Stimulation in prefrontal cortex area inhibits cardiovascular and motor components of the defence reaction in rats

Maskati, Haifa Ali Al; Zbrożyna, A. W.

doi:10.1016/0165-1838(89)90084-2

Cited by 66 publications

(35 citation statements)

References 12 publications

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“…For example, stimulation of the vmPFC in rats dampened amygdala-induced increases in blood pressure and defensive behavior (41). Human neuroimaging studies have shown that mPFC areas are functionally associated with skin conductance (42).…”

Section: Discussionmentioning

confidence: 99%

Thickness of ventromedial prefrontal cortex in humans is correlated with extinction memory

Milad

Quinn

Pitman

et al. 2005

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

378

306

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Here, we test the hypothesis that the cortical thickness of vmPFC regions is associated with how well healthy humans retain their extinction memory a day after having been conditioned and then extinguished. Fourteen participants underwent a 2-day fear conditioning and extinction protocol. The conditioned stimuli (CSs) were pictures of virtual lights, and the unconditioned stimulus (US) was an electric shock. On day 1, participants received 5 CS؉US pairings (conditioning), followed by 10 CS trials with no US (extinction). On day 2, the CS was presented alone to test for extinction memory. Skin conductance response (SCR) was the behavioral index of conditioning and extinction. Participants underwent MRI scans to obtain structural images, from which cortical thickness was measured. We performed a vertexbased analysis across the entire cortical surface and a region-ofinterest analysis of a priori hypothesized territories to measure cortical thickness and map correlations between this measure and SCR. We found significant, direct correlation between thickness of the vmPFC, specifically medial orbitofrontal cortex, and extinction retention. That is, thicker medial orbitofrontal cortex was associated with lower SCR to the conditioned stimulus during extinction recall (i.e., greater extinction memory). These results suggest that the size of the vmPFC might explain individual differences in the ability to modulate fear among humans.cortical thickness ͉ fear conditioning ͉ orbitofrontal cortex E xtinction of conditioned fear is of substantial basic and clinical neuroscientific interest. To describe posttraumatic stress disorder (PTSD), the Diagnostic and Statistical Manual of Mental Disorders (1) gives the example of a woman who is raped in an elevator and subsequently comes to fear all elevators. Recovery from PTSD entails, among other things, learning not to fear situations associated with the traumatic event (i.e., to extinguish conditioned fear responses) (2). It has been reported that 2 weeks after a rape, 92% of victims met symptom criteria for PTSD, but 3 months later only 47% did (3). Such individual differences in recovery from PTSD are likely related to genetically influenced individual differences in fear extinction and its retention (4). It is quite possible that these differences are mediated by variance in regional brain structures.Under a Pavlovian (classical) conditioning model, a onceneutral conditioned stimulus (CS) (e.g., a light) is paired with an aversive unconditioned stimulus (US) (e.g., a shock). After a few pairings, the CS comes to elicit various manifestations of a fear conditioned response, including freezing in rodents (5) and increased skin conductance in humans (6). When the CS is then repeatedly presented in the absence of the shock, the conditioned response is extinguished. There is substantial evidence indicating that fear extinction results in the formation of a new memory that coexists with, but opposes, the initial conditioning memory (7,8). Under favorable circumstances, the extinctio...

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Section: Discussionmentioning

confidence: 99%

Thickness of ventromedial prefrontal cortex in humans is correlated with extinction memory

Milad

Quinn

Pitman

et al. 2005

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

378

306

View full text Add to dashboard Cite

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“…Studies in rodents and non-human primates have shown regulation by the PFC of emotional/motivational processes linked to the amygdala (Rosenkranz and Grace, 1999;Maskati and Zbrozyna, 1989;Dias et al, 1996). In humans, functional magnetic resonance imaging (fMRI) studies and 18 fluorodeoxyglucose (FDG)-PET studies have provided evidence of a link between the amygdala and PFC (for example, see Pezawas et al, 2005;Hariri et al, 2000Hariri et al, , 2003.…”

Section: Introductionmentioning

confidence: 99%

The Neural Circuitry of Executive Functions in Healthy Subjects and Parkinson's Disease

