Amygdala and fear conditioning pathways,the secrets in their eyes review,secret world endless night hacked,site secret de gta 4 download - PDF Books


During fear conditioning, the conditioned stimulus (CS) and unconditioned stimulus (US) are relayed to the lateral nucleus of the amygdala (LA) from thalamic and cortical regions of the auditory and somatosensory systems, respectively. We will be provided with an authorization token (please note: passwords are not shared with us) and will sync your accounts for you.
Neural plasticity in the amygdala is necessary for the acquisition and storage of memory in Pavlovian fear conditioning, but most neuroimaging studies have focused only on stimulus-evoked responses during the conditioning session.
Learning and memory are supported by a variety of neurobiological processes that ultimately modify the structure and function of the nervous system. In Pavlovian fear conditioning a previously neutral conditional stimulus (CS) is paired with an aversive unconditional stimulus (UCS).
Functional connectivity can be assessed using neuroimaging tools to understand changes in the fear circuit that occur during consolidation.
Thirty-two (15 women) right-handed, neurologically normal undergraduates from the University of Wisconsin-Milwaukee ranging from 18 to 37 years old (M = 22 years, SEM = 0.85) volunteered for the study. Participants manipulated a custom-made rotary dial to report their expectancy of receiving the UCS throughout the conditioning portion of the study.
Skin conductance was recorded using a Contact Precision Instruments unit (Boston, MA) with a SC5 24-bit digital amplifier from Contact Precision Instruments at 80 Hz. The experiment was conducted using Presentation software (Albany, CA) on a Dell Inspiron 9300 (Round Rock, TX) laptop computer.
Participants were instructed on how to use the UCS expectancy dial and the UCS intensity work up was completed prior to them entering the scanner.
The UCS expectancy measure was defined as the mean expectancy rating during the last 4 s of the CS period on each trial for each participant. SCR was analyzed by subtracting the mean of a 2 s baseline period prior to CS onset from the peak of the response during the entire CS presentation (Pineles et al., 2009) on each trial for each participant. High-resolution structural scans were warped to Talairach space by manually placing anatomical markers consistent with previous studies (Balderston et al., 2011).
Variability in the BOLD time series accounted for by respiration and cardiac rhythm was removed from the raw data using previously published methods (Birn et al., 2006) in which cardiac and respiratory signals and their first harmonics serve as variables in a multiple regression analysis. To examine the relationship between behavioral performance and the change in amygdala connectivity from the pre-conditioning to post-conditioning resting-state scans we created a metric for both UCS expectancy and SCR performance. We did not observe any laterality effects in the amygdala data from the conditioning session so we correlated the mean amygdala signal during the pre-conditioning resting-state scan with the signal from all of the voxels in the brain during the same scan.
We examined amygdala connectivity at two time points, once prior to conditioning task, and once following conditioning. Amygdala connectivity is relatively consistent before and after the conditioning task, but some the connectivity of some regions is different following conditioning. In order to explore the differences between the pre- and post-conditioning amygdala connectivity maps we directly compared the two; see Figure 5. We examined the relationship between changes in amygdala connectivity before and after conditioning and behavioral performance using a step-wise multiple regression analysis. This study examined changes in the functional connectivity of the amygdala before and after subjects encoded a new fear conditioning memory. Fear memory enhances connectivity in cortical and limbic circuits but whether treatments disrupting fear reset connectivity to pre-trauma level is unknown. The present study examines the extent to which β-ARs antagonists, that interfere with fear memory and p-ERK signaling, reinstate pre-trauma levels connectivity in fear-activated neural circuits. The behavioral protocol was based on the one designed by Debiec and LeDoux (2004) in which TFC takes place in one context (chamber A), while the reactivation trial and the memory test take place in another context (chamber B). On day 5, conditioned mice were injected with saline or propranolol, and pseudo-conditioned mice were injected with saline and immediately after they were submitted to a reactivation trial taking place in chamber B and consisting of a 2-minute habituation period followed by a single CS presentation.
Forty-eight hours after the reactivation trial, mice were exposed to four CSs presentations in context B, delivered at a variable inter-tone interval (120 s on average). Behavior during conditioning, reactivation trial, and memory test was recorded by means of a video camera mounted 60 cm above the ceiling of chamber A or B, which was connected to a computer equipped with the Ethovision software (Noldus, The Netherlands).
