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At least 19 recordsLinked to original sources
PubMed1978

Parameters of the dorsal bundle extinction effect: previous extinction experience.

Lesion to the dorsal noradrenergic bundle using the selective neurotoxin 6-hydroxydopamine which depleted telencephalic noradrenaline to less than 5% of control values was found to cause prolonged responding in extinction of a continuously reinforced (CRF) operant lever pressing response (a further replication of the dorsal bundle extinction effect). The parameters involved in causing this effect). The parameters involved in causing this effect were investigated, particularly the role of previous extinction experience. Although resistance to extinction was seen the first time animals were placed in extinction, it disappeared when they were retrained on CRF and extinguished a second time. Experience of extinction as part of the acquisition process, brought about by training on a successive visual discrimination, also prevented the development of over-responding in subsequent extinction. These results are discussed in the context of related demonstrations of the absence of the dorsal bundle extinction effect after partially reinforced acquistion training.

Animals↗
PubMed1979

The asymmetric lateralization of tactile extinction in patients with unilateral cerebral dysfunction.

Two hundred and thirty-four patients with unilateral cerebral pathology and 175 control subjects were examined with a sensitive test for tactile extinction. Damage to the right hemisphere was associated with extinction slightly (but not significantly) more often than damage to the left hemisphere; the asymmetry may be due to selective exclusion of aphasics with damage to the left hemisphere. Extinction of the left side of the body, however, was significantly more common than of the right side; this asymmetry could not be accounted for by exclusion of untestable aphasics, but was a consequence of frequent ipsilateral (left side) extinction among the group with damage to the left hemisphere while the group with damage to the right hemisphere extinguished the contralateral (left) side almost exclusively. Although the hemispheres as a whole did not differ in their association with extinction, lesions in the right parietal lobe were significantly more effective in producing extinction than lesions in the left; in both cases the contralateral side of the body was affected. By contrast, lesions in the left frontal lobe were moderately but not significantly more effective in producing extinction than right frontal damage; in almost all these cases the left side of the body was affected, regardless of which frontal lobe was damaged. A relationship between extinction and pathology in the vicinity of the anterior callosum, as determined from CT scan and angiography, was found among the frontal cases. We propose an anatomical model to explain tactile extinction and its asymetric characteristics in the human. During the extinction tests a response mechanism in the left (speech) hemisphere bases its perceptual output on the relative strengths of two simultaneous sensory inputs. Damage at any point in the channel from the periphery to the response mechanism weakens one signal in comparison to the other, resulting in a response bias favouring the stronger stimulus. Tactile information from the left hand, after reaching the somatosensory zone in the right hemisphere, is transmitted to the left hemisphere by a diffuse, widespread network including the frontal lobes and the anterior callosum. This anatomical arrangement renders left-hand information more vulnerable to chance lesions than right-hand information, which has direct access to the response mechanism via a more compact projection system.

Adolescent↗
PubMed1979

Differential extinction of 2-way active avoidance in young and adult rats.

Three experiments examined age-related differences in extinction of active avoidance in rats through manipulation of the stimulus context. In Experiment I, 36 weanlings and 36 adults acquired comparable avoidance levels to a tonal conditioned stimulus (CS), and novel stimuli consisting of either the presence of a naive rat or a light were presented during 2 tests in extinction. Results indicated more pronounced disruption of extinction in the pups, compared to adults, with the animate novel stimulus having the greater effect. Eighteen pups of 22 days of age and 18 adults in Experiment II were trained to avoid shock with a CS consisting of simultaneous tone and light onset. During extinction responses did not terminate 1 of the CS elements, but rather produced continuation of either the tone or light for an additional 5 sec. Continuation of the tonal element resulted in greater disruption of extinction trials than the light in the adults, although the pups had faster, but nondifferential, extinction rates. A 3rd experiment presented 36 pups and adults with either 0-, 5-, or 10-sec delays of tonal CS reactivation after extinction responses. Both 5- and 10-sec delays resulted in increased numbers of extinction trials in the adults, but the pups failed to respond differentially to any of the delay intervals. Results of all of the experiments were considered in light of species-specific behaviors in avoidance extinction relative to environmental and associative saliencies between ages.

Age Factors↗
PubMed1979

Extinction and synesthesia in patients with spinal cord injuries.

