Inhibitory avoidance learning paradigm,read the secrets of chinese meditation online,how to be disciplined at work,benefits of traditional safety razor - New On 2016

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Rats were trained on an inhibitory avoidance task to study the effects of post-training administration of tetrodotoxin (TTX, which temporarily inactivates neural activity) on memory consolidation. Due to an error in the citation line, this revised PDF (published in December 2003) deviates from the printed version, and is the correct and authoritative version of the paper. ReferencesAmbrogi Lorenzini CG, Baldi E, Bucherelli C, Sacchetti B, Tassoni G (1999) Neural topography and chronology of memory consolidation: a review of functional inactivation findings. JavaScript is currently disabled, this site works much better if you enable JavaScript in your browser. ASA members enjoy complimentary access to ASA publications, as well as a variety of educational resources. Received from the Departments of Anesthesiology and Neurobiology and Behavior and the Center for the Neurobiology of Learning and Memory, University of California, Irvine, California. You will receive an email whenever this article is corrected, updated, or cited in the literature. IT has been hypothesized that two characteristics define inhaled compounds as general anesthetic agents, namely, the capacity to cause (1) immobility in response to a noxious stimulus and (2) amnesia. The memory modulation effects of the amygdala occur partly through ?-aminobutyric acid–mediated (GABAergic) mechanisms. After obtaining Institutional Animal Care and Use Committee (University of California, Irvine, CA) approval, 85 male Sprague-Dawley rats (weight, 250–280 g on arrival) were obtained from Charles River Laboratories (Wilmington, MA).
Sham operations used the same general procedure except that an empty needle was lowered only to the level of the caudate. The rats were trained on an inhibitory avoidance apparatus, 20 which was located in a sound-shielded room.
Because the behavioral data were not normally distributed, we used a nonparametric analysis approach. After histologic examination, 28 animals were excluded from further analysis, 11 from the BLAC-saline–treated group, and 17 from the BLAC-propofol–treated group. Figure 1shows a schematic composite diagram of the minimum and maximum lesion extents for the animals included in the final analyses.
Figure 3shows the number of trials each group of animals needed to learn the task to the 60-s acquisition criterion.
Figure 4shows memory performance as determined by differences in median retention latency (with interquartile ranges).
In contrast to the sham-propofol–treated animals, the BLAC-propofol–treated animals (n = 9) showed a robust memory with a median latency of 323 (143–480) s (not significantly different from sham-saline–treated or BLAC-saline–treated control animals). Despite being a well-established clinical phenomenon, anesthetic-induced amnesia remains poorly understood in terms of its neurobiology. There is a “reverse logic” element that must be considered, to fully appreciate the findings. The present findings will, in all likelihood, generalize to animal studies involving other paradigms. For this study, an amnestic effect of propofol had to be demonstrated, to show its reversal or blockade with a BLAC lesion. The potential effects of propofol on task acquisition cannot account for our primary findings, namely, that lesions of the BLAC prevented propofol-induced amnesia, because these potential acquisition effects were identical for the sham-treated and the BLAC-lesioned rats exposed to the same dose of propofol and there was no difference between these two groups in their acquisition performance (fig. In contrast to their clear effect on propofol-induced amnesia, the BLAC lesions did not appear to greatly change the sedative effect of the drug.
Except where otherwise noted, this work is licensed under Creative Commons Attribution-NonCommercial 4.0 International License. Background: Neurohormones like testosterone and estrogen play important roles in learning and memory. Materials and MethodsAnimalsAdult male Wistar rats (200–250g) were obtained from the breeding colony of the Pasteur Institute of Iran. Microinjection procedureIntra-hippocampal injections were given via guided cannulae with injection needles (30-gauge) that were connected by polyethylene tubing to a 10-μl Hamilton micro-syringe.
ProcedureThe stepthrough type of passive avoidance task was used to examine the long-term memory based on the negative reinforcement. Experimental protocolExperiment 1The aim of this experiment was to assess the effect of pre-training injections of EV into the CA1 region of hippocampus on passive avoidance task.
Experiment 2The aim of this experiment was to assess the effect of pre-training injections of DPN into the CA1 region of hippocampus on passive avoidance task.
