Dual functions of perirhinal cortex in fear conditioning

Kent, Brianne A.; Brown, Thomas H.

doi:10.1002/hipo.22058

Cited by 43 publications

(45 citation statements)

References 120 publications

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“…Together with the accompanying study (Tomás Pereira et al, submitted) this indicates strong reciprocal connections between these regions. The strong connectivity reinforces the role both the amygdala and the PER have in emotional processing (Janak and Tye, 2015; Kent and Brown, 2012; LeDoux, 1992). The PER connection to olfactory subcortical nuclei is consistent with the findings from the cortical connectivity (Agster and Burwell, 2009) and highlight the multisensory nature of stimulus processing that occurs in the PER (Albasser et al, 2011; Burwell, 2001).…”

Section: Discussionsupporting

confidence: 60%

Subcortical connections of the perirhinal, postrhinal, and entorhinal cortices of the rat. II. efferents

et al. 2016

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This is the second of two studies detailing the subcortical connections of the perirhinal (PER), the postrhinal (POR) and entorhinal (EC) cortices of the rat. In the present study, we analyzed the subcortical efferents of the rat PER areas 35 and 36, POR, and the lateral and medial entorhinal areas (LEA and MEA). Anterograde tracers were injected into these five regions, and the resulting density of fiber labeling was quantified in an extensive set of subcortical structures. Density and topography of fiber labeling were quantitatively assessed in 36 subcortical areas, including olfactory structures, claustrum, amygdala nuclei, septal nuclei, basal ganglia, thalamic nuclei, and hypothalamic structures. In addition to reporting the density of labeled fibers, we incorporated a new method for quantifying the size of anterograde projections that takes into account the volume of the target subcortical structure as well as the density of fiber labeling. The PER, POR and EC displayed unique patterns of projections to subcortical areas. Interestingly, all regions examined provided strong input to the basal ganglia, although the projections arising in the PER and LEA were stronger and more widespread. PER areas 35 and 36 exhibited similar pattern of projections with some differences. PER area 36 projects more heavily to the lateral amygdala and much more heavily to thalamic nuclei including the lateral posterior nucleus, the posterior complex, and the nucleus reuniens. Area 35 projects more heavily to olfactory structures. The LEA provides the strongest and most widespread projections to subcortical structures including all those targeted by the PER as well as the medial and posterior septal nuclei. POR shows fewer subcortical projections overall, but contributes substantial input to the lateral posterior nucleus of the thalamus. The MEA projections are even weaker. Our results suggest that the PER and LEA have greater influence over olfactory, amygdala, and septal nuclei, whereas PER area 36 and the POR have greater influence over thalamic nuclei.

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Section: Discussionsupporting

confidence: 60%

Subcortical connections of the perirhinal, postrhinal, and entorhinal cortices of the rat. II. efferents

et al. 2016

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“…These structures are extensively interconnected with multiple pathways involving bidirectional synaptic plasticity (Kent and Brown 2012). However, the effect of foot shock on IL-1β levels was observed only in the DH, with no change in immunoreactivity observed in the BLA or PrhC.…”

Section: Discussionmentioning

confidence: 97%

“…In Experiment 1, we examined the time course of IL-1β expression following the severe stressor in SEFL. Our analysis focused on the dorsal hippocampus (DH, including the dentate gyrus (DG), CA1, and CA3), basolateral amygdala (BLA), and perirhinal cortex (PrhC) -three regions that have been shown to be critical to fear conditioning (Anagnostaras, Gale et al 2001;Kim, Loucks et al 2011;Acheson, Gresack et al 2012;Kent and Brown 2012). In Experiment 2, we tested whether blocking central IL-1β signaling with an infusion of interleukin-1 receptor antagonist (IL-1ra) in the 48 hours following the severe stressor prevented the development of SEFL.…”