Punches for western blots were taken 90 min after the memory test from the BLA and the DH of mice experiencing the three conditions (4 mice per group) using a 1 mm punch tool (Fine Science Tools, Foster City, CA) from 1 mm thick sections cut on a frozen brain matrix (ASI Instruments).
Figure 1 shows a cartoon depicting the three phases of the behavioral protocol (Figure 1A) and the freezing scores of the three experimental groups during the conditioning, the reactivation trial, and the memory test (Figure 1B).
The time spent freezing in chamber B 48 h after the reactivation trial was then taken as an index of long term fear memory.
Western blots were carried out in amygdala and hippocampus homogenates collected 90 min after the memory test and normalized for tubulin levels. There is a complicated series of events in the nervous system that leads to the¬†physical sensations and behaviors of fear (the thoughts, we can’t localize so well). You can imagine the temporal lobe on your side of these central structures, the one that was removed so that you could see almost to the middle of the brain in the line drawing above. This hopefully will look like something you understand, if you’ve had the Tour of the hippocampus. This means that you will not need to remember your user name and password in the future and you will be able to login with the account you choose to sync, with the click of a button.
This page doesn't support Internet Explorer 6, 7 and 8.Please upgrade your browser or activate Google Chrome Frame to improve your experience. This study examined changes in the resting-state functional connectivity (RSFC) of the amygdala before and after Pavlovian fear conditioning, an emotional learning task. Through repeated pairings the CS can evoke a learned conditional response (CR) that is typically similar to the fearful unconditional response (UCR) that is evoked by the UCS (Pavlov, 1927). Connectivity approaches can provide information about which brain regions share correlated activity.
Three participants were excluded from analysis due to excessive head movement and two were excluded due to recording errors. The electrodes were filled with electrolyte gel (Signa Gel, Parker Laboratories, Fairfield, NJ) and placed on the skin over the subject's right tibial nerve above the right medial malleous. Visual stimuli and the UCS expectancy rating bar were presented to participants while they were in the scanner using a back projection system with prism glasses mounted on the head coil. Functional images were collected using a T2* weighted gradient-echo, echoplanar pulse sequence.
The high-resolution structural data was collected before the resting-state and conditioning task functional scans. Raw data was motion corrected, passed through an edge detection algorithm and registered to the fifth volume of the functional run. Baseline, drift, and head motion effects were removed from the time series using AFNI's 3dDeconvolve command. However, we did not observe a significant conditioning effect in the amygdala with the whole brain ANOVA.
The left and right amygdala both demonstrate differential responses to the CSs in the conditioning phase of the experiment.
The same analysis was conducted with the mean amygdala signal during the post-conditioning resting-state scan. Amygdala functional connectivity before and after the conditioning task shows some similarities and some differences.
The second resting-state scan began approximately 12 min after the completion of the first resting-state scan. The medial PFC shows a significant positive correlation with amygdala activity following the conditioning task that was not present prior to conditioning.
A cluster in the superior frontal gyrus was the only region that was characterized by a significant difference in connectivity between the pre- and post-conditioning resting-state scans.
The dorsal medial prefrontal cortex (superior frontal gyrus) [Talairach coordinates: 24, 30, 45] shows a significant increase in its connectivity with the amygdala following the conditioning task. In humans, comparisons of EEG signal coherence in adult individuals reporting childhood, adulthood, or no history of traumatic experience points to a positive correlation between connectivity over frontal, central, temporal and parietal areas and intensity of the trauma (Cook et al., 2009).


Importantly, the BLA controls adaptation to stress via a β-ARs-mediated regulation of phosphorylated ERK (Grissom and Bhatnagar, 2011). An ethanol solution (70%) was used to clean the chamber after each mouse underwent the conditioning trial.
The time spent freezing (absence of all but respiratory movements) after CS-US presentation was used to score fear during the conditioning and the retrieval while the time spent freezing during the four CSs presentation was averaged and used as a long term fear memory index (Blanchard and Blanchard, 1969). Brains were dissected and immediately immersed in a Golgi-Cox solution at room temperature for 6 days (Glaser and Van der Loos, 1981). The immunohistochemistry protocol was performed according the manufacturing procedure of ULTRATEK HRP KIT (ScyTek laboratories). Between-group differences in freezing behavior, spine density, protein levels were estimated by means of a One-Way ANOVA with group as the main factor. Propranolol prevents the increase in spine density observed in basolateral amygdala, but not in CA1 dorsal hippocampus, neurons upon fear memory testing. Propranolol prevents the increase in p-ERK signaling observed in basolateral amygdala upon fear memory testing. The amygdala is part of the¬†temporal lobe, way on the toward-the-middle side of it, and rather near the front. But you don’t know, at least from these MRI scans, where it is relative to your two ears.