Extinction and synesthesia were studied in 50 patients with spinal cord injury with various levels and extents. Extinction was found in 20 (40 per cent) and synesthesia in 6 (12 per cent) of the 40 males and 10 females. No correlations were found between either of the two phenomena and parameters of patient's age, lesion's age, lesion's level and extent, or accompanying head injury. The latter occurred in 22/50 patients (44 per cent), diagnosed by a history of amnesia. Extinction was tested by synchronous double stimulation unilaterally and bilaterally, symmetrically and asymmetrically. It was more frequent unilaterally than bilaterally. The modalities of superficial sensibility were prone to be extinct but those of deep sensibility (pallesthesia from bone conduction and kinesthesia) were not. Extinction of tactile responses did not imply that all other skin modalities (pain, temperature, pressure, skin pallesthesia) will also be extinct in an all or nothing fashion. Modalities could become extinct either singly or in combination. Extinction in spinal man was presumed to be caused by a reduction of perception in hypesthetic areas and was of diagnostic value insofar as its segmental distribution suggested the longitudinal extent of a cord lesion. This concept is in accord with the results of monkey experiments by Eidelberg and Schwartz (1971). Synesthia in spinal man is not identical with synchiria of the monkey. It is not in a reciprocal relationship with extinction and both phonemena co-existed in four of the six patients. Synesthesia is elicited by a stimulus delivered to the normesthetic skin above the level of the lesion with two responses: one well localised at the site of stimulation and the other unilaterally or bilaterally in anaesthetic parts of the body. Five of the six patients reported volitional phantom movements of somatic (toes) and/or visceral (micturition-defaecation) structures. Such sensations are elicited by remembering the engrams of pre-traumatic experiences in areas of the body image connected with motor function. Synesthesia could be understood as a sensory counterpart in areas of the body image when ascending impules of actual perception are mixed with impulses modulated at the artifical synapse of the rostral cord stump creating a phantom sensation.

Adolescent↗
PubMed1976

Hormonal influences of the extinction of conditioned taste aversion.

Conditioned taste aversion for a 5% glucose solution (sugar water) was induced in rats by an i.p. injection of LiCl 30 min after the first presentation of sugar water. Extinction of conditioned taste aversion was measured either in the forced-drinking test or in the preference-drinking test. In the forced-drinking test sugar water was the only fluid presented to the animals during extinction sessions. In the preference-drinking test the animals had the choice of tap water or sugar water. The rate of extinction was much slower in the preference test. The ACTH-analogues, ACTH 4-10 and ACTH 4-10 7d Phe, and alpha-MSH delayed extinction in the preference test but not extinction in the forced-drinking test. ACTH 11-24 was without any effect. MSH-release inhibiting factor (MIF) facilitated extinction in the forced-drinking test but did not alter extinction in the preference test. The peptides did not affect intake of tap water of preference of sugar water over tap water by control rats.

Adrenocorticotropic Hormone↗
PubMed1978

The effect of morphine on fear extinction in rats.

Rats were trained on an appetitive discretetrial discriminated-punishment task in which they learned to suppress responding when an intense flashing light predicting punishment was present and to respond rapidly on trials when the flashing light was absent. Once animals were performing discriminatively, 0.75, 3.0, or 6.0 mg/kg of morphine (base) was administered and a fear extinction session consisting of 60 nonshocked presentations of the flashing light was given. Two saline control groups, one that received fear extinction and one that did not, were also included in the experiment. On the day following fear extinction, all rats were tested in the undrugged state on the discriminated punishment problem, but without shock. The rats receiving 3.0 and 6.0 mg/kg of morphine before the fear extinction session were suppressed by the flashing light more than the saline extinction group or the 0.75 mg/kg morphine treatment group. Moreover, the two higher dose morphine groups were suppressed as readily as the saline group that received no fear extinction. These results are attributed to the antiemotionality effects of morphine.

Animals↗
PubMedDate not supplied

[Effect of mammillary body ablation on extinctive inhibition in cats].

Chronic extinction of chain closed conditioned reflex in intact rabbits took five to six days. The order of extinction of the reflex links was as follows: the nearer to reinforcement the link of the chain, the sooner it was inhibited. In the course of extinction different "compensatory" movements appeared with a high frequency. Unlike the conditioned movements they were not fully extinguished: in the rest periods (lying for 4 to 10 min.), running and sniffing took place 4 to 8 times in the session. After the ablation of the mammilary bodies, extinctive inhibition was developing slower (9 to 13 days) than in the norm. The order of extinction became reverse: the nearer the link of the chain to reinforcement, the greater the difficulty of inhibition. The appearance of "compensatory" movements sharply differed from the norm. The general behaviour of the operated rabbits was peculiar in that during extinction of conditioned movements the short periods of rest (1 to 3 min.) alternated with running, sitting, scratching, washing, etc.

Animals↗
PubMed2026

De-extinction technology and its application to conservation.