Experiment 3The aim of this experiment was to assess the effect pre-training injections of Cyclofenil into the CA1 region of hippocampus on passive avoidance task. Experiment 4The aim of this experiment was to assess the effect pre-training injections of Cyclofenil plus DPN into the CA1 region of hippocampus on passive avoidance task.
HistologyFollowing behavioral testing, animals were sacrificed by decapitation and the brains were removed and fixed in formalin. Statistical analysisResults of STL during the training session, and STL and time spent in the dark chamber during the retrieval for groups are expressed as one way ANOVA followed by Tukey or LSD test.
Experiment 4: Effect of Cyclofenil plus DPN on acquisition of passive avoidance taskThe results showed that pre-training injections of Cyclofenil plus DPN had no significant effects on STL during the training session as compared to the DMSO group. 1 Given two defining characteristics for anesthetic agents and a multiple-mechanism framework for anesthetic action, it would seem equally important for an understanding of anesthesia to determine the brain sites mediating anesthetic-induced amnesia as it is to determine the neurobiology of anesthetic-induced immobility. 4 The amygdala appears to modulate the strength of a memory according to how physiologically arousing and emotionally relevant a “to-be-remembered” situation is to an organism. 10 Systemically administered diazepam (a GABA agonist) fails to cause amnesia if the basolateral amygdala subnuclei are lesioned.
We chose propofol as the first general anesthetic agent to examine because it is thought to have GABA agonist properties 17,18 and clinically it appears to induce a level of amnesia similar to that of the benzodiazepines. The apparatus consisted of a V-trough–shaped alley (91 cm long, 15 cm deep, 20 cm wide at the top, and 6.4 cm wide at the floor) which was divided into two compartments separated by a manually controlled sliding door that opened by retracting into the floor. Each rat was placed back into the starting light–safe side of the apparatus and the time taken (maximum, 600 s) for each rat to again cross into the dark–shock side was recorded. Brains were removed from each animal and placed into a 10% formalin solution overnight, then transferred to a 20% sucrose–10% formalin solution for 3–5 days. Twenty-six of these animals had massive lateral damage in the temporal lobes, as if they had undergone temporal lobectomies. Clearly, these lesions all centered around the basolateral amygdala subnucleus within the BLAC. Propofol impaired task acquisition equally for both the sham-operated control animals and the BLAC-lesioned group; this is evidenced by an increased number of trials to approximately 4 for each group.
Thus, as expected on the basis of previous studies, 11 BLAC lesions did not, by themselves, have a significant effect on memory retention performance. The present study examined the hypothesis, derived from an extensive prior animal literature, 8,9 that the BLAC may be a critical brain region involved with mediating general anesthetic–induced amnesia, as assessed in the current study with propofol. Because the experiment removed a part of the brain by lesioning it and the amnestic effect of propofol was eliminated, it can be concluded by reverse logic that the BLAC must be mechanistically involved with producing the amnesia of propofol-induced general anesthesia. 24 One suggests that the amygdala is the structure in the brain that modulates the strength of memory traces, allowing things that are the most relevant to be the best remembered. The literature on amygdala function clearly documents effects of BLAC manipulations on modulating memory in studies involving many tasks including not only one-trial and multitrial avoidance learning but also, discrimination learning, reinforcer devaluation learning, active avoidance learning, pavlovian “fear conditioning” and both spatial and cued water maze learning.
It would have been preferable if the amnestic potency of propofol, relative to its sedative effects, had been strong enough to produce amnesia without also causing a significant increase in the number of trials needed to learn the inhibitory avoidance (IA) task. This is evidenced by the similar increase in number of trials to criterion needed for both BLAC-treated and sham-treated rats to learn the task under the influence of the propofol.
