Dopamine gates LTP induction in lateral amygdala by suppressing feedforward inhibition

Bissière, Stéphanie; Humeau, Yann; Lüthi, Andreas

doi:10.1038/nn1058

Cited by 369 publications

(383 citation statements)

References 43 publications

Supporting

Mentioning

352

Contrasting

Unclassified

Order By: Relevance

“…For example, GABAergic cells within intercalated cell masses (ICM), which lie at the anatomical interface of the BLA and CeA, generate feedforward inhibition of CeA neurons in response to BLA activation (Royer et al, 1999(Royer et al, , 2000, and are regulated by extrinsic glutamatergic afferents from the prefrontal cortex and dopaminergic afferents from the ventral midbrain (Bissiere et al, 2003;. Therefore, cannabinoid actions within these regions, which are known to occur (French et al, 1997;Gessa et al, 1998;Auclair et al, 2000;Patel and Hillard, 2003), could modulate CeA activity independently of the BLA, via modulation of ICM neuronal activity.…”

Section: Discussionmentioning

confidence: 99%

Synergistic Interactions between Cannabinoids and Environmental Stress in the Activation of the Central Amygdala

Patel

Cravatt

Hillard

2004

Neuropsychopharmacol

147

100

View full text Add to dashboard Cite

Anxiety and panic are the most common adverse effects of cannabis intoxication; reactions potentiated by stress. Data suggest that cannabinoid (CB 1 ) receptor modulation of amygdalar activity contributes to these phenomena. Using Fos as a marker, we tested the hypothesis that environmental stress and CB 1 cannabinoid receptor activity interact in the regulation of amygdalar activation in male mice. Both 30 min of restraint and CB 1 receptor agonist treatment (D 9 -tetrahydrocannabinol (2.5 mg/kg) or CP55940 (0.3 mg/kg); by i.p. injection) produced barely detectable increases in Fos expression within the central amygdala (CeA). However, the combination of restraint and CB 1 agonist administration produced robust Fos induction within the CeA, indicating a synergistic interaction between environmental stress and CB 1 receptor activation. An inhibitor of endocannabinoid transport, AM404 (10 mg/kg), produced an additive interaction with restraint within the CeA. In contrast, fatty acid amide hydrolase (FAAH) inhibitor-treated mice (URB597, 1 mg/kg) and FAAH À/À mice did not exhibit any differences in amygdalar activation in response to restraint compared to control mice. In the basolateral (BLA) and medial amygdala, restraint stress produced a low level of Fos induction, which was unaffected by cannabinoid treatment. Interestingly, the CB 1 receptor antagonist SR141716 dose-dependently increased Fos expression in the BLA and CeA. These data suggest the CeA is an important neural substrate subserving the interactions between cannabinoids and environmental stress, and could be relevant to understanding the context-dependent emotional and affective changes induced by marijuana intoxication and the role of endocannabinoid signaling in the modulation of amygdalar activity.

show abstract

Section: Discussionmentioning

confidence: 99%

Synergistic Interactions between Cannabinoids and Environmental Stress in the Activation of the Central Amygdala

Patel

Cravatt

Hillard

2004

Neuropsychopharmacol

147

100

View full text Add to dashboard Cite

show abstract

“…Theoretically dopamine might modulate extinction through its effects on the amygdala, [192][193][194][195] prefrontal cortex, [196][197][198][199] and/or the interaction between these structures. 139,200 Acetylcholine Only two studies have examined the contribution of cholinergic neurotransmission to fear extinction and both focus on the expression rather than the development of extinction.…”

Section: Neurotransmitter Systemsmentioning

confidence: 99%

Mechanisms of fear extinction

2006

View full text Add to dashboard Cite

Excessive fear and anxiety are hallmarks of a variety of disabling anxiety disorders that affect millions of people throughout the world. Hence, a greater understanding of the brain mechanisms involved in the inhibition of fear and anxiety is attracting increasing interest in the research community. In the laboratory, fear inhibition most often is studied through a procedure in which a previously fear conditioned organism is exposed to a fear-eliciting cue in the absence of any aversive event. This procedure results in a decline in conditioned fear responses that is attributed to a process called fear extinction. Extensive empirical work by behavioral psychologists has revealed basic behavioral characteristics of extinction, and theoretical accounts have emphasized extinction as a form of inhibitory learning as opposed to an erasure of acquired fear. Guided by this work, neuroscientists have begun to dissect the neural mechanisms involved, including the regions in which extinction-related plasticity occurs and the cellular and molecular processes that are engaged. The present paper will cover behavioral, theoretical and neurobiological work, and will conclude with a discussion of clinical implications. Molecular Psychiatry (2007) 12, 120-150.

