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[Determination of prostaglandinum E1 by fluorescence extinction method].

In this paper, we have studied the fluorescence extinction effect of methyl alcohol by prostaglandinum E1 (PG E1) and found the linear relation between the fluorescence extinction intensity and prostaglandinum E1 concentration. Its linear equation is deltaF = 0.222c + 9.33 x 10(-2)(deltaF: fluorescence extinction value; c: PG E1 concentration microg/mL), correlation coeficient r = 0.99930. The results derived from fluorescence extinction method correspond to the results from violet spectrophotometric method.

Alprostadil↗

The evolution of California's wild radish has resulted in the extinction of its progenitors.

If two previously isolated taxa mutually assimilate through hybridization and subsequent biparental introgression, and if their introgressed descendants have the same or higher fitness than their parents, then gene flow should result in the local extinction of parental taxa via replacement by hybrid derivatives. These dramatic events may occur rapidly, even in a few generations. Given the speed at which such extinction by hybridization may occur, it may be difficult to identify that the process has occurred. Thus, documented instances of extinction by hybridization are rare, and especially so for cases in which both parents are replaced by the hybrid lineage. Here we report morphological and allozyme evidence for the local extinction of two Raphanus species in California via replacement by their hybrid-derived descendants. The results from a greenhouse experiment demonstrate that California wild radishes have a specific combination of traits from their progenitors, and comparison of our results to that of an earlier report indicate that pure parental types are no longer present in the wild. Our results also show the hybrid-derived lineage has transgressive fruit weight compared to its parents. Allozyme analysis demonstrates that California wild radishes are derived from hybridization between the putative parental species. However, that analysis also demonstrates that California wild radish has now become an evolutionary entity separate from both of its parents. We suggest that the aggressive colonizing behavior of the hybrid-derived lineage probably results from a novel combination of parental traits, rather than genetic variability of the population per se.

Biodiversity↗

[Short and long latent effects of 15-hydroxyeicosatetraenoic acid on the extinction of the acetylcholine-induced inward current in neurons of the Helix lucorum].

The impact of a non-cyclized arachidonic acid derivative 15S-hydroxy-5Z, 8Z, 11Z, 13E-eicosatetraenoic acid (15-HETE) upon the dynamics of the inward current extinction, caused by repeated ion-tophoretic acetylcholine applications on the soma, was studied through a double electrode voltage clamp technique on the Helix lucorum identified neurons RPa3 and LPa3. The extracellular effect of 15-HETE (4-16 microM) was found to have a two phase influence on the inward current extinction, depending on the time of exposure to the compound. The short-latent effect (up to 60-80 min) displays itself as an extinction decrease, whereas the long-latent effect (after 60-80 min) - as an enhanced extinction. The effects caused by 15-HETE are irreversible. The short-latent one was probably due to the earlier described inhibition of 5- and 12-lipoxygenase enzymes by 15-HETE while the long-latent one - due to its intrinsic function.

Acetylcholine↗

Extinction of expression of the PU.1/Sfpi-1 putative oncogene encoding a B-cell- and macrophage-specific transcription factor in somatic cell hybrids.

Several examples of extinction of cell type-specific gene expression have been observed following fusion of different cell types. Possible mechanisms of the extinction include loss of transcriptional activators and acquisition of repressor factors responsible for cell type-specific gene expression. In this study, we demonstrated the extinction of expression of the PU.1/Sfpi-1 putative oncogene encoding a B-cell- and macrophage-specific transcription factor when plasmacytoma cells are fused with embryonal carcinoma (EC) cells. The hybrid cells retained most chromosome complements from both parental lines including chromosome 2 on which the PU.1 gene is located. Therefore, extinction of PU.1 gene expression in the hybrids is not likely the result of chromosome segregation but rather due to a transacting negative factor(s) present in EC cells. On the contrary, expression of the PU.1 mRNA in plasmacytoma cells was not extinguished upon cell fusion with T-lymphoma cells, although the parental T-lymphoma cells did not express PU.1 transcripts. Hence, T-lymphoma cells seemed to be permissive to PU.1 gene expression, while EC cells were repressive. These results suggest that PU.1 gene expression which positively regulates some B cell- and macrophage-specific gene expression is a target of negative regulatory mechanisms during cell differentiation, and the regulatory mechanisms repressing PU.1 gene expression is different between EC cells and T-cells.

Animals↗

[Tactile extinction following the cerebral sinus thrombosis. A study using event-related potentials].

