Fear Incubation Using an Extended Fear-Conditioning Protocol for Rats

Emotional memory has been primarily studied with fear-conditioning paradigms. Fear conditioning is a form of learning through which individuals learn the ...

UNIVERSIDAD DE LOS ANDES

In despite the similarity of mechanisms of action between both selective serotonin reuptake inhibitors (SSRI) and MDMA (main compound of "Ecstasy") there are relatively few reports on the effects of the later on animal models of depression. There are many animal models designed to create or to assess depression. Mild chronic stress (MCS) is a procedure designed to create depression. MCS includes the chronic exposure of the animal to several stressors. After that, rats show behavioural changes associated to depression. In the other hand, the active avoidance task (AAT) is an experimental situation in which an animal has to accomplish a particular behaviour in order to avoid the application of a stressor. Animals exhibiting depression fail to acquire avoidance responses as rapidly as normal animals do. In order to assess the effect of MDMA on the acquisition of an active avoidance response, forty-five rats were divided in two groups exposed or not exposed to MCS. Rats also received chronic intracerebroventricular MDMA (0.2microg/microl; 1microl), fluoxetine (2.0microg/microl; 1microl) or saline solution (0.9%; 1microl). Our results showed that the effect of MDMA depends upon the level of stress. MDMA treated animals showed better acquisition (F([2,37])=7.046; P=0.003) and retention (F([2,37])=3.900; P=0.029) of the avoidance response than fluoxetine or saline treated animals when exposed to MCS. This finding suggests that MDMA (and no fluoxetine) was able to change the aversive valence of the stressors maybe enhancing coping strategies. This effect could serve as a protective factor against helplessness and maybe post-traumatic stress.

Effects of chronic intracerebroventricular 3,4-methylenedioxy-N-methamphetamine (MDMA) or fluoxetine on the active avoidance test in rats with or without exposure to mild chronic stress.

Animal models of fear extinction have an important clinical relevance to pharmacological and exposure-based therapies for anxiety disorders. Lesions of prefrontal structures impair fear extinction. On the other hand, d-cycloserine is able to enhance this process. We hypothesize that the integrity of cortical structures involved in inhibitory control of emotional responses is crucial for the facilitatory effects of d-cycloserine. Here, we showed that medial orbitofrontal cortex lesion prevents d-cycloserine enhancement of fear extinction. These preliminary results suggest that effects of pharmacological treatments could be dependent on cortical activity state to promote fear memory reduction. 

Medial orbitofrontal cortex lesion prevents facilitatory effects of d-cycloserine during fear extinction.

In many species, chronic stress due to overcrowding during the juvenile period triggers several metabolic and behavioral pathologies in adulthood. The aim of this study was to determine whether a chronic stress condition (overcrowding) induces changes in plasma and hair corticosterone concentrations, overall growth, and organ weights in young Wistar rats. The experimental subjects were divided into 2 groups (control and overcrowded); the overcrowded subjects were exposed to overcrowding during days 38 through 65 after birth. Plasma and hair corticosterone concentrations were higher in overcrowded rats compared with control subjects. In addition, overcrowding reduced body and organ weight gains. These results demonstrate that measuring the concentration of corticosterone in hair samples is an effective, noninvasive method for monitoring chronic stress in rats.

Effect of Overcrowding on Hair Corticosterone Concentrations in Juvenile Male Wistar Rats.

The strength and efficiency of synaptic connections are affected by the environment or the experience of the individual. This property, called synaptic plasticity, is directly related to memory and learning processes and has been modeled at the cellular level. These types of cellular memory and learning models include specific stimulation protocols that generate a long-term strengthening of the synapses, called long-term potentiation, or a weakening of the said long-term synapses, called long-term depression. Although, for decades, researchers have believed that the main cause of the cognitive deficit that characterizes Alzheimer's disease (AD) and aging was the loss of neurons, the hypothesis of an imbalance in the cellular and molecular mechanisms of synaptic plasticity underlying this deficit is currently widely accepted. An understanding of the molecular and cellular changes underlying the process of synaptic plasticity during the development of AD and aging will direct future studies to specific targets, resulting in the development of much more efficient and specific therapeutic strategies. In this review, we classify, discuss, and describe the main findings related to changes in the neurophysiological mechanisms of synaptic plasticity in excitatory synapses underlying AD and aging. In addition, we suggest possible mechanisms in which aging can become a high-risk factor for the development of AD and how its development could be prevented or slowed.

Synaptic plasticity in Alzheimer's disease and healthy aging.

The bidirectional selection of high and low anxiety-like behavior is a valuable tool for understanding the neurocircuits that are responsible for anxiety disorders. Our group developed two breeding lines of rats, known as Carioca High- and Low-conditioned Freezing (CHF and CLF), based on defensive freezing in the contextual fear conditioning paradigm. A random selected line was employed as a control (CTL) comparison group for both CHF and CLF lines of animals. The present study performed Fos immunochemistry to investigate changes in neural activity in different brain structures among CHF and CLF rats when they were exposed to contextual cues that were previously associated with footshock.

Fernando P. Cardenas

Department of Psychology

UNIVERSIDAD DE LOS ANDES

Fear Incubation Using an Extended Fear-Conditioning Protocol for Rats

Fernando P. Cardenas

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Department of Psychology

UNIVERSIDAD DE LOS ANDES

Fear Incubation Using an Extended Fear-Conditioning Protocol for Rats

Department of Psychology