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PubMed2002

Split-second escape decisions in blue tits (Parus caeruleus).

Bird mortality is heavily affected by birds of prey. Under attack, take-off is crucial for survival and even minor mistakes in initial escape response can have devastating consequences. Birds may respond differently depending on the character of the predator's attack and these split-second decisions were studied using a model merlin (Falco columbarius) that attacked feeding blue tits (Parus caeruleus) from two different attack angles in two different speeds. When attacked from a low attack angle they took off more steeply than when attacked from a high angle. This is the first study to show that escape behaviour also depends on predator attack speed. The blue tits responded to a high-speed attack by dodging sideways more often than when attacked at a low speed. Escape speed was not significantly affected by the different treatments. Although they have only a split-second before escaping an attack, blue tits do adjust their escape strategy to the prevailing attack conditions.

Animals↗
PubMed2002

5-HT2C receptor mediation of unconditioned escape behaviour in the unstable elevated exposed plus maze.

RATIONALE AND OBJECTIVES: m-Chlorophenylpiperazine (mCPP) induces panic in humans and dose dependently increases unconditioned escape behaviour in a novel pre-clinical model of extreme anxiety in rats, the unstable elevated exposed plus maze (UEEPM). Numerous studies indicate that the anxiogenic effects of mCPP may be mediated by its action at the 5-HT2C receptor. This study aimed to examine the involvement of the 5-HT2C receptor in the unconditioned fear responses observed in the UEEPM (after an acute dose of mCPP) by pre-treatment with the selective 5-HT2C receptor antagonist SB-242084. METHODS: Male Hooded Lister rats received a single dose of SB-242084 (0.1-1.0 mg/kg IP) or vehicle 40 min pre-test followed by a single dose of mCPP (1.0 mg/kg IP) or saline 30 min before being exposed to the UEEPM for a period of 5 min. Subjects' behaviour was analysed to determine the effects of SB-242084 on mCPP-induced increases in escape behaviour. RESULTS: mCPP alone increased animals' propensity to escape from the UEEPM despite producing marked decreases in locomotor/exploratory behaviour. SB-242084 dose dependently inhibited the increases in escape and hypolocomotor effects induced by mCPP. CONCLUSIONS: These results suggest that the escape-related behaviours exhibited by animals in the UEEPM are mediated, at least in part, by activation of the 5-HT2C receptor subtype.

Aminopyridines↗
PubMed2003

Acute effects of gabapentin on laboratory measures of aggressive and escape responses of adult parolees with and without a history of conduct disorder.

RATIONALE: The possible role of GABA in human aggression was evaluated by administering gabapentin to subjects with and without a history of conduct disorder and comparing the effects on laboratory measures of aggression and escape. METHODS: Eighteen male and two female subjects with a history of criminal behavior participated in experimental sessions, which measured aggressive and escape responses. Ten subjects had a history of childhood conduct disorder (CD+) and ten subjects with no history (non-CD controls). Aggression was measured using the Point Subtraction Aggression Paradigm (PSAP), which provided subjects aggressive, escape and monetary reinforced response options. RESULTS: Acute doses (200, 400 and 800 mg) of gabapentin had similar effects on aggressive responses among CD+ subjects compared to non-CD control subjects. Aggressive responses of CD+ and non-CD control subjects increased at lower gabapentin doses, and decreased at the highest 800 mg gabapentin dose. Gabapentin increased escape responses for both CD+ and non-CD controls CD- subjects at the lowest dose, but then produced dose-related decreases at the two higher doses in both groups. No changes in monetary reinforced responses were observed, indicative of no CNS stimulation or sedation. CONCLUSIONS: Gabapentin produced similar bitonic effects upon aggressive and escape responses in subjects with and without a history of childhood conduct disorder. This is in marked contrast to prior differential effects of baclofen on aggressive responses between CD+ and non-CD control subjects in a previous study.

Acetates↗
PubMed1991

Working memory and the aged rat: deficient two-choice win-stay water-escape acquisition and retention.

Twelve aged (22 months), 12 adult (12 months) and 12 young (3 months) male Fisher 344 rats were compared on acquisition of a two-choice win-stay (spatial delayed matching-to-sample) water-escape working memory task. The 7 aged, 10 adult and 10 young animals that attained criterion were then compared on performance of the task when the retention interval (RI) was 5, 15, 30, 60 and 120 min. They were also compared on retention after being forced to perform an unsolvable water-escape task in a second maze during the first 5 minutes of a 30-minute RI. The aged animals had longer escape latencies, and required more trials and made more errors in attaining a criterion of 9 correct choices over 10 test trials than did the adult and young animals, who did not differ from one another. Also, comparisons of the animals that attained the acquisition criterion revealed that the aged animals had longer escape latencies and made more errors across all RIs and during trials including an interpolated distraction task than did the adult and young animals. The aged animals failed to perform above chance level on tests at any of the RIs or following the distraction task, while the young animals performed above chance level on tests at all intervals and following distraction. The adult animals failed to perform above chance on tests with the 120-minute RI or following distraction. The aged rats were clearly deficient on acquisition and retention of a two-choice water-escape working memory task.

Aging↗
PubMed1976

A dose-response study of anorectic drug effects on food intake, self-stimulation, and stimulation-escape.

