The Basomedial and Basolateral Amygdaloid Nuclei Contribute to the Induction of Long‐term Potentiation in the Dentate Gyrus In Vivo

Ikegaya, Yuji; Saito, Hiroshi; Abe, Kazuho

doi:10.1111/j.1460-9568.1996.tb01327.x

Cited by 100 publications

(61 citation statements)

References 40 publications

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“…Previous research has shown that the amygdala influences emotional memory formation through connections to the hippocampus (Phelps 2004). Animal studies have demonstrated that amygdala stimulation facilitates hippocampal-dependent learning (Ikegaya et al 1996;Packard et al 1994). The enhancing effect of amygdala activity on emotional memory consolidation is a wellestablished finding in the imaging literature relating activity in the amygdala to later retrieval success (Cahill et al 1996;Canli et al 2000;Dolcos et al 2004Dolcos et al , 2005Hamann et al 1999;rev: LaBar and Cabeza 2006).…”

Section: Discussionmentioning

confidence: 99%

Role of FKBP5 in emotion processing: results on amygdala activity, connectivity and volume

et al. 2014

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Accumulating evidence suggests a role of FKBP5, a co-chaperone regulating the glucocorticoid receptor sensitivity, in the etiology of depression and anxiety disorders. Based on recent findings of altered amygdala activity following childhood adversity, the present study aimed at clarifying the impact of genetic variation in FKBP5 on threat-related neural activity and coupling as well as morphometric alterations in stress-sensitive brain systems. Functional magnetic resonance imaging during an emotional face-matching task was performed in 153 healthy young adults (66 males) from a high-risk community sample followed since birth. Voxel-based morphometry was applied to study structural alterations and DNA was genotyped for FKBP5 rs1360780. Childhood adversity was measured using retrospective selfreport (Childhood Trauma Questionnaire) and by a standardized parent interview assessing childhood family adversity. Depression was assessed by the Beck Depression Inventory. There was a main effect of FKBP5 on the left amygdala, with T homozygotes showing the highest activity, largest volume and increased coupling with the left hippocampus and the orbitofrontal cortex (OFC). Moreover, amygdala-OFC coupling proved to be associated with depression in this genotype. In addition, our results support previous evidence of a gene-environment interaction on right amygdala activity with respect to retrospective assessment of childhood adversity, but clarify that this does not generalize to the prospective assessment. These findings indicated that activity in T homozygotes increased with the level of adversity, whereas the opposite pattern emerged in C homozygotes, with CT individuals being intermediate. Abstract Accumulating evidence suggests a role of FKBP5, a co-chaperone regulating the glucocorticoid receptor sensitivity, in the etiology of depression and anxiety disorders. Based on recent findings of altered amygdala activity following childhood adversity, the present study aimed at clarifying the impact of genetic variation in FKBP5 on threat-related neural activity and coupling as well as morphometric alterations in stresssensitive brain systems. Functional magnetic resonance imaging during an emotional face-matching task was performed in 153 healthy young adults (66 males) from a high-risk community sample followed since birth. Voxelbased morphometry was applied to study structural alterations and DNA was genotyped for FKBP5 rs1360780. Childhood adversity was measured using retrospective selfreport (Childhood Trauma Questionnaire) and by a standardized parent interview assessing childhood family adversity. Depression was assessed by the Beck Depression Inventory. There was a main effect of FKBP5 on the left amygdala, with T homozygotes showing the highest activity, largest volume and increased coupling with the left hippocampus and the orbitofrontal cortex (OFC). Moreover, amygdala-OFC coupling proved to be associated with depression in this genotype. In addition, our results support previous evidence of a gene-env...

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Section: Discussionmentioning

confidence: 99%

Role of FKBP5 in emotion processing: results on amygdala activity, connectivity and volume

et al. 2014

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“…For instance, immediate posttraining pharmacological manipulations that alter noradrenergic, acetylcholinergic, GABAergic, and opioid activities in the amygdala can enhance or impair memory consolidation in hippocampal-dependent tasks (McGaugh, 2000). Amygdalar lesions, drug infusions, and stimulations have also been reported to influence DG LTP (Ikegaya et al, 1994(Ikegaya et al, , 1995(Ikegaya et al, , 1996Akirav and Richter-Levin, 1999). Therefore, it has been suggested that posttraining amygdalar manipulations influence memory consolidation in the hippocampus by altering LTP or LTP-like changes (McGaugh, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…Ikegaya and colleagues (1994) have shown that electrolytic lesions to the basolateral (but not central) nuclei of the amygdala significantly attenuate the DG LTP in vivo, whereas high-frequency stimulation of the amygdala augment LTP (Ikegaya et al, 1996). Moreover, amygdalar infusions of NMDA receptor antagonist have been shown to decrease DG LTP without affecting the baseline synaptic response (Ikegaya et al, 1995), a finding which suggests that amygdalar NMDA receptors influence LTP in the hippocampus.…”

Section: Discussionmentioning

confidence: 99%

Amygdalar Inactivation Blocks Stress-Induced Impairments in Hippocampal Long-Term Potentiation and Spatial Memory

