Pain Pathways Involved in Fear Conditioning Measured with Fear-Potentiated Startle: Lesion Studies

Shi, C.-J.R.; Davis, Michael

doi:10.1523/jneurosci.19-01-00420.1999

Cited by 252 publications

(200 citation statements)

References 55 publications

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“…Neural correlates of learned safety E Kong et al that the insula is not necessary for fear learning (Romanski and LeDoux, 1992;Shi and Davis, 1999). This would also propose an exclusive involvement of this structure in learned safety, independently of learned fear.…”

Section: Other Brain Regions Potentially Involved In Learned Safetymentioning

confidence: 99%

Learning not to Fear: Neural Correlates of Learned Safety

Kong

Monje

Hirsch

et al. 2013

Neuropsychopharmacol

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The ability to recognize and properly respond to instances of protection from impending danger is critical for preventing chronic stress and anxiety-central symptoms of anxiety and affective disorders afflicting large populations of people. Learned safety encompasses learning processes, which lead to the identification of episodes of security and regulation of fear responses. On the basis of insights into the neural circuitry and molecular mechanisms involved in learned safety in mice and humans, we describe learned safety as a tool for understanding neural mechanisms involved in the pathomechanisms of specific affective disorders. This review summarizes our current knowledge on the neurobiological underpinnings of learned safety and discusses potential applications in basic and translational neurosciences.

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Section: Other Brain Regions Potentially Involved In Learned Safetymentioning

confidence: 99%

Learning not to Fear: Neural Correlates of Learned Safety

Kong

Monje

Hirsch

et al. 2013

Neuropsychopharmacol

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“…The amygdala is critical for the formation, consolidation, and retrieval of fear memories (Davis, 1992;Schafe et al, 2001;Maren and Quirk, 2004;Paré et al, 2004;Lüthi and Lüscher, 2014). Principal cells of the basolateral amygdala (BLA) receive glutamatergic inputs from thalamus and cortex conveying information about the conditioned stimulus (CS) and aversive footshock unconditioned stimulus (US) (Farb and Ledoux, 1999;Shi and Davis, 1999;Sah et al, 2003;Lanuza et al, 2008), and their activity is sufficient for fear learning (Johansen et al, 2010a). These glutamatergic neurons are subject to complex regulation by multiple families of GABAergic interneurons (Ehrlich et al, 2009;Tovote et al, 2015), show synaptic plasticity during fear conditioning, and form fear memories in an NMDA receptordependent manner (McKernan and Shinnick-Gallagher, 1997;Maren and Quirk, 2004;Marek et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Disrupted Prediction Error Links Excessive Amygdala Activation to Excessive Fear

et al. 2016

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Basolateral amygdala (BLA) is critical for fear learning, and its heightened activation is widely thought to underpin a variety of anxiety disorders. Here we used chemogenetic techniques in rats to study the consequences of heightened BLA activation for fear learning and memory, and to specifically identify a mechanism linking increased activity of BLA glutamatergic neurons to aberrant fear. We expressed the excitatory hM3Dq DREADD in rat BLA glutamatergic neurons and showed that CNO acted selectively to increase their activity, depolarizing these neurons and increasing their firing rates. This chemogenetic excitation of BLA glutamatergic neurons had no effect on the acquisition of simple fear learning, regardless of whether this learning led to a weak or strong fear memory. However, in an associative blocking task, chemogenetic excitation of BLA glutamatergic neurons yielded significant learning to a blocked conditioned stimulus, which otherwise should not have been learned about. Moreover, in an overexpectation task, chemogenetic manipulation of BLA glutamatergic neurons prevented use of negative prediction error to reduce fear learning, leading to significant impairments in fear inhibition. These effects were not attributable to the chemogenetic manipulation enhancing arousal, increasing asymptotic levels of fear learning or fear memory consolidation. Instead, chemogenetic excitation of BLA glutamatergic neurons disrupted use of prediction error to regulate fear learning.

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“…TRPC5 is also present in the hippocampus and dentate gyrus that project to the amygdala, and in the perirhinal cortex (PRh) that relays CS and somatosensory US information (Lanuza et al, 2004;LeDoux, 2000;Shi and Davis, 1999;Shumyatsky et al, 2005). Our findings show that responses to the CCK 2 receptor agonist, and cortico-amygdala EPSPs, mediated by Group I mGluRs, were significantly diminished in slices from TRPC5 −/− mice, while basal synaptic transmission in cortical and thalamic inputs to the LA and inputs from the LA to intercalated cells (Pare et al, 2004) was unaltered.…”

Section: Discussionmentioning

confidence: 99%

“…Regions of the auditory cortex (AuD, Au1, and AuV) that process conditioned stimulus information bound for the LA during auditory fear conditioning (Maren and Quirk, 2004), the somatosensory cortex (S1 and S2 areas) and the parietal insular cortex, regions that transmit somatosensory unconditioned stimulus (US) information to the LA, also contain TRPC5 mRNA ( Figure 1A). Finally, TRPC5 is present in the perirhinal cortex (PRh), an area involved in processing CS and somatosensory US information (Lanuza et al, 2004;LeDoux, 2000;Shi and Davis, 1999;Shumyatsky et al, 2005). Interestingly, TRPC5 mRNA was not observed in the auditory thalamus, another auditory CS area ( Figure 1B).…”

Section: Trpc5 Expression In the Mouse Brainmentioning

confidence: 99%

Essential Role for TRPC5 in Amygdala Function and Fear-Related Behavior

RICCIO¹

2009

Journal of End-to-End-testing

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SummaryThe transient receptor potential channel 5 (TRPC5) is predominantly expressed in the brain where it can form heterotetrameric complexes with TRPC1 and TRPC4 channel subunits. These excitatory, non-selective cationic channels are regulated by G protein, phospholipase C-coupled receptors. Here, we show that TRPC5 −/− mice exhibit diminished innate fear levels in response to innately aversive stimuli. Moreover, mutant mice exhibited significant reductions in responses mediated by synaptic activation of Group I metabotropic glutamate and cholecystokinin 2 receptors in neurons of the amygdala. Synaptic strength at afferent inputs to the amygdala was diminished in P10-P13 null mice. In contrast, baseline synaptic transmission, membrane excitability, and spike timing-dependent longterm potentiation at cortical and thalamic inputs to the amygdala were largely normal in older null mice. These experiments provide genetic evidence that TRPC5, activated via G protein-coupled neuronal receptors, has an essential function in innate fear.

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Pain Pathways Involved in Fear Conditioning Measured with Fear-Potentiated Startle: Lesion Studies

Cited by 252 publications

References 55 publications

Learning not to Fear: Neural Correlates of Learned Safety

Learning not to Fear: Neural Correlates of Learned Safety

Disrupted Prediction Error Links Excessive Amygdala Activation to Excessive Fear

Essential Role for TRPC5 in Amygdala Function and Fear-Related Behavior

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