Amygdaloid D1 dopamine receptor involvement in Pavlovian fear conditioning

Guarraci, Fay A.; Frohardt, Russell J.; Kapp, Bruce S.

doi:10.1016/s0006-8993(99)01291-3

Cited by 183 publications

(157 citation statements)

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“…For example, in the dimension of emotional dysregulation, hyper-reactive response to salient stimuli by the amygdala may result in enhanced conditioned fear responses in individuals with BPD. These enhanced responses could result from an increase in DA activity in the amygdala (Guarraci et al, 1999) that is inadequately modulated by medial prefrontal cortical inhibition (Rosenkranz and Grace, 2001).…”

Section: Discussionmentioning

confidence: 99%

“…This proposal is supported by the relationships of DA activity in the extended amygdala, NAC, and PFC to fear conditioning (Guarraci et al, 1999), motivation, reward, and stress (Horvitz, 2000;Finlay and Zigmond, 1997), and of DA and 5-HT activity in these structures in anger (Swann, 2003). Of interest is the recent report by Jentsch et al (2002) that cAMP-dependent protein kinase (PKA) activity in the amygdala can facilitate reward-related learning.…”

Section: Da Effects On Emotion In Human and Animal Studiesmentioning

confidence: 96%

“…Other human and animal studies DA modulates responses to positive/negative rewards, salient events and arousal-producing stimuli (Everitt et al, 2000;Liberzon et al, 2003;Horvitz, 2000) CSF HVA levels are related to impulsivity in BPD (Coccaro, 1998;Chotai et al, 1998); to self-injurious and violent behavior (Winchel and Stanley, 1991;Soderstrom et al, 2001) DA receptor activity in the DLPFC modulates working memory and cognition (Arnsten et al, 1994;Goldman-Rakic, 1996;Arnsten and Goldman-Rakic, 1998) DA modulates emotional responses mediated by the amygdala-VTA-PFC circuits (Horvitz, 2000) DA dysfunction is involved in drug addiction (Modell et al, 1993;Volkow and Fowler, 2000) PCP-induced cognitive impairment correlates with DA levels in the DLPFC (Jentsch et al, 1997) Stress alters DA activity in the amydala and PFC (Finlay and Zigmond, 1997;Doherty and Gratton, 1999) DA mediates aggression and attack in rats (Wade et al, 2000;Vukhac et al, 2001) DA modulates cognitive processes at NMDA receptors (Williams and Goldman-Rakic, 1995) DA modulates conditioned fear responses (Guarraci et al, 1999) DA stimulates impulsive behavior in rats (Harrison et al, 1997) D1 agonist dilhydrexidine enhances cognitive performance and stimulates Ach release in the PFC (Steele et al, 1997;Schneider et al, 1994) Microdialysates of the PFC and the NAC suggest DA dysfunction is a risk factor for impulsivity (Van Erp and Miczek, 2000;Dalley et al, 2002) DA dysfunction in the DLPFC is related to cognitive impairment in SCZ, SPD, and normal subjects (Goldberg et al, 2003;Siever et al, 2002) DAFdopamine; CSF HVAFspinal fluid homovanillic acid; DLPFCFdorsolateral prefrontal cortex; PCPFphencylclidine; VTAFventral tegmental area; PFCFprefrontal cortex; AchFacetylcholine; NACFnucleus accumbens; SCZFschizophrenia; SPDFschizotypal personality disorder.…”

Section: The Effects Of Dopamine In Human and Animal Studiesmentioning

confidence: 99%

“…that DA activity in the amygdala is involved in fear conditioning (Guarraci et al, 1999). Dysregulated DA activity in the neural system regulating conditioned fear could result in the abnormal fear and anxiety responses prominent in BPD.…”

Section: Pfcmentioning

confidence: 99%

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Dopamine Dysfunction in Borderline Personality Disorder: A Hypothesis