Estrogen receptors, densely expressed in the CA1 region of rat hippocampus, mediate the effects of estrogen on learning and memory. The effect of pre-training infusions of estrogen receptor ligands in the CA1 region of hippocampus on passive avoidance task. Performance on place learning tasks, requiring the use of spatial location is enhanced by estrogen treatment to ovariectomized rats (2, 3). A rectangular opening (8 cm × 8 cm) was located between the two chambers and could be closed by an opaque guillotine door. A day before initiation of tests, animals were familiarizedand habituated to the testing room, for which on day one, 30 min before training, rats were placed in the lighted chamber and were allowed to explore for 30 s, and then guillotine door was raised. For histological examination of cannulae and injection placement in CA1 area, 100-μm thick sections were taken and cannulae and injection tracks were examined for each side with light microscopy. The effects of EV on acquisition of inhibitory avoidance learning (A) step-through latency and (B) time spent in dark chamber.
Low levels of estradiol facilitate, whereas high levels of estradiol impair, working memory performance on the radial arm maze.


Distribution and differences of estrogen receptor beta immunoreactivity in the brain of adult male and female rats. The human forebrain has discrete estrogen receptor alpha messenger RNA expression: high levels in the amygdaloid complex. Estradiol targets synaptic proteins to induce glutamatergic synapse formation in cultured hippocampal neurons: critical role of estrogen receptor-alpha. Comparison between basal and apical dendritic spines in estrogen-induced rapid spinogenesis of CA1 principal neurons in the adult hippocampus. Stress facilitates classical conditioning in males, but impairs classical conditioning in females through activational effects of ovarian hormones.
High levels of estradiol disrupt conditioned place preference learning, stimulus response learning and reference memory but have limited effects on working memory.
ERbeta-selective SERMs produce mnemonic-enhancing effects in the inhibitory avoidance and water maze tasks. Antidepressant effects of ERbeta-selective estrogen receptor modulators in the forced swim test. Bridged bicyclic cores containing a 1,1-diarylethylene motif are high-affinity subtype-selective ligands for the estrogen receptor.
Intra hippocampal injection of testosterone impaired acquisition, consolidation and retrieval of inhibitory avoidance learning and memory in adult male rats.
Estrogen receptor transcription and transactivation: Structure-function relationship in DNA- and ligand-binding domains of estrogen receptors. Posttraining intrahippocampal estradiol injections enhance spatial memory in male rats: interaction with cholinergic systems. Androgen inhibits neurotransmitter turnover in the medial prefrontal cortex of the rat following exposure to a novel environment. Estrogen receptor-beta colocalizes extensively with parvalbumin-labeled inhibitory neurons in the cortex, amygdala, basal forebrain, and hippocampal formation of intact and ovariectomized adult rats. Prior non-spatial pretraining eliminates sensorimotor disturbances and impairments in water maze learning caused by diazepam. Propofol facilitates the development of long-term depression (LTD) and impairs the maintenance of long-term potentiation (LTP) in the CA1 region of the hippocampus of anesthetized rats. Neuroactive steroid effects on cognitive functions with a focus on the serotonin and GABA systems. Knockout Corner: Neurobehavioural consequences of a serotonin 5-HT(2C) receptor gene mutation. Impaired hippocampal-dependent learning and functional abnormalities in the hippocampus in mice lacking serotonin(1A) receptors. Age-related cognitive deficits in rats are associated with a combined loss of cholinergic and serotonergic functions. Molecular cloning and characterization of human estrogen receptor betacx: a potential inhibitor ofestrogen action in human.
Transcriptional activities of estrogen receptor alpha and beta in yeast properties of raloxifene. ADHD can be conceptualized as a disorder of executive function; specifically, ADHD is characterized by reduced ability to exert and maintain cognitive control of behavior. At any age across the life cycle EFs can be improved, including in the elderly and in infants. TTX was administered bilaterally into the dorsal hippocampus immediately after training, and memory of the task was measured 48 h later.
However, identifying which brain regions mediate anesthetic-induced amnesia is a difficult proposition, especially because it is likely that memory processing involves many brain structures and anesthetics tend to globally depress brain activity. 5–9 There has been a remarkable convergence of recent studies demonstrating the critical role of the BLAC (but not the central amygdala) in memory modulation by every class of drug or hormone tested to date.
