Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0598853 (forgetting)
 3,232 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The spontaneous forgetting model has been used to demonstrate the possibility of the memory forgetten trace extraction under the dopamine reuptake blockade by nomifensine and bupropion, increase of its quantity by amfonelic acid, activation of the postsynaptic dopaminergic receptors by (+)3-PPP, blockade of the latter by (-)3-PPP, and under the blockade of separate links of the GABA-benzodiazepine-ionophore complex by bicuculline, picrotoxin, flumazepil and R015-3505. Effectiveness of the neuropharmacological actions improving the memory forgotten trace retrieval is shown to depend upon the duration of the spontaneous forgetting process. The presynaptic receptors are involved in the retrieval process control--improvement of the conditioned habit performance after forgetting due to the activation of presynaptic dopaminergic receptors by specific agonist (-)3-PPP is clearly correlated with the initial retrieval level. The above facts underlie a hypothesis about the neurochemical forgetting mechanisms.
 ...
PMID:[The role of the dopaminergic system and GABA-benzodiazepine- ionophore complex in the regulation of memory retrieval]. 197 48

The results of study testify to a stimulating effect of benzodiazepine receptors blocators RO15-1788 and RO15-3505 on reproduction of conditioned reaction of passive avoidance in mice disturbed as a result of various procedures-"psychogenic" and cycloheximide amnesia, extinction and forgetting. A considerable antiamnesic effect of the drugs on cycloheximide amnesia models is noted, in comparison with the "psychogenic" one. RO15-3505 is more effective in the processes of extraction of memory traces under amnesia. The obtained results testify to an important contribution of benzodiazepine-GABA-ergic brain systems in inhibitory regulation of the processes of stored memory traces reproduction.
 ...
PMID:[Effect of benzodiazepine receptor blockade on memory processes in the mouse]. 311 78

Inability to remember and amnesia have been shown to be active neurochemical processes. The coupled processes (blockade of the triggering DA stimulating system and activation of the inhibitory GABA-ergic system with the predominant value of postsynaptic D-2 receptors) are a neurochemical basis for development of amnesia. The mechanisms of spontaneous forgetting is provided by a decrease in the activity of the dopaminergic system along with the enhancement of benzodiazepine-GABA-ergic interferentional inhibition. The observed changes in dopamine metabolism, para-tyramine appearance, as well as restructure of D-2 receptors provide the activity of dopamine increasing mechanism which determines the retention of memory traces. A computer model of the spatial interaction of the dopamine membrane-receptor complex was constructed by scanning the samples of synaptic membranes after learning and amnesia. A new method of inducing psychogenic amnesia in human beings has been elaborated. Amnesia is characterized by the absence of increases in the number of cortical connections reflecting the emotional factor of information.
 ...
PMID:[Forgetfulness and amnesia: receptor mechanisms and brain mapping]. 751 Jan 70

Short-term memory in pigeons is studied in the delayed matching-to-sample procedure where information is forgotten over short periods of time. Performance in this task reflects the separate influences of attention to the sample stimuli and memorial processes and is determined by a range of procedural variables. Forgetting functions can be obtained by varying the duration of the retention interval and can be quantified in terms of the parameters of a fitted function, such as the negative exponential. These parameters provide measures of initial discriminability and rate of forgetting and are sensitive to the effects of drugs known to influence the cholinergic, GABA and dopaminergic systems. The results of behavioral pharmacological studies suggest that the effects of a variety of drugs on initial discriminability and rate of forgetting are quite similar for pigeons and monkeys. We conclude that pigeons serve as an effective model to examine the effects of agonist and antagonist drugs on memory.
 ...
PMID:Memory procedures, performance and processes in pigeons. 880 32

The determining mechanism of memory regulation is a system involving the right temporal region and two anterior frontal regions. This is a cortical part of the integral system of the emotional regulation of memory. The dopaminergic mechanism forms the basis for fortifying the emotiogenic memory system, promoting the facilitation of retrieval. The selective emotional set of aggressive and submissive mice determines both the processes of extinction, development of amnesia, and subsequent reactivation of a memory trace induced by neuropharmacological agents. The GABA system is shown to enter the mechanism that controls the activity of dopamine system--dopamine release from the terminals of the nigrostriatal and mesolimbic dopaminergic systems is stimulated. The neurochemical background in the development of amnesia or forgetting determines the subsequent retrieval of a memory trace. The dopamine and GABA systems are common links in the retrieval of amnestic and forgetting memory traces, respectively. A substantial rise of met-enkephaline levels along with the maximum increase of D2-receptor density in the frontal cortex, amygdala, striatum, and hippocampus were observed in rats after learning. In vitro experiments indicated that met-enkephaline and beta-endorphine stabilized the kinetics of dopamine-receptor interactions.
 ...
PMID:[The mechanisms of the emotiogenic regulation of memory]. 981

Infantile amnesia is a ubiquitous phenomenon, but its neural bases remain largely unknown. The authors identify a role for GABAergic transmission in suppressing retrieval of memories acquired in infancy. Eighteen-day-old rats received pairings of white noise and shock; considerable forgetting of this experience (assessed by freezing) occurred after 10 days. The memory was recovered by pretest administration of the GABAA inverse agonist FG7142 10 days, but not 2 months, after training. This effect of FG7142 generalized when a passive avoidance procedure was used. Also, FG7142 decreased fear of a latently inhibited conditioned stimulus, showing that the observed memory recovery effect was not due to a state-dependent process. It appears that GABA may be involved in infantile amnesia regardless of the emotional content of the memory.
 ...
PMID:Recovery of fear memories in rats: role of gamma-amino butyric acid (GABA) in infantile amnesia. 1649 15