We reported a 46-year-old woman in whom cerebral sinus thrombosis manifested itself in headache and weakness while she was on an oral estrogen preparation. The neurological examinations revealed monoparesis of the right upper extremity, hyperactive right deep tendon reflex and disturbance of the joint sense, stereognostic sense, two-point discrimination and skin writing sense in the right upper extremity, in addition to tactile extinction. Brain CT showed empty triangle sign. MRI revealed infarction near the left postcentral gyrus and thrombosis of right sigmoid sinus. In the MRA study, there was low signal intensity in the posterior portion of the superior sagittal sinus and right transverse sinus. Short latency SEP in upper extremity showed that the central conduction time was normal, while the amplitude of wave components after N20 was reduced on the right side. Both palms were given bilateral or unilateral pressure stimuli. When event-related potentials (ERP) were evoked, using bilateral stimuli as a rare target, and left unilateral stimuli as a non-target, the P 300 latency was prolonged to 450 msec but was restored to normal with the improvement of tactile extinction. These results seem to suggest that the tactile extinction is ascribable to a disturbance of recognition at the higher brain function level and that ERP can be a useful objective yardstick in the evaluation of extinction phenomenon.

Event-Related Potentials, P300↗

Migration, extinction, and alary morphism in water-striders (Gerris Fabr.)

A migration-extinction model has been developed for the analysis of alary polymorphism and its adaptive significance in univoltine populations of water-striders (Gerris). It is assumed that all actual and potential population sites are identical with respect to all relevant variables, i.e. that populations do not live in a 'harlequin' environment. The model can be applied to other groups with alary polymorphism. The effects of isolation, environmental stability, and environmental productivity are discussed, with numerical examples. Isolation and stability enhance the optimality of short-wingedness, while temporariness of population sites selects for long-wingedness. Optima cannot always be realized. The models reveal several critical variables which are of interest in the ecological genetics of Gerris and which should be measured in natural populations: (a) extinction probabilities (a distinction being drawn between extinction due to drying up of the population site and extinction due to other causes), (b) extent of passive dispersal, and (c) the proportion of colonized population sites in a large geographical region.

Adaptation, Biological↗

Effect of amount of training on rate and duration of responding during extinction.

Four experiments are reported in which the amount of CRF training prior to extinction is examined as it effects transient changes in response frequency and duration immediately following extinction onset. The first two experiments, using albino rats as subjects and water reinforcement, revealed a reliable relationship between length of time on CRF and the tendency to increase response frequency, duration, and the variability of response frequency and duration. Two comparative experiments were conducted using 53-to-69-month old children as subjects, and recorded music as reinforcement. The results of the first child study failed to conform with those obtained in the rat experiments. However, manipulation of the reinforcer in a subsequent study reproduced the rat extinction effect. Despite the differences in the rat and child experiments, the qualitative similarity of the results of the four studies suggests a basic underlying comparability of the relationship between the amount of training and transient changes in response frequency.

Animals↗

Extinction deficits in male rhesus macaques with a history of self-injurious behavior.

Self-injurious behavior (SIB) occurs in both human and nonhuman primate populations. Despite the potential for harm, SIB may persist in part because of an inability to inhibit behavior that results in wounding. A lever-pressing task was used to test the prediction that monkeys with SIB would show greater persistence in lever-pressing on extinction trials than monkeys without the disorder. The subjects were 15 individually-housed adult male rhesus macaques, 10 of which (the SIB group) had a veterinary record of self-inflicted wounding. All of the monkeys were trained to lever-press for food rewards to a criterion of 400 total responses. The test procedures consisted of five daily 30-min sessions divided into six 5-min intervals. On day 1, the subjects received continuous reinforcement. On days 2-4, testing consisted of alternating reinforced/unreinforced 5-min intervals, beginning with reinforcement. Reinforced intervals were cued with a buzzer. On day 5, the subjects received no reinforcement. The number of lever-presses and behavioral responses were recorded during each session. Saliva samples were collected for cortisol measurement before and after test sessions on days 1, 2, and 5. As predicted, monkeys with SIB lever-pressed more than controls during extinction intervals on days 2-4. There was no difference on day 1 or day 5. The frequency of scratching, yawning, and abnormal behavior increased when reinforcement was intermittent (days 2-4) or absent (day 5). Cortisol levels were highest with continuous reinforcement (day 1), and may reflect differential levels of food intake rather than stress. The presence of extinction deficits suggests that SIB may persist in some monkeys because they lack the ability to regulate the intensity of their biting behavior.

Analysis of Variance↗

The role of NMDA glutamate receptors, PKA, MAPK, and CAMKII in the hippocampus in extinction of conditioned fear.

