A Functional Role for Dopamine Transmission in the Amygdala during Condtioned Fear

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

doi:10.1111/j.1749-6632.1999.tb09312.x

Cited by 38 publications

(23 citation statements)

References 10 publications

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“…This effect would be sensitized by the repeated conditioning sessions, allowing a potentiated DA modulation on BLA outputs. This hypothesis is in line with data using other models showing that increased DA activity in the amygdala is critical for mediating aversive conditioning (Coco et al, 1992;Guarraci et al, 1999;Nader and Le Doux, 1999).…”

Section: Differential Involvement Of Vta Neuronssupporting

confidence: 91%

A Specific Limbic Circuit Underlies Opiate Withdrawal Memories

Frenois

Stinus²,

Blasi³

et al. 2005

J. Neurosci.

108

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Compulsive drug-seeking behavior and its renewal in former drug addicts is promoted by several situations, among which reactivation of drug withdrawal memories plays a crucial role. A neural hypothesis is that such memories reactivate the circuits involved in withdrawal itself and promote a motivational state leading to drug seeking or taking. To test this hypothesis, we have analyzed the neural circuits and cell populations recruited when opiate-dependent rats are reexposed to stimuli previously paired with withdrawal (memory retrieval) and compared them with those underlying acute withdrawal during conditioning (memory formation). Using in situ hybridization for c-fos expression, we report here that reexposure to a withdrawal-paired environment induced conditioned c-fos responses in a specific limbic circuit, which can be partially dissociated from the structures involved in acute withdrawal. At the amygdala level, c-fos responses were doubly dissociated between the central and basolateral (BLA) nuclei, when comparing the two situations. Detailed phenotypical analyses in the amygdala and ventral tegmental area (VTA) show that specific subpopulations in the BLA are differentially involved in the formation and retrieval of withdrawal memories, and strikingly that a population of VTA dopamine neurons is activated in both situations. Together, this indicates that withdrawal memories can drive activity changes in specific neuronal populations of interconnected limbic areas known to be involved in aversive motivational processes. This first study on the neural substrates of withdrawal memories strongly supports an incentive-motivational view of withdrawal in opiate addiction that could be crucial in compulsive drug seeking and relapse.

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Section: Differential Involvement Of Vta Neuronssupporting

confidence: 91%

A Specific Limbic Circuit Underlies Opiate Withdrawal Memories

Frenois

Stinus²,

Blasi³

et al. 2005

J. Neurosci.

108

View full text Add to dashboard Cite

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“…lITC cells are densely innervated by putative dopaminergic terminals and are inhibited by dopamine (Marowsky et al, 2005). Dopamine is released into the amygdala during stressful episodes (Inglis and Moghaddam, 1999), and dopamine receptor activity is known to affect fear learning (Guarraci et al, 1999). Our results suggest that dopaminergic input to the amygdala would result in widespread reduction of auditory feed-forward inhibition, disinhibiting pyramidal neurons in the BLA.…”

Section: Discussionmentioning

confidence: 89%

Prefrontal and Auditory Input to Intercalated Neurons of the Amygdala

et al. 2015

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The basolateral amygdala (BLA) and prefrontal cortex (PFC) are partners in fear learning and extinction. Intercalated (ITC) cells are inhibitory neurons that surround the BLA. Lateral ITC (lITC) neurons provide feed-forward inhibition to BLA principal neurons, whereas medial ITC (mITC) neurons form an inhibitory interface between the BLA and central amygdala (CeA). Notably, infralimbic prefrontal (IL) input to mITC neurons is thought to play a key role in fear extinction. Here, using targeted optogenetic stimulation, we show that lITC neurons receive auditory input from cortical and thalamic regions. IL inputs innervate principal neurons in the BLA but not mITC neurons. These results suggest that (1) these neurons may play a more central role in fear learning as both lITCs and mITCs receive auditory input and that (2) mITC neurons cannot be driven directly by the IL, and their role in fear extinction is likely mediated via the BLA.

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“…We have recently described a profound defective GABAergic transmission in the basolateral nucleus of the amygdala [18], but to our knowledge there is not a single study focusing on GABAergic transmission within the lateral amygdala in Fmr1 KO mice. Since decreasing GABAergic transmission can improve learning or retrieval of conditioned fear memories and impairs extinction memory retrieval in a context-specific manner [45,46,47], it might be possible that GABAergic transmission is enhanced in the lateral amygdala, and reducing GABAergic transmission might have different outcomes in this behavioral paradigm.…”

Section: Discussionmentioning

confidence: 99%

The GABA<sub>A</sub> Receptor Agonist THIP Ameliorates Specific Behavioral Deficits in the Mouse Model of Fragile X Syndrome

2011

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Hyperactivity, hypersensitivity to auditory stimuli, and exaggerated fear are common behavioral abnormalities observed in individuals with fragile X syndrome (FXS), a neurodevelopmental disorder that is the most common genetic cause of autism. Evidence from studies of the Fmr1 knockout (KO) mouse model of FXS supports the notion that impaired GABAergic transmission in different brain regions such as the amygdala, striatum or cerebral cortex is central to FXS behavioral abnormalities. This suggests that the GABAergic system might be an intriguing target to ameliorate some of the phenotypes in FXS. Our recent work revealed that THIP (gaboxadol), a GABA_A receptor agonist, can restore principal neuron excitability deficits in the Fmr1 KO amygdala, suggesting that THIP may also restore some of the key behavioral abnormalities in Fmr1 KO mice. Here, we reveal that THIP significantly attenuated hyperactivity in Fmr1 KO mice, and reduced prepulse inhibition in a volume-dependent manner. In contrast, THIP did not reverse the deficits in cued fear or startle response. Thus, this study shows that enhancing GABAergic transmission can correct specific behavioral phenotypes of the Fmr1 KO mouse further supporting that targeting the GABAergic system, and specifically tonic inhibition, might be important for correcting or ameliorating some key behaviors in FXS.

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A Functional Role for Dopamine Transmission in the Amygdala during Condtioned Fear

Cited by 38 publications

References 10 publications

A Specific Limbic Circuit Underlies Opiate Withdrawal Memories

A Specific Limbic Circuit Underlies Opiate Withdrawal Memories

Prefrontal and Auditory Input to Intercalated Neurons of the Amygdala

The GABA<sub>A</sub> Receptor Agonist THIP Ameliorates Specific Behavioral Deficits in the Mouse Model of Fragile X Syndrome

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