Temporal dynamic of the hippocampal structural plasticity associated with the fear memory destabilization/reconsolidation process.

Reconsolidation of a contextual fear memory is a protein synthesis-dependent process in which a previously destabilized memory returns to a stable state. This process has become the subject of many studies due to its importance in memory processing, maintenance and updating, and its potential role as a therapeutical target in fear memory disorders such as phobias and post-traumatic stress disorder. In this sense, understanding the underlying mechanisms of memory reconsolidation is paramount in developing potential treatments for such memory dysfunctions.

Stress-induced resistance to fear memory destabilization is associated with an impairment of Lys-48-linked protein polyubiquitination in the Basolateral Amygdala: Influence of D-cycloserine.

The destabilization/reconsolidation process can be triggered by memory recall, allowing consolidated memories to be modified. We have previously reported that stress prior to fear conditioning induces memories that exhibit resistance to the engagement of some molecular events associated with the destabilization/reconsolidation process. Here, we evaluated whether stress could affect the expression of Lys-48 polyubiquitinated proteins within the basolateral amygdala complex, a phenomenon crucially linked to memory destabilization.

Resistance to fear memory destabilization triggers exaggerated emotional-like responses following memory reactivation.

Fear memory reactivation does not always lead to memory destabilization-reconsolidation. For instance, fear memories formed following withdrawal from chronic ethanol consumption or a stressful event are less likely to become destabilized after reactivation, with the effect of recall of these memories on the affective state still requiring elucidation. Here, we investigated the negative emotional-like responses following fear memory reactivation in ethanol-withdrawn (ETOH) rats by focusing on the possible role played by destabilization.

Ethanol withdrawal limits fear memory reactivation-induced molecular events associated with destabilization phase: Influence of d-cycloserine.

A 1-day fear memory in ethanol withdrawn (ETOH) rats is resistant to destabilization-reconsolidation process. However, d-cycloserine (DCS) reverts this disturbance. Considering that the formation of pathological fear memories in humans often occurs long time before the requirement of an intervention, the study of older memories is relevant in ETOH rats.

GABAergic signaling within the Basolateral Amygdala Complex modulates resistance to the labilization/reconsolidation process.

It is well known that stress can affect mnemonic processes. In particular, stress before contextual fear conditioning induces a memory which exhibits resistance to being interfered with by Midazolam (MDZ) when applied after memory retrieval. Moreover, stress exposure strongly affects GABAergic transmission within the Basolateral Amygdala Complex (BLA), a brain structure critically involved in fear memory processing.

Effect of a positive reinforcing stimulus on fear memory reconsolidation in ethanol withdrawn rats: Influence of d-cycloserine.

The pharmacological blockade of memory reconsolidation has been suggested as a potential treatment to the attenuation of maladaptive memories associated to psychiatric disorders and drug addiction. To interfere with the process of fear memory reconsolidation using a manipulation safer than pharmacological interventions, here we examined whether a positive reinforcing stimulus (non-alcoholic beer, NB) post-memory retrieval can decrease the fear response in ethanol withdrawn (ETOH) animals. We first evaluated the potential interfering effect of NB on memory reconsolidation in non-ethanol dependent (control, CON) rats.

Stress-induced resistance to the fear memory labilization/reconsolidation process. Involvement of the basolateral amygdala complex.

Consolidated memories can enter into a labile state after reactivation followed by a restabilization process defined as reconsolidation. This process can be interfered with Midazolam (MDZ), a positive allosteric modulator of the GABA-A receptor. The present study has evaluated the influence of prior stress on MDZ's interfering effect.

The effect of Midazolam and Propranolol on fear memory reconsolidation in ethanol-withdrawn rats: influence of d-cycloserine.

Background: Withdrawal from chronic ethanol facilitates the formation of contextual fear memory and delays the onset to extinction, with its retrieval promoting an increase in ethanol consumption. Consequently, manipulations aimed to reduce these aversive memories, may be beneficial in the treatment of alcohol discontinuation symptoms. Related to this, pharmacological memory reconsolidation blockade has received greater attention due to its therapeutic potential.