Pavlovian conditioning involves the association of initially neutral conditioned stimuli (CS) with unconditioned stimuli (US) that elicit a response. In contextual fear conditioning in rodents, the CS is the context of a training apparatus and the US is a foot shock. Retrieval of memory of the training is tested by presenting the CS alone. But a retrieval test also initiates extinction of the conditioned response. That is, presentation of the CS alone results in new learning, i.e., the CS no longer predicts the US. Here we report that extinction is triggered by two hippocampal signaling pathways underlying retrieval (the cAMP-dependent protein kinase and the mitogen-activated protein kinase pathways) and two other mechanisms that become activated at the same time and are not necessary for retrieval (N-methyl-D-aspartate glutamatergic receptors and the calcium/calmodulin-dependent protein kinase II signaling pathway). Thus, the molecular mechanisms underlying acquisition and/or consolidation of the memory for extinction are similar to those described for the acquisition and/or consolidation of the original contextual fear.

Animals↗

Contribution of ventrolateral prefrontal cortex to the acquisition and extinction of conditioned fear in rats.

The ventrolateral, agranular insular portion of prefrontal cortex (PFC) in rats is involved in visceral functions and has been shown to be involved in emotional processes. However, its contribution to aversive learning has not been well defined. Classical fear conditioning has been a powerful tool for illuminating some of the primary neural structures involved in aversive emotional learning. We measured both the acquisition and the extinction of conditioned fear following lesions of the ventrolateral PFC of rats. Lesions reduced fear reactivity to contextual stimuli associated with conditioning without affecting CS acquisition, and had no effect on response extinction. Ventrolateral PFC may normally be involved in the processing of contextual information while not being directly involved in extinction processes within the aversive domain.

Animals↗

No sex difference in contextual control over the expression of latent inhibition and extinction in Pavlovian fear conditioning in rats.

Three experiments with Wistar rats searched for a sex difference in contextual control over the expression of latent inhibition and extinction. Experiment 1 used a latent inhibition procedure; Experiments 2 and 3 employed an extinction preparation. All experiments used a shock as the unconditioned stimulus, a tone as the conditioned stimulus, and suppression of food magazine visits as the measure of conditioned responding to the tone. Each experiment revealed a reliable context effect on conditioned responding to the tone; after conditioning in a separate context, conditioned responding in the former latent inhibition or extinction context was attenuated relative to conditioned responding in a control context. There was no sex difference in the magnitude of this effect. These results are discussed in the framework of sex differences in the hippocampus and of the putative role of this structure in various instances of contextual learning.

Acoustic Stimulation↗

The effects of compounds related to gamma-aminobutyrate and benzodiazepine receptors on behavioural responses to anxiogenic stimuli in the rat: extinction and successive discrimination.

In a first set of experiments rats were trained to run in a straight alley for food reward on a continuous reinforcement schedule and the running response was then extinguished. On the last 2 days of training and daily throughout extinction different groups of animals were injected IP with saline, 5 mg/kg chlordiazepoxide, 0.75 mg/kg picrotoxin, chlordiazepoxide + picrotoxin, chlordiazepoxide + 1.5 mg/kg bicuculline, 0.00125 or 0.25 mg/kg muscimol, 1 mg/kg baclofen, chlordiazepoxide + baclofen, or 0.00125 mg/kg muscimol + baclofen. Chlordiazepoxide increased resistance to extinction, a well-known anxiolytic effect. This effect was blocked by both picrotoxin and bicuculline. Picrotoxin on its own reduced resistance to extinction (an anxiogenic-like effect). Whether given alone or in combination with other drugs, muscimol and baclofen had no effect. In a second set of experiments rats were trained in a successive operant discrimination (signalled by a flashing or steady light) between components in which sucrose reward was available on a variable-interval schedule for barpressing and components in which no reward was given. Chlordiazepoxide at 10 mg/kg increased responding in both rewarded and nonrewarded components, but more in the latter than could be accounted for by change in the former. This effect is as expected with an anxiolytic drug. It was not altered by administration of bicuculline at 1.5 or 1.75 mg/kg; at 2 mg/kg bicuculline acted synergistically with chlordiazepoxide. Picrotoxin (1 and 1.5 mg/kg) also acted synergistically with chlordiazepoxide, enhancing the latter's rate-increasing effects, but only during rewarded components. Neither muscimol (0.00125 and 0.25 mg/kg) nor baclofen (0.01 mg/kg) affected response rates, whether given alone or in combination. However, baclofen in a dose of 1 mg/kg, provided it was given to rats also injected with muscimol (0.00125 or 0.25 mg/kg) at other times, significantly reduced responding during nonrewarded components (an apparently anxiogenic effect). The results of the two sets of experiments are discussed in relation to the hypothesis that anxiolytic drugs affect behaviour by increasing GABAergic inhibition.

Animals↗

Tests of functional equivalence between pimozide pretreatment, extinction and free feeding.