Kim¹,

Koo²,

Lee³

et al. 2005

J. Neurosci.

167

145

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Electrolytic lesions to the amygdala, a limbic structure implicated in stress-related behaviors and memory modulation, have been shown to prevent stress-induced impairments of hippocampal long-term potentiation (LTP) and spatial memory in rats. The present study investigated the role of intrinsic amygdalar neurons in mediating stress effects on the hippocampus by microinfusing the GABA A receptor agonist muscimol into the amygdala and examining stress effects on Schaffer collateral/commissural-CA1 LTP and spatial memory. The critical period of the amygdalar contribution to stress effects on hippocampal functions was determined by applying muscimol either before stress or immediately after stress. Our results indicate that intra-amygdalar muscimol infusions before uncontrollable restrainttailshock stress effectively blocked stress-induced physiological and behavioral effects. Specifically, hippocampal slices prepared from vehicle-infused stressed animals exhibited markedly impaired LTP, whereas slices obtained from muscimol-infused stressed animals demonstrated robust LTP comparable with that of unstressed animals. Correspondingly, vehicle-infused stressed animals displayed impaired spatial memory (on a hidden platform version of the Morris water maze task), whereas muscimol-infused stressed animals revealed unimpaired spatial memory. In contrast to prestress muscimol effects, however, immediate poststress infusions of muscimol into the amygdala failed to interfere with stress impairments of LTP and spatial memory. Together, these results suggest that the amygdalar neuronal activity during stress, but not shortly after stress, is essential for the emergence of stress-induced alterations in hippocampal LTP and memory.

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“…Electrophysiological studies show that stimulation of the amygdala enhances synaptic transmission, plasticity, and long-term potentiation in the dentate gyrus (DG) of the hippocampus (27,28). Furthermore, recent evidence demonstrated synchronization of amygdala and hippocampal theta rhythm during retrieval of conditioned fear (29).…”

Section: Discussionmentioning

confidence: 99%

β-Adrenergic modulation of emotional memory-evoked human amygdala and hippocampal responses

Strange

Dolan

2004

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

267

191

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Human emotional experience is typically associated with enhanced episodic memory. We have used functional magnetic resonance imaging to demonstrate that successful encoding of emotional, compared to neutral, verbal stimuli evokes increased human amygdala responses. Items that evoke amygdala activation at encoding evoke greater hippocampal responses at retrieval compared to neutral items. Administration of the ␤-adrenergic antagonist propranolol at encoding abolishes the enhanced amygdala encoding and hippocampal retrieval effects, despite propranolol being no longer present at retrieval. Thus, memory-related amygdala responses at encoding and hippocampal responses at recognition for emotional items depend on ␤-adrenergic engagement at encoding. Our results suggest that human emotional memory is associated with a ␤-adrenergic-dependent modulation of amygdalahippocampal interactions.T he human hippocampus is critical for episodic memory (1). By contrast, enhanced memory for emotional events is amygdaladependent, as it is abolished by human amygdala lesions (2). Animal data suggest that the amygdala enhances emotional stimulus encoding by modulating responses in other brain regions (3). In the case of episodic memory, engagement of amygdala by emotional stimuli is thought to up-regulate responses in hippocampus, resulting in memory enhancement (3).The amygdala is thought to exert its modulatory effect on hippocampus by means of a ␤-adrenergic system. ␤-adrenergic blockade with the ␤ 1 ␤ 2 antagonist propranolol selectively impairs episodic memory for emotionally arousing material without affecting memory for neutral stimuli (4, 5). This modulation of emotional memory by propranolol is centrally mediated, as peripheral ␤-adrenergic blockade has no such effect (6). A previous study demonstrated amygdala modulation of hippocampal͞parahippocampal function by using path analysis (7). However, studies in humans have yet to provide evidence for an adrenergic-dependent amygdala-mediated modulation of hippocampal function during emotional encoding.To investigate the roles of amygdala and hippocampus in emotional memory, and their ␤-adrenergic dependency, we conducted an event-related functional MRI experiment in which 24 subjects received either 40 mg of propranolol or placebo in a double-blind experimental design. There were two distinct scanning sessions corresponding to encoding and retrieval respectively (Fig. 1A). Drug͞placebo was administered in the morning, with the encoding scanning session coinciding with propranolol's peak plasma concentration. The retrieval session, scanned 10 h later, was not contaminated by the presence of drug. During encoding, subjects viewed nouns presented serially, every 3 s, in semantically related lists. Each list contained two ''oddball'' nouns: an emotionally aversive noun (E) and a perceptual oddball (P) presented in a different font (Fig. 1B). Because all other nouns in each list were emotionally neutral, the E nouns constituted emotional oddballs. Perceptual oddballs were presented ...

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The Basomedial and Basolateral Amygdaloid Nuclei Contribute to the Induction of Long‐term Potentiation in the Dentate Gyrus In Vivo

Cited by 100 publications

References 40 publications

Role of FKBP5 in emotion processing: results on amygdala activity, connectivity and volume

Role of FKBP5 in emotion processing: results on amygdala activity, connectivity and volume

Amygdalar Inactivation Blocks Stress-Induced Impairments in Hippocampal Long-Term Potentiation and Spatial Memory

β-Adrenergic modulation of emotional memory-evoked human amygdala and hippocampal responses

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