Again you see that it is located on the inner fold of the temporal lobe, circled in yellow. 3, the CS inputs enter the dorsal subregion of the LA, where interactions with the US induce plasticity in two functional cell types (so-called 'trigger' and 'storage' cells). Behavioral results from the conditioning session revealed that participants learned normally and fMRI data recorded during learning identified a number of stimulus-evoked changes that were consistent with previous work.
The process of changing these neural connections begins during exposure to the events and relationships to be encoded and continues after this initial experience as long term memory is formed and stored (for review see Kandel, 2001; Squire and Bayley, 2007). Each participant determined the maximum UCS intensity used in the experiment individually prior to the start of the experiment in a work up procedure.
Skin conductance data was collected with electrodes (Biopac, Goleta, CA; Model EL258-RT) filled with electrolytic gel (Signagel, Parker Laboratories, Fairfield, NJ).
Head motion and motor processes associated with the gross movement of the UCS expectancy dial were included as regressors of no interest. The mean signal from the Freesurfer created white matter and ventricle maps, as well as a global signal measure were also included as regressors of no interest as discussed by Fox and colleagues (2009). A correlation map with the mean amygdala signal was created for the pre-conditioning resting-state scan and the post-conditioning resting-state scan.
Brain images depict the pre- and post-conditioning connectivity maps as well as where those maps overlap. Amygdala activity was positively correlated with activity in the medial temporal lobe and ventral portions of the prefrontal cortex (PFC) before and after the conditioning task. The left angular gyrus and right posterior temporal lobe show a similar pattern with a significant positive correlation with the amygdala after the conditioning task that was not present prior to conditioning. The superior frontal gyrus cluster showed a significant increase in connectivity between the two scans. UCS expectancy performance positively correlated with the change in amygdala connectivity for a cluster in the superior frontal gyrus; see Figures 6A,B.
This intense fear response is associated with a massive increase in dendritic spines and phospho-Erk (p-ERK) signaling in basolateral amygdala (BLA) but neurons. There is evidence that β-ARs antagonists disrupt fear memory (Soeter and Kindt, 2011), but whether they also block fear-induced phospho-Erk (p-ERK) enhancement has not yet been investigated. This intense freezing response is accompanied by an increase in dendritic spines and p-ERK signaling in BLA neurons. Chamber B differed from chamber A in shape (trapezoidal shape), color (black walls with a plain gray floor), odor (70% ethanol solution with lemon odor), and light intensity (40 W lamp).
On the seventh day, brains were transferred in a 30% sucrose solution for cryoprotection and then sectioned with a vibratome. The supernatant was collected, and protein content was quantified by Bradford colorimetric assay (Biorad, Milano, Italy). In supplemental experiment 1, differences in freezing behavior during the long term memory test between mice receiving pre-reactivation injections of sotalol or saline were estimated by means of a t-test. Post-hoc comparisons between the two trained groups revealed that although mice injected with propranolol showed less freezing that their saline-injected counterpart, these scores did not differ significantly. Importantly, no difference in spine density was found between the two latter groups (propranolol-injected trained mice vs. In the trained mice, spine density did not significantly differ between those injected with saline or propranolol (p = 0.90, NS) therefore revealing that DH spines were unaffected by the treatment. CS information is then transmitted through further stations in the LA to the central nucleus of the amygdala (CE).
A direct comparison between the pre- and post-conditioning amygdala connectivity revealed a region of dorsal prefrontal cortex (PFC) in the superior frontal gyrus that showed a significant increase in connectivity following the conditioning session. Previous neuroimaging studies on memory have primarily focused on stimulus evoked activity during the encoding or retrieval phases, and little attention has been paid to the neural processes that occur in the absence of direct external stimulation following learning.
Participants were offered extra-credit in a psychology course, $20 and a picture of their brain.