De-extinction, once the realm of science fiction, has evolved into a tangible scientific endeavor thanks to breakthroughs in genome sequencing, engineering, advanced assisted reproductive technologies, and stem cell biology. Alongside this work are innovations in reintroduction science and artificial intelligence, which are refining strategies for species translocations, rewilding, and long-term ecosystem monitoring of de-extinct species and populations. While the primary motivation for de-extinction is restoring lost ecological functions to eroded ecosystems, each of these technologies can also be applied to conservation biology for de-endangerment, offering new solutions for biodiversity preservation. This review synthesizes the technological advancements emerging from de-extinction science and explores their broad applications in conservation, demonstrating how de-extinction is both about resurrecting lost species and about expanding the conservation toolkit to sustain and rebuild biodiversity in the face of accelerating environmental change.

Conservation of Natural Resources↗
PubMed2025

PUS7-dependent Ψ reshapes specific synaptic gene exons to facilitate fear extinction memory formation.

RNA modifications serve as dynamic regulators of neural plasticity through their ability to fine-tune transcript stability and splicing. Pseudouridine (Ψ), an evolutionarily conserved RNA modification catalyzed by pseudouridine synthases, plays established roles in neurodevelopment, yet its functional significance in activity-dependent behavioral adaptation remains poorly defined. Here, we investigate Ψ-mediated epitranscriptomic regulation within the infralimbic prefrontal cortex (ILPFC), a brain region requiring precise synaptic remodeling for the clinically relevant form of fear extinction memory. Combining transcriptome-wide pseudouridylation profiling with behavioral analysis in mice, we identified selective Ψ enrichment at exons of synaptic regulatory genes within ILPFC during fear extinction learning. Fear extinction in the ILPFC drives concomitant exonic Ψ deposition and upregulation of synaptogenic transcripts, processes that involve pseudouridine synthase PUS7. Crucially, PUS7 knockdown in the ILPFC selectively impaired fear extinction memory formation without altering baseline fear expression, establishing a causal link between Ψ-dependent RNA processing and activity-dependent synaptic structural remodeling in this microcircuit. Our findings demonstrate that PUS7-mediated Ψ modification spatiotemporally regulates activity-dependent RNA dynamics in the ILPFC, providing the evidence that epitranscriptomic mechanisms precisely coordinate synaptic gene expression within behaviorally defined brain sub-region. This work bridges molecular RNA biology with systems neuroscience, revealing a novel mechanism for activity-dependent regulation of fear extinction in ILPFC.

Animals↗
PubMed1978

Sensory extinction: a procedure form eliminating self-stimulatory behavior in developmentally disabled children.

This study was designed to investigate the role of sensory reinforcement in the motivation of self-stimulation. If self-stimulatory behavior is maintained by its sensory consequences, such as the proprioceptive, auditory, or visual stimulation it produces, then such behavior should extinguish when those sensory consequences are not permitted. The present study introduces a new procedure, Sensory Extinction, in which certain sensory consequences are masked or removed, to examine whether self-stimulation is operant behavior maintained by sensory reinforcement. The effectiveness of Sensory Extinction was assessed by a reversal design for each of three autistic children, and the results showed the following. First, self-stimulation reliably extinguished when a certain sensory consequence was removed, then increased when that consequence was permitted. This was replicable within and across children. Second, different Sensory Extinction procedures were required for different self-stimulatory behaviors, since the sensory reinforcers supporting them were idiosyncratic across children. Finally, regarding clinical gains, the data suggest that Sensory Extinction may be a relatively convenient and rapid alternative for the treatment of self-stimulation. The present findings extend the efficacy of extinction as a behavior-modification technique to instances in which the reinforcer is purely sensory. The implications of these results for the treatment of other forms of deviant behavior are discussed.

Autistic Disorder↗
PubMed1979

Modulation of behavioral inhibition in appetitive extinction following manipulation of adrenal steroids in rats: implications for involvement of the hippocampus.

Corticosterone, the principal glucocorticoid in the rat, binds selectively to the CA1 pyramidal neurons of the hippocampus where the hormone has been demonstrated to exert a moderate chronic suppression of spontaneous activity. In the first experiment of the current study, the functional behavioral significance of this hormone--brain interaction was investigated in the extinction of an appetitive runway response in normal rats and those with lesions of the hippocampus. During extinction, half of the animals in each group were given daily subcutaneous injections of corticosterone. Whie the classical retardation effect of hippocampal lesions on appetitive extinction was replicated, hormone treatment was without effect in normal or hippocampally damaged subjects. The absence of a hormone effect in normals was primarily attributed to a saturated limited-binding system operating in the normal animal. Experiment 2 tested this notion, repeating the first experiment, with adrenal-ectomized (ADX), ADX + corticosterone replacement, and normal groups of animals. Adrenalectomy produced a striking facilitation of extinction which was speculated to be the result of a hyperactive inhibitory neural organ free from an inhibitory endocrine feedback. Corticosterone treatment normalized the progress of extinction in ADX animals, providing support for the afore-mentioned speculation. In the normal animal, it appears that a stress-induced surge in hormone level interacts with a limited-capacity neural binding to produce a transient dynamic range of behavioral disinhibition, perhaps promoting persistence during initial stages of frustrative nonreward in moderate stress tasks.

