scholarly journals Increased c-fos expression in the central nucleus of the amygdala and enhancement of cued fear memory in Dyt1 ΔGAG knock-in mice

2009 ◽  
Vol 65 (3) ◽  
pp. 228-235 ◽  
Author(s):  
Fumiaki Yokoi ◽  
Mai T. Dang ◽  
Courtney A. Miller ◽  
Andrea G. Marshall ◽  
Susan L. Campbell ◽  
...  
Keyword(s):  
Fear Memory ◽  
Central Nucleus ◽  
Fos Expression

scholarly journals A Fear-Inducing Odor Alters PER2 and c-Fos Expression in Brain Regions Involved in Fear Memory

PLoS ONE ◽  
2011 ◽  
Vol 6 (5) ◽  
pp. e20658 ◽  
Author(s):  
Harry Pantazopoulos ◽  
Hamid Dolatshad ◽  
Fred C. Davis
Keyword(s):  
Fear Memory ◽  
Brain Regions ◽  
Fos Expression

scholarly journals Prefrontal dopamine regulates fear reinstatement through the downregulation of extinction circuits

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Natsuko Hitora-Imamura ◽  
Yuki Miura ◽  
Chie Teshirogi ◽  
Yuji Ikegaya ◽  
Norio Matsuki ◽  
...  
Keyword(s):  
Anxiety Disorders ◽  
Synaptic Input ◽  
Dopaminergic Neurons ◽  
Contextual Fear Conditioning ◽  
Central Nucleus ◽  
Infralimbic Cortex ◽  
Contextual Fear ◽  
Fear Reduction ◽  
Dependent Inactivation ◽  
Fos Expression

Prevention of relapses is a major challenge in treating anxiety disorders. Fear reinstatement can cause relapse in spite of successful fear reduction through extinction-based exposure therapy. By utilising a contextual fear-conditioning task in mice, we found that reinstatement was accompanied by decreased c-Fos expression in the infralimbic cortex (IL) with reduction of synaptic input and enhanced c-Fos expression in the medial subdivision of the central nucleus of the amygdala (CeM). Moreover, we found that IL dopamine plays a key role in reinstatement. A reinstatement-inducing reminder shock induced c-Fos expression in the IL-projecting dopaminergic neurons in the ventral tegmental area, and the blocking of IL D1 signalling prevented reduction of synaptic input, CeM c-Fos expression, and fear reinstatement. These findings demonstrate that a dopamine-dependent inactivation of extinction circuits underlies fear reinstatement and may explain the comorbidity of substance use disorders and anxiety disorders.

Vestibular-mediated increase in central serotonin plays an important role in hypergravity-induced hypophagia in rats

2010 ◽  
Vol 109 (6) ◽  
pp. 1635-1643 ◽  
Author(s):  
Chikara Abe ◽  
Kunihiko Tanaka ◽  
Chihiro Iwata ◽  
Hironobu Morita
Keyword(s):  
Area Postrema ◽  
Vestibular Nucleus ◽  
Central Nucleus ◽  
Medial Vestibular Nucleus ◽  
Hypothalamic Nucleus ◽  
Solitary Tract ◽  
Afferent Pathway ◽  
Vestibular Input ◽  
Paraventricular Hypothalamic Nucleus ◽  
Fos Expression

Exposure to a hypergravity environment induces acute transient hypophagia, which is partially restored by a vestibular lesion (VL), suggesting that the vestibular system is involved in the afferent pathway of hypergravity-induced hypophagia. When rats were placed in a 3-G environment for 14 days, Fos-containing cells increased in the paraventricular hypothalamic nucleus, the central nucleus of the amygdala, the medial vestibular nucleus, the raphe nucleus, the nucleus of the solitary tract, and the area postrema. The increase in Fos expression was completely abolished or significantly suppressed by VL. Therefore, these regions may be critical for the initiation and integration of hypophagia. Because the vestibular nucleus contains serotonergic neurons and because serotonin (5-HT) is a key neurotransmitter in hypophagia, with possible involvement in motion sickness, we hypothesized that central 5-HT increases during hypergravity and induces hypophagia. To examine this proposition, the 5-HT concentrations in the cerebrospinal fluid were measured when rats were reared in a 3-G environment for 14 days. The 5-HT concentrations increased in the hypergravity environment, and these increases were completely abolished in rats with VL. Furthermore, a 5-HT2A antagonist (ketanserin) significantly reduced 3-G (120 min) load-induced Fos expression in the medial vestibular nucleus, and chronically administered ketanserin ameliorated hypergravity-induced hypophagia. These results indicate that hypergravity induces an increase in central 5-HT via the vestibular input and that this increase plays a significant role in hypergravity-induced hypophagia. The 5-HT2A receptor is involved in the signal transduction of hypergravity stress in the vestibular nucleus.