11 Furthermore, intra-BLAC doses of bicuculline (a GABA antagonist) given before or just after learning block the amnestic effect of systemically administered midazolam. 19 To put the essence of this experiment in simple terms, if activity within the BLAC is required for propofol amnesia to occur, then if the BLAC is removed, propofol should no longer cause amnesia. The rats were randomly assigned to one of two surgery groups: sham-operated control animals and animals with bilateral NMDA-produced lesions of the BLAC. The starting compartment (31 cm long) was colored white and illuminated, whereas the shock compartment (60 cm long) was dark and not illuminated.
This dose of propofol was chosen on the basis of pilot work, which demonstrated it to be the minimal dose consistently producing anterograde amnesia in this paradigm. Longer latencies to cross into the dark side were interpreted as indicating better retention of the training experience. Brains were sectioned into 40-?m sections using a freezing microtome and stained with thionin. The smaller lesions affected an area approximately equal in size to that of the entire basolateral amygdala subnuclei, and the larger lesions extended this area of damage to encompass most of the lateral subnuclei.
Schematic representation of the minimal (black hatched) and maximal (white hatched) extent of the lesions involving the basolateral amygdala complex.
6,7,9 The other suggests that the amygdala is the site in the brain where emotional or fearful memories are formed and stored in the brain.
8 In addition, it is likely that the present findings will generalize to studies of human subjects.
In other words, both sham-treated and BLAC-lesioned rats had the same trouble learning the task under propofol, but only the sham-treated animals seemed to “forget it,” whereas the BLAC-lesioned animals still “remembered it.” Given the influence of propofol on task acquisition, postlearning propofol administration and the use of a retrograde amnestic effect might have been a useful technique to employ to negate any drug-induced acquisition deficits.
The number of trials to criterion increased from the 1–2 range for both groups trained without propofol and to the 3–5 range for both groups trained with propofol.
The floor of both chambers was made of stainless steel rods (2mm diameter), spaced 1 cm apart. After entering of the rats to the dark chamber, the guillotine door was lowered and the rats remained there for 30s. STL during the training session and STL and the time spent in dark compartment during the retrieval test were recorded. STL during the training session, and STL and the time spent in dark compartment during the retrieval test were recorded. Only data obtained from animals, whose cannulae and injections were inserted precisely in the CA1 region, were used for analysis. Figure 2B shows the effect of pre-training injections of DPN on time-spent in the dark chamber. Figure 3B shows the effect of pre-training injections of Cyclofenil on time-spent in the dark chamber.
The first test that was given was the door task; in this task children were asked to sit in front of an item or electronic device that consisted of a pathway where balls could be rolled down into different slots. There has been much work with excellent results on improving EFs in the elderly by improving physical fitness (Erickson & Kramer 2009, Voss et al. We corroborated the typical amnesic effect of intrahippocampal infusions of TTX in those rats trained with the mild-intensity foot shock.
2,3 Nevertheless, a candidate site for mediating drug-induced amnesia has emerged from the learning and memory literature. 12,13 Because a GABAergic mechanism of action could underlie the mechanisms of anesthesia, 14–16 it seems likely that part of the amnestic effects produced by anesthetics could depend on BLAC-mediated mechanisms.
Each animal was placed into the light–safe compartment of the training apparatus facing away from the door. One animal showed no damage to the BLAC, and one animal had only unilateral damage to the BLAC.
Figure 2shows two representative photomicrographs of thionin-stained rat brain sections at the level of the BLAC for both a sham-operated control animal (fig. The median values and the interquartile ranges for the number of trials each group of animals required to learn the inhibitory avoidance task.
Thus, rats with discrete BLAC lesions, which had acquired the task under the influence of propofol, showed memory performance no different from rats that had acquired the task without propofol. Studies both of patients with amygdala damage and of healthy subjects with human brain imaging from several laboratories have consistently confirmed the “memory modulation” view of the amygdala derived from the animal studies. A lesser dose of propofol may have allowed the animals to learn the task more easily (as evidenced by fewer learning trials), but it also would not have resulted in the required anterograde amnesia.
However, retrograde memory effects of propofol have not been consistently reported, 32,33 and we were unable to find any retrograde memory effect in pilot experiments. Furthermore, there was no objective difference in the effectiveness of the propofol evident in the behavior of the rats with confined BLAC lesions compared with the sham-operated control animals.