Animals↗
PubMed2025

Illuminating the mystery of thylacine extinction: a role for relaxed selection and gene loss.

Gene loss shapes lineage-specific traits but is often overlooked in species survival. In this study, we investigate the role of ancestral gene loss using the extinction icon-thylacine (Thylacinus cynocephalus). While studies of neutral genetic variation indicate a population decline before extinction, the impact of thylacine-specific ancestral gene losses remains unexplored. The availability of a chromosomal-level genome of the extinct thylacine offers a unique opportunity for such comparative studies. Here, we leverage palaeogenomic data to compare gene presence/absence patterns between the Tasmanian devil and thylacine. We discovered ancestral (between 13-1 Ma) loss of SAMD9L, HSD17B13, CUZD1 and VWA7 due to multiple gene-inactivating mutations, corroborated by short-read sequencing. The timing of gene loss mirrors the thylacine's shift towards hypercarnivory and increased body size. Notably, the loss of SAMD9 correlates with a carnivorous diet. Our genome-wide analysis reveals olfactory receptor loss and relaxed selection, aligning with reduced olfactory lobes in the thylacine, indicating olfaction is not its primary hunting sense. By integrating palaeogenomic data with comparative genomics, our study reveals ancestral gene losses and their impact on species survival and resilience to environmental changes. Our approach can be extended to other extinct and endangered species, helping to identify genetic factors for conservation efforts.

Animals↗
PubMed1979

Piracetam facilitates retrieval but does not impair extinction of bar-pressing in rats.

Rats were trained on a continuously reinforced bar-press response for water reward. Seven days later they were retested for retention, with or without pretest injection of the nootropic drug, piracetam. Drug-treated animals had significantly shorter response latencies than saline-treated animals. The results are interpreted as a facilitation of retrieval processes after forgetting. The experiment was extended under extinction conditions and it was found that after three sessions there was a tendency to facilitate extinction when response latency is used as the extinction index. The clinical interest of a drug which facilitates the retrieval aspect of the memory process without impairing extinction is discussed.

Animals↗
PubMed1979

The dorsal bundle extinction effect:dependence on subtle changes in acquisition.

Destruction of the ascending noradrenergic innervation to the forebrain in rats by intracerebral injection of the selective neurotoxin 6-hydroxydopamine (4 microgram in 2 microliter injected bilaterally into the dorsal bundle in the mesencephalon) was found to cause resistance to extinction of a continuously reinforced lever press response. However, this effect occurred only if the lesion were present during acquisition training on the reinforced schedule and not if intact animals were trained and the lesion inflicted after completion of acquisition training and just prior to the extinction phase. Thus, the behavioural effect that manifests itself during extinction appears to be due to subtle changes in the acquisition learning process. This is consistent with the predictions of an attentional theory of noradrenergic function and appears to exclude most other suggested explanations of the dorsal bundle extinction effect.

Animals↗
PubMed1979

Dorsal bundle extinction effect: motivation or attention?

Male albino Wistar rats were injected bilaterally with 4 micrograms of 6-hydroxydopamine into the dorsal noradrenergic bundle to deplete forebrain noradrenaline to less than 5% of control values. Acquisition learning of a fixed interval schedule or a continuously reinforced schedule was not altered but resistance to extinction was seen after food reinforced training on either schedule but not after water reinforced training. A possible increase in food motivation was tested by the use of preloading with free food prior to a fixed interval session but both control and lesioned rats reacted similarly to this manipulation thus appearing to exclude an increase in food motivation. An attentional explanation is proposed and tested by the demonstration that resistance to extinction does not occur after a partially (variable ratio 4), as opposed to a continuously, reinforced schedule. Further evidence in favour of an attentional mechanism comes from the finding that on both a fixed interval and a continuously reinforced schedule the lesion has to be present during the acquisition phase to result in subsequent resistance to extinction. Intact animals trained on either schedule and subsequently subjected to the lesion failed to show an increased resistance to extinction.

Animals↗
PubMed1979

Possible involvement of serotonin in extinction.

In Experiment 1, rats were trained to leverpress for continuous reinforcement with food; half were then intubated with the serotonin synthesis inhibitor parachlorophenylalanine (PCPA: 400 mg/kg) and half with water. In extinction the PCPA-treated rats responded at a higher rate. In Experiment 2, rats were trained on a random interval schedule and then assigned to two groups, treated as in Experiment 1, and tested in extinction. There was no significant difference in the resistance to extinction of the two groups. In Experiment 3, the responding of rats trained in a punished stepdown response paradigm and then given an intragastric injection of PCPA took longer to recover than the responding of water-injected controls. These observations suggest that serotonergic neurons might play a role in extinction processes.

Animals↗