The work up procedure consisted of no more than five presentations of the electrical stimulation. The pre-conditioning and post-conditioning resting state runs consisted of 240 whole brain scans. Six images starting at stimulus onset were used to calculate the percent area under the curve (%AUC) of the mean IRF for each stimulus type. The change in amygdala connectivity was calculated by subtracting the normalized amygdala correlation coefficient from the pre-conditioning resting-state scan from the post-conditioning resting-state scan.
The color scale corresponds to the probability that the region is included in any of the participants' amygdala ROIs. These maps were layered on top of one another creating a map that displays areas that show significant positive and negative correlations with the mean amygdala signal during pre- and post-conditioning scans. Amygdala activity was negatively correlated with activity in the dorsal lateral PFC, precuneus, posterior cingulate cortex, and an area of parietal cortex near the junction of the inferior parietal lobule and the supramarginal gyrus before and after the conditioning task. This cluster neighbors the superior frontal gyrus cluster that was identified in the pre- versus post-conditioning amygdala connectivity contrast. In rodents, tone fear conditioning (TFC) drives structural alterations in basolateral amygdala (BLA) neurons consistent with an enhancement in the strength and in the number of synapses. This point is of importance considering that p-ERK regulates the activity of downstream pathways implicated in the synthesis of proteins involved in synaptic plasticity and experience-dependent structural re-arrangements (Sweatt, 2004). Administration of the β-ARs blocker propranolol before, but not immediately after, the reactivation test attenuates fear memory assessed drug-free 48 h later but completely prevents the increase in dendritic spines and of p-ERK signaling in BLA neurons. Coronal sections (100 μm) were collected and stained according to the method described by Gibb and Kolb (1998).
On the next day, frontal 30 um cryostat slices were sectioned from entire brain and immediately prepared for immunohistochemistry. Section were then washed with PBS and incubated with biotinylated goat antirabbit secondary antibody. Pre-reactivation injections of sotalol did not decrease freezing during the memory test (sotalol- vs. Interactions between the lateral and central amygdala are more complex than illustrated, and involve local-circuit connections (see main text).
A behavioral measure of explicit memory performance was positively correlated with the change in amygdala connectivity within a neighboring region in the superior frontal gyrus. If neural connections are being strengthened during the post training consolidation period we would expect changes in connectivity, even at rest, between the brain regions involved in memory formation.


Resting-state connectivity measures are relatively stable across time (Shehzad et al., 2009).
Each presentation was rated by the participant on a scale from 0 to 10 (0 = no sensation, 10 = painful, but tolerable). Participants with excessive head movement (greater than 2.5 mm displacement or more than five examples of discrete head movement) were excluded from further analysis. The amygdala time series was extracted from the individual Freesurfer generated amygdala masks for the left and right hemisphere for each participant. We ran a step-wise multiple regression using the AFNI command 3dRegAna with UCS expectancy and SCR performance as regressors and the change in amygdala connectivity as the dependent variable. We conducted a ROI analysis of the amygdala due to our strong a priori prediction that it would be involved in this task. This map also displays regions that are significantly positively or negatively correlated with the amygdala at both resting-state scans and regions that changed from a positive to negative correlation from pre- to post-conditioning or vice versa; see Figure 4. The second step of the regression analysis examined if any of the residual variance in the change in amygdala connectivity could be accounted for by SCR performance.
An increase in spines, but not of p-ERK, was also detected in the dorsal hippocampus (DH) of the conditioned mice. The formation of fear memory also promotes an increase in spines, but not of p-ERK levels, in the dorsal hippocampus (DH) of the conditioned mice. Spine density was analyzed on class I spiny neurons which represent the predominant cell type in the basolateral amygdala nuclei (McDonald, 1982). Pre-reactivation injections of sotalol did not affect freezing during the reactivation trial (sotalol- vs. Pre-reactivation injections of propranolol blocked the increase in spines in BLA but not in CA1 DH neurons.
The LA also communicates with the CE by way of connections with other amygdala regions (not shown), but the direct pathway seems to be sufficient to mediate fear conditioning. Additionally, an implicit autonomic measure of conditioning was positively correlated with the change in connectivity between the amygdala and the anterior cingulate cortex (ACC). One way to examine changes in resting-state connectivity during memory formation is to examine functional connectivity before and after a well understood form of learning such as Pavlovian fear conditioning.