Activation of ERK2 in basolateral amygdala underlies the promoting influence of stress on fear memory and anxiety: influence of midazolam pretreatment.

Exposure to emotionally arousing experiences elicits a robust and persistent memory and enhances anxiety. The amygdala complex plays a key role in stress-induced emotional processing and in the fear memory formation. It is well known that ERK activation in the amygdala is a prerequisite for fear memory consolidation.

The influence of stress on fear memory processes.

It is well recognized that stressful experiences promote robust emotional memories, which are well remembered. The amygdaloid complex, principally the basolateral complex (BLA), plays a pivotal role in fear memory and in the modulation of stress-induced emotional responses. A large number of reports have revealed that GABAergic interneurons provide a powerful inhibitory control of the activity of projecting glutamatergic neurons in the BLA.

Facilitating influence of stress on the consolidation of fear memory induced by a weak training: reversal by midazolam pretreatment.

It is well known that an emotionally arousing experience usually results in a robust and persistent memory trace. The present study explored the potential mechanisms involved in the influence of stress on the consolidation of a contextual fear memory in animals subjected to a weak fear training protocol, and whether pretreatment with intra-basolateral amygdala or systemic administration of midazolam (MDZ) prevents the potential stress-induced influence on fear memory formation. A previous restraint session facilitated fear retention, this effect was not due to a sensitized effect of restraint on the footshock experience.

ERK activation in the amygdala and hippocampus induced by fear conditioning in ethanol withdrawn rats: modulation by MK-801.

The extracellular signal-regulated kinase (ERK) pathway, which can be activated by NMDA receptor stimulation, is involved in fear conditioning and drug addiction. We have previously shown that withdrawal from chronic ethanol administration facilitated the formation of contextual fear memory. In order to explore the neural substrates and the potential mechanism involved in this effect, we examined: 1) the ERK1/2 activation in the central (CeA) and basolateral (BLA) nuclei of the amygdala and in the dorsal hippocampus (dHip), 2) the effect of the NMDA receptor antagonist MK-801 on fear conditioning and ERK activation and 3) the effect of the infusion of U0126, a MEK inhibitor, into the BLA on fear memory formation in ethanol withdrawn rats.

Increased voluntary ethanol consumption and c-Fos expression in selected brain areas induced by fear memory retrieval in ethanol withdrawn rats.

Withdrawal from chronic ethanol administration facilitated the formation of contextual fear memory. The effect of fear memory retrieval on subsequent ethanol consumption, by employing a two-bottle free-choice procedure with either water or ethanol (2-8% v/v), was investigated in ethanol withdrawn rats. The effect of fear memory extinction with or without d-cycloserine (DCS, 5mg/kgi.

Lack of feedback inhibition on rat basolateral amygdala following stress or withdrawal from sedative-hypnotic drugs.

Previous research has demonstrated that suppression of inhibition in projection neurons of the basolateral complex of the amygdala (BLA) represents an essential mechanism underlying the emergence of negative emotional responses, including exaggerated fear and anxiety. The present work evaluates inhibitory postsynaptic potentials (IPSPs) in pyramidal projection neurons of the BLA in rats subjected to either diazepam or ethanol withdrawal or uncontrollable stress. These are experimental paradigms conducive to a negative emotional state.

Prenatal stress and early adoption effects on benzodiazepine receptors and anxiogenic behavior in the adult rat brain.

Chronic maternal stress during pregnancy has been associated with behavioral alterations that persist into adulthood. Moreover, adoption procedures performed immediately after birth can reverse these alterations. In this study, we examined the effects of prenatal restraint stress and adoption at birth (cross-fostering) on the behavioral response to an anxiety-provoking situation and on the adult male offspring expression of benzodiazepine (BDZ) receptors in selected brain areas.

Influence of ethanol withdrawal on fear memory: Effect of D-cycloserine.

Animals made dependent via an ethanol (ETOH) -containing liquid diet (6% v/v) for 14 days were subjected to a contextual fear conditioning paradigm 3 days after the last consumption day. After conditioning, rats were subjected to four extinction trials by exposing the animals to the conditioned context and their freezing was evaluated for each trial. Immediately after the first extinction trial, animals were injected with D-cycloserine (DCS) 5 mg/kg i.