Recently, studies from our laboratory have shown that 16-day-old rats, in contrast to 23-day-old rats, fail to show either ABA renewal or recovery of an extinguished fear response following a pre-test injection of FG7142 [Kim, J. H. & Richardson, R. (2007). A developmental dissociation of context and GABA effects on extinguished fear in rats. Behavioral Neuroscience; Yap & Richardson, unpublished data]. The present study, using freezing as a measure of learned fear, extends these findings by examining whether there is a developmental difference in susceptibility to reinstatement following extinction. 16- and 23-day-old rats were trained to fear a white-noise conditioned stimulus (CS) by pairing it with a shock unconditioned stimulus (US). This fear was subsequently extinguished by non-reinforced presentations of the CS. Some rats received a post-extinction Reminder which consisted of a single presentation of a reduced-intensity US. Experiments 1 and 2 demonstrated that this Reminder was effective in reinstating extinguished fear in 23-day-olds, and that this reinstatement effect was context-specific in rats this age. In contrast, 16-day-old rats failed to show the reinstatement effect in either experiment. The failure to observe a post-extinction reinstatement effect in the 16-day-olds was not due to a general ineffectiveness of the Reminder treatment at this age because it did alleviate spontaneous forgetting in rats this age (Experiment 3). Taken together, the results suggest that fundamentally different processes may mediate extinction early in development compared to later in development.
 ...
PMID:A developmental dissociation in reinstatement of an extinguished fear response in rats. 1745 34

The paper reviews the existing and future nootropic drugs (cognition enhancers) with different mechanisms of action and heterogenous chemical structures, which have been developed on the basis of knowledge of the mechanisms of learning, memory and forgetting, as well as degenerative processes in aging brain and disease-associated cognitive impairments. These agents influence on acetylcholine-, glutamate-, GABA-, 5-HT-, dopamine-, histamine-, adenosine-, phosphodiesterase-, neurotrophic- systems, and neurohormones. Neuropeptides and their analogs, blood flow enhancers, calcium-channel blockers, antioxidants and vitamins and herbal preparations, and some other agents improving cerebral metabolism and influencing the neurodegeneracy involved in Alzheimer's disease are considered. An original classification of cognition enhancers, based on mechanisms of their action, includes more than 200 drugs in current use and those currently under development.
 ...
PMID:[Nootropes (cognition enhancers) and neuroprotectors]. 1807 43

J. H. Kim, G. McNally, and R. Richardson (2006) reported that pretest injection of FG7142, a GABA inverse agonist, alleviated infantile amnesia in rats. From this, it was concluded that GABAergic neurotransmission is involved in the forgetting seen in the developing rat. The present study extends that finding by examining the role of GABA in the reactivation of a forgotten memory in the infant rat. Sixteen-day-old rats were conditioned to fear a white noise. When tested 3 days later, rats that had not received a reminder treatment exhibited substantial forgetting. Reactivation of memory (as assessed by high levels of freezing) was observed in rats that were given a reminder shock and injected with saline the day before test. However, rats given a reminder shock and injected with midazolam immediately afterward failed to exhibit the reactivation effect. A subsequent experiment replicated this finding and further showed that midazolam did not reduce the memory reactivation effect when injected 2 hr after the reminder episode. From this, it appears that alterations in GABAergic neurotransmission may be an underlying process mediating memory reactivation in the infant rat.
 ...
PMID:Immediate post-reminder injection of gamma-amino butyric acid (GABA) agonist midazolam attenuates reactivation of forgotten fear in the infant rat. 1808 85

In women, medroxyprogesterone acetate (MPA) is the most commonly used progestin component of hormone therapy (HT). In vitro, MPA negatively impacts markers of neuronal health and exacerbates experimentally-induced neurotoxicity. There is in vitro evidence that these factors are driven by GABAergic and neurotrophic systems. Whether these effects translate to a negative impact on brain function has not been tested in vivo, clinically or preclinically. Here we evaluate the mnemonic and neurobiological effects of MPA in the surgically menopausal rat. Aged ovariectomized (OVX) rats were given subcutaneous vehicle, natural progesterone, low-dose MPA or high-dose MPA. Multiple cognitive domains were analyzed via the water radial-arm maze (WRAM) and Morris maze (MM). Cognitive brain regions were assayed for changes in the GABAergic system by evaluating GAD protein, the synthesizing enzyme for GABA, and neurotrophins. On the WRAM, both progestin types impaired learning. Further, high-dose MPA impaired delayed memory retention on the WRAM, and exacerbated overnight forgetting on the MM. While neurotrophins were not affected by progesterone or MPA treatment, both progestin types altered GAD levels. MPA significantly and progesterone marginally decreased GAD levels in the hippocampus, and both MPA and progesterone significantly increased GAD levels in the entorhinal cortex. These findings suggest that MPA, the most commonly used progestin in HT, is detrimental to learning and two types of memory, and modulates the GABAergic system in cognitive brain regions, in aged surgically menopausal rats. These findings, combined with in vitro evidence that MPA is detrimental to neuronal health, indicates that MPA has negative effects for brain health and function.
 ...
PMID:Medroxyprogesterone acetate impairs memory and alters the GABAergic system in aged surgically menopausal rats. 2007 54


1