement of the Basolateral Amygdala

Ferry¹,

Quírarte²

2012

The Amygdala - A Discrete Multitasking Manager

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Amnesia after Diazepam Infusion into Basolateral But Not Central Amygdala of Rattus norvegicus

Cited by 48 publications

References 36 publications

Effects on Anxiety and Memory of Systemic and Intra-Amygdala Injection of 5-HT<sub>3</sub> Receptor Antagonist BRL 46470A

Effects on Anxiety and Memory of Systemic and Intra-Amygdala Injection of 5-HT<sub>3</sub> Receptor Antagonist BRL 46470A

Involvement of the amygdala in memory storage: Interaction with other brain systems

Role of Norepinephrine in Modulating Inhibitory Avoidance Memory Storage: Critical Involvement of the Basolateral Amygdala

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