scholarly journals Fluoxetine acts concomitantly on dorsal and ventral hippocampus to Trk-dependently modulate the extinction of fear memory

2021 ◽  
Author(s):  
Cassiano Ricardo Alves Faria Diniz ◽  
Leandro Antero da Silva ◽  
Luana Barreto Domingos ◽  
Andreza Buzolin Sonego ◽  
Leonardo Resstel Barbosa Moraes ◽  
...  
Keyword(s):  
Acute Treatment ◽  
Wistar Rats ◽  
Opposite Effect ◽  
Antidepressant Drugs ◽  
Longitudinal Axis ◽  
Fear Memory ◽  
Fear Response ◽  
Direct Infusion ◽  
Extinction Memory ◽  
Fos Expression

ABSTRACTBackgroundHippocampus can be divided along its longitudinal axis into dorsal and ventral parts. Both are usually committed to modulate different aspects of behavior and stress response. However, it is not clear whether the hippocampal subregions could differently modulate the effect of antidepressant drugs. Since fluoxetine (FLX) effect on extinction of aversive memory is well known to depend on hippocampal BDNF levels, we hypothesized that the hippocampal subregions might play different roles in fluoxetine efficacy in decreasing fear response.MethodWistar rats were fear-cued conditioned and treated chronically with fluoxetine to enhance their subsequent extinction memory. First, FLX effect on BDNF levels was assessed considering the dorsal (dHC) and ventral (vHC) hippocampus apart. Then, K252a (a functional Trk blocker) was infused either into the dHC or vHC to assay its interaction with FLX treatment over the fear response. Next, BDNF was directly infused into either the dHC or vHC to compare its behavioral effects with FLX. Finally, FLX effect on c-Fos expression was evaluated also considering the dHC and vHC apart, along with subareas of amygdala and medial prefrontal cortex.ResultsChronic FLX treatment increased BDNF in the dHC, whereas BDNF was increased in the vHC after acute treatment only. K252a infused after the extinction protocol into either dHC or vHC was able to prevent FLX effect on fear response. BDNF directly infused into the dHC increased fear response, however its administration into the vHC induced an opposite effect. Besides, a negative correlation between the fear response and c-Fos expression was observed after chronic FLX treatment specifically in the dHC CA3/CA1 and vHC CA1/DG.ConclusionBoth dHC and vHC are important for the Trk-dependent FLX effect on extinction memory, although a discrepancy on the fear response was observed with the direct infusion of BDNF into the dHC or vHC.

Plasma hormone levels and central c-Fos expression in ferrets after systemic administration of cholecystokinin

2001 ◽  
Vol 281 (4) ◽  
pp. R1243-R1255 ◽  
Author(s):  
I. Billig ◽  
B. J. Yates ◽  
L. Rinaman
Keyword(s):  
Brain Stem ◽  
Area Postrema ◽  
Hormone Secretion ◽  
Early Gene ◽  
Central Nucleus ◽  
Ventrolateral Medulla ◽  
Pituitary Hormone ◽  
Bed Nucleus ◽  
Fos Expression ◽  
Glucagon Like Peptide 1

Posterior pituitary hormone secretion and central neural expression of the immediate-early gene product c-Fos was examined in adult ferrets after intravenous administration of CCK octapeptide. Pharmacological doses of CCK (1, 5, 10, or 50 μg/kg) did not induce emesis, but elicited behavioral signs of nausea and dose-related increases in plasma vasopressin (AVP) levels without significant increases in plasma oxytocin (OT) levels. CCK activated neuronal c-Fos expression in several brain stem viscerosensory regions, including a dose-related activation of neurons in the dorsal vagal complex (DVC). Activated brain stem neurons included catecholaminergic and glucagon-like peptide-1-positive cells in the DVC and ventrolateral medulla. In the forebrain, activated neurons were prevalent in the paraventricular and supraoptic nuclei of the hypothalamus and also were observed in the central nucleus of the amygdala and bed nucleus of the stria terminalis. Activated hypothalamic neurons included cells that were immunoreactive for AVP, OT, and corticotropin-releasing factor. Comparable patterns of brain stem and forebrain c-Fos activation were observed in ferrets after intraperitoneal injection of lithium chloride (LiCl; 86 mg/kg), a classic emetic agent. However, LiCl activated more neurons in the area postrema and fewer neurons in the nucleus of the solitary tract compared with CCK. Together with results from previous studies in rodents, our findings support the view that nauseogenic treatments activate similar central neural circuits in emetic and nonemetic species, despite differences in treatment-induced emesis and pituitary hormone secretion.

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