These animal experiments were carried out in accordance with the recommendations of the Helsinki declaration and the internationally accepted principles for the use of experimental animals. Following the habituation of all animals, the first rat was again placed into the lighted chamber for 10 s, the door was lifted, and the crossover latency was recorded; the door was closed behind it and a shock was delivered (1 mA, 5-s duration). STL during the training session, STL and the time spent in the dark compartment during the retrieval test were recorded. It is well established that many of the actions of steroid hormones occur by means of activation of intracellular hormones (23), which diffuse into the cell, bind to their individual receptors and transformation and activation of the receptors occur; activation is dissociation of the receptor-heat shock protein complex, formed with unbound receptors in order to stabilize, keep inactive and protect the receptor. A barrier was included to mislead the child and test the memory of what slot the ball went into.[8] They were then instructed to search or point at where the hidden ball had landed. More importantly, with the stronger foot shock, the same treatment was ineffective in producing amnesia. The NMDA solution was back-filled into a 30-gauge needle, which was attached by a polyethylene tube to a 10-?l syringe (Hamilton Co., Reno, NV) driven by a minipump (Sage Instruments, Boston, MA). When the animal turned to face the door, the door was lowered out of the way to reveal the dark–shock compartment. In addition, 15 animals were dropped from analysis for behavioral reasons: seven animals failed to learn the task secondary to an excessive sedative effect of the propofol, and eight animals apparently had inadequate intraperitoneal injections because they failed to show any sedative effect during training, with two of these animals excreting propofol per rectum immediately after injection (a clear indication of an intraintestinal rather than a proper intraperitoneal injection). 8,9 These facts make clear that, although the present conclusions must be evaluated with other species and tests, the available evidence strongly supports their general validity and the general hypothesis that the amygdala may be a site that is critically involved with producing anesthetic-induced amnesia. This relatively weak amnestic potency of propofol contrasts with the apparently more potent amnestic effect of diazepam.
The apparatus was placed in an acoustically insulated room, kept under standard conditions. These results suggest that, after an enhanced learning experience, other brain regions are also activated, which may compensate for the amnesic effect of TTX infusions into the hippocampus. Lesions were histologically classified into one of the following categories: (1) discrete–confined lesions of the BLAC, (2) inadequate or missing lesions, or (3) extensive lesions of the BLAC with significant collateral damage to surrounding structures. In consideration of previous evidence indicating that anesthetic-induced immobility is mediated through anesthetic actions in the spinal cord 26 and that anesthetic-induced unconsciousness may be mediated through anesthetic actions in the thalamus, 27–30 there would now seem to be strong neuroanatomic support for the “multiple sites, multiple mechanisms” concept of anesthetic action. 11 Diazepam produced anterograde amnesia without increasing the number of trials needed to learn the IA task.
Several studies have shown that ERβ is an important modulator of cell proliferation and learning and memory (7, 8). The rats were placed in the lighted chamber, 10 s later the door was opened, and the step-through latency (STL) and the time spent in dark compartment during the retrieval test was recorded, up to 600 s, during which time electric shocks were not applied to the grid floor(22). The injection needle remained in place for an additional 3 min to maximize diffusion of the solution.
As the rat stepped into the dark–shock compartment with all four paws, a foot shock (0.4 mA) was delivered until the animal escaped back into the starting light–safe compartment.
Confined lesions had to include bilateral damage to the BLAC at a minimum of 1.5 mm anteroposterior to the injection site, as well as minimal damage to surrounding structures (confined to borderline areas around the BLAC). An amnestic effect of propofol is clearly seen in the sham-operated control animals exposed to propofol 24 h earlier. Midazolam, on the other hand, did cause an increase in the number of trials needed to learn the IA task.
Localized predominantly in the limbic system, like amygdala, septum, and also in the hippocampus, and hypothalamus, ERs are involved in emotional processing and cognition (9, 10). ERs consist of different domains: N-terminal domain, DNA-binding domain, hinge region, large ligand binding domain, and the C-terminal domain (25).
The last test consisted of a three peg task, this measured inhibitory control, in this test children were asked to identify pegs.
Thus, inhibitory control makes it possible for us to change and for us to choose how we react and how we behave rather than being unthinking creatures of habit.