Leh

Petrides

Strafella

2009

Neuropsychopharmacol

177

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In our constantly changing environment, we are frequently faced with altered circumstances requiring generation and monitoring of appropriate strategies, when novel plans of action must be formulated and conducted. The abilities that we call upon to respond accurately to novel situations are referred to as 'executive functions', and are frequently engaged to deal with conditions in which routine activation of behavior would not be sufficient for optimal performance. Here, we summarize important findings that may help us understand executive functions and their underlying neuronal correlates. We focus particularly on observations from imaging technology, such as functional magnetic resonance imaging, position emission tomography, diffusion tensor imaging, and transcranial magnetic stimulation, which in the past few years have provided the bulk of information on the neurobiological underpinnings of the executive functions. Further, emphasis will be placed on recent insights from Parkinson's disease (PD), in which the underlying dopaminergic abnormalities have provided new exciting information into basic molecular mechanisms of executive dysfunction, and which may help to disentangle the cortical/subcortical networks involved in executive processes.

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“…The medial prefrontal cortex (mPFC) also projects to the BLA (Sesack et al, 1989;McDonald et al, 1996) and may regulate the expression of some amygdala-mediated behaviors by selection of a set of BLA outputs or general inhibition of output. Thus, stimulation of the mPFC will inhibit the production of affective behavior produced by BLA (Al Maskati and Zbrozyna, 1989;Zbrozyna and Westwood, 1991), and PFC lesions appear to disinhibit some affective behaviors or result in perseverative affective responses to stimuli (Jaskiw and Weinberger, 1992;Morgan and LeDoux, 1995;Dias et al, 1996;Jinks and McGregor, 1997) (see also Powell et al, 1994;Gewirtz et al, 1997). The balance of sensory and mPFC inputs may determine whether an amygdala-mediated affective response will be produced in the presence of an affective sensory stimulus.…”

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confidence: 99%

Dopamine Attenuates Prefrontal Cortical Suppression of Sensory Inputs to the Basolateral Amygdala of Rats

Rosenkranz¹,

2001

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The basolateral complex of the amygdala (BLA) plays a significant role in affective behavior that is likely regulated by afferents from the medial prefrontal cortex (mPFC). Studies suggest that dopamine (DA) is a necessary component for production of appropriate affective responses. In this study, prefrontal cortical and sensory cortical [temporal area 3 (Te3)] inputs to the BLA and their modulation by DA receptor activation was examined using in vivo single-unit extracellular recordings. We found that Te3 inputs are more capable of driving BLA projection neuron firing, whereas mPFC inputs potently elicited firing from BLA interneurons. Moreover, mPFC stimulation before Te3 stimulation attenuated the probability of Te3-evoked spikes in BLA projection neurons, possibly via activation of inhibitory interneurons. DA receptor activation by apomorphine attenuated mPFC inputs, while augmenting Te3 inputs. Additionally, DA receptor activation suppressed mPFC-induced inhibition of Te3-evoked spikes. Thus, the mPFC may attenuate sensorydriven amygdala-mediated affective responses via recruitment of BLA inhibitory interneurons that suppress sensory cortical inputs. In situations of enhanced DA levels in the BLA, such as during stress and after amphetamine administration, mPFC regulation of BLA will be dampened, leading to a disinhibition of sensory-driven affective responses. : dopamine; amygdala; prefrontal cortex; temporal area 3; Te3; electrophysiology Disorders of the nervous system that include an affective component are believed to involve dysfunction within the amygdala. Thus, evidence of morphological or functional abnormalities of the amygdala have been found in schizophrenia, depression, anxiety, and temporal lobe epilepsy (Breier et al Key words

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Stimulation in prefrontal cortex area inhibits cardiovascular and motor components of the defence reaction in rats

Cited by 66 publications

References 12 publications

Thickness of ventromedial prefrontal cortex in humans is correlated with extinction memory

Thickness of ventromedial prefrontal cortex in humans is correlated with extinction memory

The Neural Circuitry of Executive Functions in Healthy Subjects and Parkinson's Disease

Dopamine Attenuates Prefrontal Cortical Suppression of Sensory Inputs to the Basolateral Amygdala of Rats

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