Section: Introductionmentioning

confidence: 99%

The Role of Brain Interleukin-1 in Stress-Enhanced Fear Learning

Jones

Lebonville

Barrus

et al. 2014

Neuropsychopharmacol

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Posttraumatic stress disorder (PTSD) has been shown to be associated with pro-inflammatory markers, including elevated plasma levels of interleukin-1β (IL-1β). However, the precise role of neuroinflammation and central immune signaling on the development of this debilitating psychological disorder is not known. Here, we used stress-enhanced fear learning (SEFL), an animal model of the disorder, to examine the role of central IL-1β in PTSD. The results show that the severe stressor in SEFL induces a time-dependent increase in IL-1β immunoreactivity and mRNA expression within the dentate gyrus of the dorsal hippocampus (DH). There was no increase in IL-1β in the basolateral amygdala or the perirhinal cortex. Moreover, blocking the action of IL-1β following the severe stressor with IL-1 receptor antagonist (10 μg, intracerebroventricular (i.c.v.), 24 and 48 h after the stressor) prevented the development of SEFL. To provide further support for the role of IL-1β in the development of SEFL, we show that systemic morphine, a treatment which is known to reduce both PTSD and SEFL, also reduces IL-1β expression in the DH induced by the severe stressor. These studies provide the first evidence that IL-1 is involved SEFL and suggest that IL-1 signaling in the brain may have a critical role in the development of PTSD.

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“…The RSC has been implicated in recent and long-term contextual fear memory (Corcoran, Donnan, Tronson, Guzman, Gao, Jovasevic, Guedea, and Radulovic, 2011), while the dHipp is critical for contextual fear memory (for reviews see Jadhav, Kemere, German, and Frank, 2012; Maren et al, 2013; Phillips and LeDoux, 1992; Quinn, Loya, Ma, and Fanselow, 2005), as well as trace fear memory (Beeman, Bauer, Pierson, and Quinn, 2013; Kent and Brown, 2012; Raybuck and Lattal, 2011), and contextual control of extinction memory retrieval (Bouton et al, 2006; Corcoran and Maren, 2004). The IL and vHipp are critical for extinction memory (Lebron, Milad, and Quirk, 2004; Milad et al, 2006; Quirk et al, 2006; Quirk, Pare, Richardson, Herry, Monfils, Schiller, and Vicentic, 2010; Sierra-Mercado et al, 2006; Sierra-Mercado, Padilla-Coreano, and Quirk, 2011; Vidal-Gonzalez, Vidal-Gonzalez, Rauch, and Quirk, 2006).…”

Section: Bf Cholinergic Neurons In Fear and Extinction Memorymentioning

confidence: 99%

The role of basal forebrain cholinergic neurons in fear and extinction memory

Knox

2016

Neurobiology of Learning and Memory

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Cholinergic input to the neocortex, dorsal hippocampus (dHipp), and basolateral amygdala (BLA) is critical for neural function and synaptic plasticity in these brain regions. Synaptic plasticity in the neocortex, dHipp, ventral Hipp (vHipp), and BLA has also been implicated in fear and extinction memory. This finding raises the possibility that basal forebrain (BF) cholinergic neurons, the predominant source of acetylcholine in these brain regions, have an important role in mediating fear and extinction memory. While empirical studies support this hypothesis, there are interesting inconsistencies among these studies that raise questions about how best to define the role of BF cholinergic neurons in fear and extinction memory. Nucleus basalis magnocellularis (NBM) cholinergic neurons that project to the BLA are critical for fear memory and contextual fear extinction memory. NBM cholinergic neurons that project to the neocortex are critical for cued and contextual fear conditioned suppression, but are not critical for fear memory in other behavioral paradigms and in the inhibitory avoidance paradigm may even inhibit contextual fear memory formation. Medial septum and diagonal band of Broca cholinergic neurons are critical for contextual fear memory and acquisition of cued fear extinction. Thus, even though the results of previous studies suggest BF cholinergic neurons modulate fear and extinction memory, inconsistent findings among these studies necessitates more research to better define the neural circuits and molecular processes through which BF cholinergic neurons modulate fear and extinction memory. Furthermore, studies determining if BF cholinergic neurons can be manipulated in such a manner so as to treat excessive fear in anxiety disorders are needed.

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Dual functions of perirhinal cortex in fear conditioning

Cited by 43 publications

References 120 publications

Subcortical connections of the perirhinal, postrhinal, and entorhinal cortices of the rat. II. efferents

Subcortical connections of the perirhinal, postrhinal, and entorhinal cortices of the rat. II. efferents

The Role of Brain Interleukin-1 in Stress-Enhanced Fear Learning

The role of basal forebrain cholinergic neurons in fear and extinction memory

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