show abstract

“…The amygdala also possesses a powerful inhibitory interneuron system (Takagi and Yamamoto, 1981;Washburn and Moises, 1992a, b), which tightly controls neuronal activity and plasticity (Li et al, 1996;Szinyei et al, 2000;Bissiere et al, 2003;Shaban et al, 2006). In fact, amygdalar disinhibition induced either by GABAergic blockade (Isoardi et al, 2004), genetic knockout of the GABA B(1a) -receptor subtype (Shaban et al, 2006), benzodiazepine withdrawal (Isoardi et al, 2004), dopamine receptor activation (Bissiere et al, 2003), or stress (Rodriguez Manzanares et al, 2005), can result in amygdaloid hyperexcitability (Isoardi et al, 2004;Rodriguez Manzanares et al, 2005) and facilitate LTP induction (Bissiere et al, 2003;Rodriguez Manzanares et al, 2005;Shaban et al, 2006), which have been associated not only with enhanced fear memories (Isoardi et al, 2004;Rodriguez Manzanares et al, 2005), but also with overgeneralization of conditioned fear to neutral stimuli (Shaban et al, 2006).…”

Section: A Novel Role Suggested For the Amygdala In Autismmentioning

confidence: 99%

“…In fact, amygdalar disinhibition induced either by GABAergic blockade (Isoardi et al, 2004), genetic knockout of the GABA B(1a) -receptor subtype (Shaban et al, 2006), benzodiazepine withdrawal (Isoardi et al, 2004), dopamine receptor activation (Bissiere et al, 2003), or stress (Rodriguez Manzanares et al, 2005), can result in amygdaloid hyperexcitability (Isoardi et al, 2004;Rodriguez Manzanares et al, 2005) and facilitate LTP induction (Bissiere et al, 2003;Rodriguez Manzanares et al, 2005;Shaban et al, 2006), which have been associated not only with enhanced fear memories (Isoardi et al, 2004;Rodriguez Manzanares et al, 2005), but also with overgeneralization of conditioned fear to neutral stimuli (Shaban et al, 2006). These reports suggest that the hyperreactivity and hyperplasticity observed in this study may be due to a deficit in inhibition in the amygdala.…”

Section: A Novel Role Suggested For the Amygdala In Autismmentioning

confidence: 99%

Abnormal Fear Conditioning and Amygdala Processing in an Animal Model of Autism

Markram

Rinaldi

Mendola

et al. 2007

Neuropsychopharmacol

319

262

View full text Add to dashboard Cite

A core feature of autism spectrum disorders is the impairment in social interactions. Among other brain regions, a deficit in amygdala processing has been suggested to underlie this impairment, but whether the amygdala is processing fear abnormally in autism, is yet not clear. We used the valproic acid (VPA) rat model of autism to (a) screen for autism-like symptoms in rats, (b) test for alterations in amygdala-dependent fear processing, and (c) evaluate neuronal reactivity and synaptic plasticity in the lateral amygdala by means of in vitro single-cell electrophysiological recordings. VPA-treated animals displayed several symptoms common to autism, among them impaired social interactions and increased repetitive behaviors. Furthermore, VPA-treated rats were more anxious and exhibited abnormally high and longer lasting fear memories, which were overgeneralized and harder to extinguish. On the cellular level, the amygdala was hyperreactive to electrical stimulation and displayed boosted synaptic plasticity as well as a deficit in inhibition. We show for the first time enhanced, overgeneralized and resistant conditioned fear memories in an animal model of autism. Such hyperfear could be caused by the hyperreactivity and hyperplasticity found in the lateral amygdala, which may in turn be due to a deficit in the inhibitory system of the amygdala. We hypothesize an 'aversive world' syndrome that could, even if not a primary cause of the disorder itself, underlie some core symptoms in autism, such as impairments in social interactions and resistance to rehabilitation.

show abstract

Dopamine gates LTP induction in lateral amygdala by suppressing feedforward inhibition

Cited by 369 publications

References 43 publications

Synergistic Interactions between Cannabinoids and Environmental Stress in the Activation of the Central Amygdala

Synergistic Interactions between Cannabinoids and Environmental Stress in the Activation of the Central Amygdala

Mechanisms of fear extinction

Abnormal Fear Conditioning and Amygdala Processing in an Animal Model of Autism

Contact Info

Product

Resources

About