All procedures were approved by the Institutional Review Boards for human subject research at the University of Wisconsin-Milwaukee and the Medical College of Wisconsin. The intensity of the electrical stimulation was increased until the participant rated it as a 10. Participants received verbal instructions on how to use the dial before the experiment began. The mean amygdala time series, including the left and right hemisphere, for each participant was calculated and then correlated with the time series from every other voxel in the brain using AFNI's 3dDeconvolve command.
These data indicate that participants did not differentially expect the UCS on early trials.
SCR performance positively correlated with the change in amygdala connectivity for a cluster in the anterior cingulate cortex (ACC); see Figures 6C,D. Although it is conceivable that connectivity in fear-activated circuits should be reduced upon fear erasure, whether pharmacological treatments reducing fear memory reset physiological levels of connectivity is unknown. DH connectivity, however, is unaffected by propranolol suggesting that it plays role in the persistence of a consistent level of fear memory. The two bands corresponding to p-ERK42 and p-ERK44 consistently varied in the same manner and were thus analyzed together. Among the trained mice, those receiving pre-reactivation injections of propranolol showed significantly less freezing during the memory test than those receiving saline injections.
The resting-state data show that amygdala connectivity is altered following Pavlovian fear conditioning and that these changes are also related to behavioral outcomes. Participants were able to rate the stimulation higher than a 10 at which point the intensity would be decreased.
They were instructed to place the cursor at 0 if they were certain that they would not experience the UCS, at 50 if they were not sure if they would experience the UCS, and at 100 if they were certain that they would experience the UCS.
The individual r statistics were then normalized using a Fisher's z transformation and resampled into 1 mm3 voxels.
The changes in connectivity that correlate with behavioral performance suggest that this phenomenon is due to associative learning. Louis, MO,USA) at the same dose and time-point as propranolol to estimate the respective role of central vs. For light microscopy immunohistochemistry, slices were mounted on superfrost plis slides, air dried, quickly dehydrated, and coverslipped. These alterations may reflect the operation of a consolidation process that strengthens neural connections to support memory after the learning event. These changes might also reflect some of the ongoing processes that support the consolidation of memory. Participants were instructed to update the position of the cursor continuously throughout the conditioning portion of the experiment. The CSs were counterbalanced across subjects and presented in one of two pseudorandom trial order sequences with the caveat that there could be no more than two consecutive trials of the same type.
In order to ensure that the changes in connectivity were not due participants having a higher level of anxiety in the resting-state scan that followed conditioning, we examined the heart rate data from both of the resting-state scans.
Pseudo-conditioning consisted in placing mice in chamber A and exposing them to the tone in the absence of foot-shock. Blots were then incubated with appropriate secondary antibody conjugated to horseradish peroxidase (Chemicon) and developed by ECL Western Blotting Analysis System (GE Healthcare). The current study was designed to determine if the resting-state connectivity between the amygdala and other brain regions changes following fear conditioning. Participants were not instructed about any of the potential relationships between the visual stimuli and the UCS.
The Freesurfer software package was used for segmentation of the white matter, ventricles, and amygdala (Fischl et al., 2002, 2004).
As a first pass analysis we calculated a whole-brain one-sample t-test on the normalized amygdala correlation coefficients for both the pre-conditioning and post-conditioning resting-state runs.
In supplemental experiment 2, we compared the effect of propranolol injected immediately before or immediately after the reactivation trial to assess whether attenuation of fear memory can be ascribed to an effect of the drug on retrieval, on reconsolidation, or both.
Only protrusions with a clear connection of the head of the spine to the shaft of the dendrite were counted as spines (Horner and Arbuthnott, 1991). Furthermore, we wanted to identify whether or not any observed changes in connectivity were related to behavioral performance. Statistical comparisons were made on single neuron values obtained by averaging the number of spines counted on segments of the same neuron. The realigned volumes were then manually edited to conform to previously published standards (Morey et al., 2009). A t-test directly comparing the pre-conditioning resting-state correlations values to the post-conditioning resting-state correlation values was also calculated. These findings therefore suggest that the effect of the drug on long term fear memory is unlikely to be ascribed to a disruption of memory reconsolidation. A CS type by laterality ANOVA was conducted on the %AUC data extracted from both the right and left amygdala ROIs. To control for the regional specificity of fear memory-induced structural changes in the hippocampus, CA1 dorsal (N = 3) and ventral (N = 3) hippocampal neurons were selected within each hemisphere in the same animals, and spine density counts were performed on basal dendrites using to the same quantification method.



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