Both pimozide pretreatment and free feeding caused within-session and between-session decrements in variable interval operant performance; response decrements generated under pimozide were maintained on transfer to free feeding, and vice versa. On subsequently testing under extinction conditions (after food deprivation and drug free) large initial increases in responding were seen in all groups, and subsequent response decrements in extinction were steeper than in either pimozide or free feeding conditions. The effects of pimozide pretreatment do not resemble those of extinction, but may in some circumstances be functionally equivalent to a decrease in drive level.

Animals↗

Resistance to extinction after schedules of partial delay or partial reinforcement in rats with hippocampal lesions.

Two experimental procedures were employed to establish the reason why hippocampal lesions apparently block the development of tolerance for aversive events in partial reinforcement experiments, but do not do so in partial punishment experiments. Rats were trained to run in a straight alley following hippocampal lesions (HC), cortical control lesions (CC) or sham operations (SO), and resistance to extinction was assessed following differing acquisition conditions. In Experiment 1 a 4-8 min inter-trial interval (ITI) was used. Either every acquisition trial was rewarded immediately (Continuous Reinforcement, CR), or only a randomly selected half of the trials were immediately rewarded, the reward being delayed for thirty seconds on the other trials (Partial Delay, PD). This delay procedure produced increased resistance to extinction in rats in all lesion groups. In Experiment 2 the ITI was reduced to a few seconds, and rats were trained either on a CR schedule, or on a schedule in which only half the trials were rewarded (Partial Reinforcement, PR). This form of partial reinforcement procedure also produced increased resistance to extinction in rats in all lesion groups. It thus appears that hippocampal lesions only prevent the development of resistance to aversive events when the interval between aversive and subsequent appetitive events exceeds some minimum value.

Animals↗

Fornix-fimbria section and the partial reinforcement extinction effect.

Rats were trained to run in an alley for food reward given on every trial (continuous reinforcement, CR) or on a random 50% of trials (partial reinforcement, PR) and were then extinguished. Sham-operated controls showed the normal partial reinforcement extinction effect (PREE), in that PR-trained animals were significantly more resistant to extinction than CR-trained animals. The PREE was significantly reduced by lesions of the fornix-fimbria. The reduction was largely a consequence of a reduction in resistance to extinction in PR-trained rats with fimbria-fornix lesions. These results are discussed in the light of other experiments that have studied disconnections in the septo-hippocampal system.

Animals↗

Comparison in the mouse of the effect of the opiate delta receptor antagonist ICI 154129 and naloxone in tests of extinction, passive avoidance and food intake.

The effects of 30 and 80 mg/kg ICI 154,129, an opiate delta receptor antagonist, were compared with those of 0.1 and 10 mg/kg naloxone using tests of food-intake, passive avoidance and extinction in mice. Whereas naloxone depressed food intake and facilitated extinction, ICI 154,129 failed to affect food intake, passive avoidance or extinction although the mice reared significantly more during the test of food intake.

Animals↗

Effects of intraventricular glutamic acid on the acquisition, performance, and extinction of an operant response, and on general activity.

This study was designed to investigate the effects of intracerebral injections of glutamic acid on acquisition and extinction of a bar-press response, performance of that response, and behavior activity. Nineteen food-deprived rats bearing chronic ventricular cannulae were tested in operant conditioning chambers or in an open field. Just prior to each testing session each animal was injected intraventricularly with 10 mul of either normal or acidified saline solution (control groups), or 10 mul of 100 mMol glutamic acid solution. Acquisition of the bar-pressing response by the glutamic acid group was significantly retarded as compared to the control groups, and the responding of the glutamic acid group was suppressed during the beginning of the first few sessions of testing on a fixed-interval schedule and during extinction. Other behavioral measures, such as operant level, performance of the response on a continuous schedule, performance on fixed-interval and extinction schedules except during the start of the first few sessions, and behavioral activity, were either unaffected or only slightly affected. It is concluded that interference with the normal neurophysiological activity of glutamic acid in the central nervous system interferes with learning and suppresses behavioral output in certain situations.

Animals↗

Effect of angiotensin II and vasopressin on acquisition and extinction of conditioned avoidance in rats.

The effect of angiotensin II on the acquisition and extinction of a conditioned avoidance response was examined in rats. Angiotensin II, 1 and 2 micrograms, given intracerebroventricularly facilitated acquisition of the conditioned avoidance response but did not influence extinction. [Sar1, Ile8]-angiotensin II (1 microgram), a specific antagonist of angiotensin II receptors, unexpectedly produced an effect quite similar to that of angiotensin II. Vasopressin (1 microgram) did not influence the rate of acquisition of the conditioned avoidance response but it markedly delayed its extinction. The data are discussed in terms of learning and memory facilitating properties of angiotensin II. This action seems to be independent of an interaction of angiotensin II with its known receptors or of release of vasopressin caused by the peptide.

Angiotensin II↗