The door to the dark compartment remained open, and the animals could choose to either stay in the light–safe compartment or again cross into the dark–shock compartment. Extensive lesions included a massive lesion of the BLAC at a minimum of 1.5 mm anteroposterior to the injection site, along with accompanying extensive damage to a number of other surrounding structures, including (1) the piriform and entorhinal cortical areas (2) the striatum, (3) the endopiriform nucleus, or (4) the central nucleus of the amygdala.
2A) shows a somewhat triangular clustering of relatively large cell bodies in the area between the central amygdala nucleus medially and superior (up and to the right) and the entorhinal–piriform cortex laterally (to the left). Estradiol mediates structural changes at synapses of the hippocampus, an area in the brain important for learning and memory (11). The results of this study found that the inhibitory control test was the most effective in allowing the child to remember things. EFs and prefrontal cortex are the first to suffer, and suffer disproportionately, if something is not right in your life. Animals crossing back into the dark–shock compartment were again given a foot shock and allowed to escape back to the light–safe compartment. Only animals with discrete–confined, approximately equivalent bilateral lesions of the BLAC were included in the behavioral analysis. In addition, estradiol has a variety of effects in the brain, including the modulation of cholinergic, serotonergic, and catecholaminergic neurons in different brain areas (12).Several concepts have been proposed to account for the mixed effects of estrogen on cognition, including the possibility that the efficacy of estrogen treatment varies with the motivating factors of the task (13), stress state of the animals (14), type of memory (15) and duration and type of hormone treatment (3).
Learning was considered to have occurred when animals would avoid the dark–shock compartment for greater than 60 consecutive s. 2B, arrowed), damaged areas are characterized by loss of neurons and gliosis in the tissue and show a significant lack of any large cell bodies. After the animals attained the 60-s learning criterion they were removed from the apparatus and returned to their home cages. In this figure, the majority of the BLAC is damaged, including all of the lateral and basolateral subnuclei.
The number of trials required for each animal to learn the task was taken as an index of how difficult the task was for a particular group of animals to learn. Given these different patterns of effects with SERMs, it is important to further investigate the role of ERβ for the effects of E2 on performance in hippocampally mediated tasks. Both receptors are widely expressed in the brain with a great overlap but also with quantitative regional and sex-specific differences in expression patterns (24).
This is clearly seen because the area of cellular damage has a crescent-moon shape to it, which curves around the central amygdala nucleus. Academic, New YorkPerez-Ruiz C, Prado-Alcala R A (1989) Retrograde amnesia induced by lidocaine injection into the striatum: protective effect of the negative reinforcer. In: McGaugh JL, Bermudez-Rattoni F, Prado-Alcala RA (eds) Plasticity in the central nervous system. It has become evident in recent years that there are important reciprocal relationships between brain steroid hormone systems and neurotransmitter systems such as the cholinergic (23, 28), dopaminergic (29, 30), GABAergic, serotonergic and the glotaminergic (23, 31, 32).
Second, serotonin neurons also express the nuclear estrogen receptors beta (ERβ) which are transcription factors. Any of these can cause you to appear to have a disorder of EFs, such as ADHD, when you do not.
5HT1B knockout mice exhibit facilitation in the acquisition of a hippocampal-dependent spatial reference memory task in the Morris water maze, but an impairment of delay-dependent working memory in the radial arm maze (37-40). Interestingly, stimulation of the 5HT1B receptor inhibits the release of acetylcholine in the hippocampus, but stimulates its release in the frontal cortex (39). Reduction in both cholinergic and serotonergic functions causes severe memory impairment in young as well as in aged rats (41). The expression of ERβ3 appears to be restricted to the testis (43) and functional studies on this isoform have not been performed.
ERβ2 lacks the AF-2 core region and has undetectable affinity for estradiol and other tested ligands.
An in vitro estrogen receptor-binding assay was used to assess the binding affinities of the yeast recombinant proteins.
This model differs from the original paradigm in which the two partners in a nuclear receptor dimer play identical roles in ligand binding and coacti-vator recruitment by way of helix 12. Hence, these data suggest that the ER- β heterodimer may recruit only one coactivator during transcriptional activation (46).



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