Antidepressants attenuate both the enhanced ethanol intake and ethanol-induced anxiolytic effects in diazepam withdrawn rats.

We have recently shown that the abrupt discontinuation of chronic diazepam (DZM) administration facilitated ethanol consumption and enhanced the anxiolytic properties of ethanol. Tricyclic antidepressants such as desipramine and the selective serotonin reuptake inhibitor fluoxetine have been shown to reduce alcohol intake in rodent models of alcoholism and in alcoholics who are depressed. In the present study, we tested whether desipramine (1.

Increased fear learning coincides with neuronal dysinhibition and facilitated LTP in the basolateral amygdala following benzodiazepine withdrawal in rats.

Animals chronically administered with diazepam (DZM -- 2 mg/kg/day i.p.) or vehicle (VEH) for 21 days were tested in a fear-conditioning paradigm 4 days after the last administration.

Early adoption modifies the effects of prenatal stress on dopamine and glutamate receptors in adult rat brain.

Stressful stimuli during pregnancy induce complex effects that influence the development of offspring. These effects can be prevented by environmental manipulations during the early postnatal period. Repeated restraint during the last week of pregnancy was used as a model of prenatal stress, and adoption at birth was used to change the postnatal environment.

Gabaergic modulation of the stress response in frontal cortex and amygdala.

GABAergic neurotransmission is thought to play an important role in the modulation of the central response to stress. In the present study we evaluate the influence of a brief restraint exposure on GABA-stimulated chloride influx in diverse brain areas presumed to have a major role in the mediation of emotional behaviors following aversive stimulation. A reduced chloride uptake after stress exposure was only observed in frontal cortex and amygdala.

A dopaminergic mechanism is involved in the 'anxiogenic-like' response induced by chronic amphetamine treatment: a behavioral and neurochemical study.

The purpose of this study was to examine the influence of chronic d-amphetamine (AMPH) treatment (2 mg/kg i.p., for 9 consecutive days) on behavioral and neurochemical responses to a subsequent exposure - 4 days after the last AMPH injection--to the elevated plus-maze (EPM), as well as to determine the involvement of a dopaminergic mechanism in that influence.

Chronic benzodiazepine administration facilitates the subsequent development of ethanol dependence.

This study investigated the effect of chronic benzodiazepine (BZD) administration and its abrupt discontinuation on later subsequent ethanol consumption employing a free choice paradigm between water and increasing ethanol concentrations. In addition, we also studied the anxiolytic and reinforcing properties of ethanol assessed in the elevated plus maze (EPM) and in the conditioned place preference paradigm, respectively. Adult male Wistar rats were subjected to a chronic diazepam (DZM) treatment (2 mg/kg/day, i.

Early exposure to chronic variable stress facilitates the occurrence of anhedonia and enhanced emotional reactions to novel stressors: reversal by naltrexone pretreatment.

The present research studied the influence of an early chronic variable stress (CVS) paradigm - an animal model of depression - on behavioral responses to subsequent environmental challenges suggested to model anhedonia and emotional reactions such as anxiety and fear. In order to explore a potential involvement of an endogenous opiate mechanism - presumably activated during CVS exposure - in the development of such behavioral reactions, in all experiments rats were administered naltrexone (NAL, 2 mg/kg, i.p.

Benzodiazepine withdrawal facilitates the subsequent onset of escape failures and anhedonia: influence of different antidepressant drugs.

The effect of benzodiazepine (BDZ) withdrawal on escape acquisition and on the behavioral response to two different reinforcing stimuli was investigated. In addition, the influence of antidepressant drugs (AD) differing in their mechanism of action on these behavioral outputs was also evaluated. Rats subjected to withdrawal from a chronic treatment with diazepam (DZM; 2 mg/kg per day, i.

Anxiogenic-like effects of Tagetes minuta L essential oil on T-maze and tonic immobility behaviour in domestic chicks.

In a first experiment, four doses (ranging between 0.04 and 0.45 mg/kg of body weight) of the essential oil from Tagetes minuta L.