Friedel

2004

Neuropsychopharmacol

121

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Research on the biological basis of borderline personality disorder (BPD) has focused primarily on the serotonin model of impulsive aggression. However, there is evidence that dopamine (DA) dysfunction may also be associated with BPD. Pertinent research and review articles, identified by Medline searches of relevant topics, books, references from bibliographies, and conference proceedings from 1975 to 2003, were reviewed. Evidence of DA dysfunction in BPD derives from the efficacy of traditional and atypical antipsychotic agents in BPD, and from provocative challenges with amphetamine and methylphenidate of subjects with the disorder. In addition, human and animal studies indicate that DA activity plays an important role in emotion information processing, impulse control, and cognition. The results of this review suggest that DA dysfunction is associated with three dimensions of BPD, that is, emotional dysregulation, impulsivity, and cognitive-perceptual impairment. The main limitation of this hypothesis is that the evidence reviewed is circumstantial. There is no study that directly demonstrates DA dysfunction in BPD. In addition, the therapeutic effects of antipsychotic agents observed in BPD may be mediated by non-DA mechanisms of action. If the stated hypothesis is correct, DA dysfunction in BPD may result from genetic, developmental, or environmental factors directly affecting specific DA pathways. Alternatively, DA dysfunction in BPD may be a compensatory response to alterations in the primary neural systems that control emotion, impulse control, and cognition, and that are mediated by the brain's main neurotransmitters, glutamate, and GABA, or in one or more other neuromodulatory pathways such as serotonin, acetylcholine, and norepinephrine.

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Section: Discussionmentioning

confidence: 99%

Section: Da Effects On Emotion In Human and Animal Studiesmentioning

confidence: 96%

Section: The Effects Of Dopamine In Human and Animal Studiesmentioning

confidence: 99%

Section: Pfcmentioning

confidence: 99%

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Dopamine Dysfunction in Borderline Personality Disorder: A Hypothesis

Friedel

2004

Neuropsychopharmacol

121

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“…Acquisition and expression of fear are facilitated by administration of dopamine receptor agonists and electrical stimulation of the ventral tegmental area [182][183][184] and are disrupted by administration of dopamine receptor antagonists or lesions of midbrain dopamine systems. [185][186][187] Several studies have implicated dopamine in fear extinction as well, although the nature of the modulation seems to be opposite that seen with acquisition. Hence, extinction is disrupted by manipulations that increase dopamine bioavailability or facilitate dopamine receptor function.…”

Section: Neurotransmitter Systemsmentioning

confidence: 99%

Mechanisms of fear extinction

2006

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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.

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Emotion

Davis

Lang

2003

Handbook of Psychology

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This chapter will present evidence to suggest that emotion is best defined, not as a single reaction, but as a process: Emotion involves multiple responses, organized according to temporal and spatial parameters. Thus, events that are positive/appetitive or aversive/threatening engage attention. They prompt information gathering, and do so more than other less motivationally relevant stimuli. Motive cues also occasion metabolic arousal, anticipatory responses that are oriented towards the engaging event, a mobilization of the organism that can lead to some action. Emotional processing can be compressed into fractions of a second or considerably extended in time. We suggest that neural networks underlying emotion include direct connections to the brain's primary motivational systems, appetitive and defensive. These neural circuits were laid down early in our evolutionary history, in primitive cortex, subcortex, and midbrain, to mediate behaviors basic to the survival of individuals and species. Unconditioned and conditioned appetitive and aversive stimuli activate these motivational circuits. They determine the general mobilization of the organism, the deployment of reflexive attentional, approach, and defensive behaviors, and mediate the formation of conditioned associations originally based on primary reinforcement.

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Amygdaloid D1 dopamine receptor involvement in Pavlovian fear conditioning

Cited by 183 publications

References 32 publications

Dopamine Dysfunction in Borderline Personality Disorder: A Hypothesis

Dopamine Dysfunction in Borderline Personality Disorder: A Hypothesis

Mechanisms of fear extinction

Emotion

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