A comparison was made of the short-term effects in rats of 3 anorectic drugs (amphetamine, fenfluramine, and phenylpropanolamine) on food intake and responses to obtain brain stimulation and to escape from automatic brain stimulation. At a dose which decreased food intake, amphetamine increased self-stimulation, but not stimulation-escape. Fenfluramine decreased both self-stimulation and stimulation-escape. Phenylpropanolamine, on the other hand, decreased self-stimulation, but not stimulation-escape. Even though all 3 drugs decreased food intake, each of them had different effects on hypothalamic self-stimulation and stimulation-escape. Only the actions of phenylpropanolamine were in agreement with the hypothesis that lateral hypothalamic reward and aversion reflect the animal's tendency to eat, suggesting that other aspects of reinforcement are also involved in lateral hypothalamic stimulation and were affected differently by these drugs.

Amphetamine↗
PubMed1981

Escape and approach induced by brain stimulation: a parametric analysis.

The study reported pursued two general aims: (a) to find out whether a brain-stimulation-induced escape response results from the bringing into play of similar mechanisms irrespective of whether the stimulation is applied to a site located in the mesencephalic central gray (CG), in the medial hypothalamus (MH) or in the lateral hypothalamus (LH); and (b) to verify whether escape and approach that can be induced by stimulating one and the same hypothalamic site result from a combined activation of two distinct neuronal systems, by means of specifying some of their functional characteristics that would possibly allow differentiation between them. Three experiments were carried out using a situation (shuttle-box) that allowed the measurement, for each given brain site, of both the time for which the rat underwent the stimulation before interrupting it (stimulation time, st., corresponding to an escape latency) and the time for which the animal remained non-stimulated before eventually restarting the stimulation himself (non-stimulation time, nst, corresponding to an approach latency). The following stimulation parameters were varied: the pulse duration (D), the stimulation intensity (I) and the interpulse interval (IPI = 1/stimulation frequency), i.e. the time interval that separated the beginning of a stimulating pulse from the beginning of the next one. The results obtained suggest the following. (1) Some of the mechanisms implicated in the elaboration of an escape response are similar irrespective of whether escape is induced by stimulating a site located in the CG, in the MH or in the LH.

Animals↗
PubMed1983

Effects of dorsal raphe stimulation on escape induced by medial hypothalamic or central gray stimulation.

Electrical stimulation of the ventral part of the mesencephalic central gray affects escape responding induced by stimulation of either the medial hypothalamus (MH) or dorsal central gray (CG) in the rat. The sign and magnitude of the effect appeared to depend on the following factors: (1) The location of the site stimulated in the ventral central gray and the intensity of the stimulation. A stimulation of the dorsal raphe nucleus (DR) which induced a marked rewarding and a low aversive effect reliably suppressed MH or CG induced escape. Stimulation of sites located at the boundary between DR and central gray enhanced escape at low intensities and suppressed it at higher intensities. When located more laterally in the ventral central gray, the stimulation induced less rewarding and more marked aversive effects and it reliably enhanced MH or CG induced escape. (2) The kind of stimulation applied (monopolar or bipolar). (3) The location of the site (MH or CG) from which the stimulation-induced escape responses were obtained.

Animals↗
PubMed1986

Approach and escape responses to mesencephalic central gray stimulation in rats: effects of morphine and naloxone.

Two experiments were conducted to examine whether regional differences in mesencephalic central gray (CG) could be delineated according to the reinforcing (rewarding and/or punishing) effects of electrical stimulation of CG, and whether such reinforcing properties of CG stimulation would be mediated by endogenous opioid system. In Expt. I, rats with electrodes in CG were trained to turn CG stimulation on and off by running from one compartment to another in a shuttlebox. Rats whose electrode tips were verified at the ventral part of CG, showed both approach and escape responses to the brain stimulation, while those stimulated to more dorsal CG yielded only escape response. In Expt. II, effects of morphine (4 and 8 mg/kg) and naloxone (2 and 10 mg/kg) were investigated for 3 h after injection in the rats which showed both approach and escape responses to CG stimulation in Expt. I. Naloxone significantly increased approach latency to CG stimulation without any effect on escape latency. On the other hand, morphine markedly enhanced the number of shuttling responses and tended to decrease approach latency to stimulation in the late postinjection period, although it increased both approach and escape latencies in the early period. The results were discussed in terms of rewarding and punishing effects of CG stimulation and their underlying endogenous opioid-opiate receptor mechanism.

Animals↗
PubMed1998

The higher the dose, the greater the sex differences in escape-avoidance response in mice after acute administration of haloperidol.

Sex differences in the effects of haloperidol in the escape-avoidance response have previously been found in various studies carried out in our laboratory in which mice were used as experimental subjects. Males were more affected than females by the disruptive effects of this neuroleptic of frequent clinical use. In the present work these sex differences were evaluated in a unique training session using several doses of the drug (0.075, 0.25, and 0.75 mg/kg i.p.). The number of avoidances, escapes, nonresponses, crossings during the adaptation period, crossings during intertrial intervals, and response latencies were analyzed. Statistically significant sex differences were found in the number of escapes and nonresponses: males showed fewer escape responses and more nonresponses than females. These sex differences were dose dependent: a positive correlation was obtained between doses of haloperidol and sex differences observed in the number of escapes and nonresponses. The higher the dose, the greater the sex differences. These are related not only to the impairment of motor activity, because no sex differences were found in the number of crossings during the adaptation period and intertrial intervals.

Animals↗
PubMed1988

Recovery of escape locomotion following a CNS lesion in Aplysia.

The recovery of escape locomotion in Aplysia following a CNS lesion was investigated. The connectives between the cerebral and pleural ganglia were crushed in anesthetized animals, producing a specific behavioral deficit. Animals with lesions failed to initiate escape locomotion in response to tail shock. Tail withdrawal and inking which were also evoked by tail shock were still present. Other behaviors such as normal locomotion and feeding were not impaired. There was gradual recovery from the effects of the lesion. Animals with lesions began to respond to tail shock with weak pedal waves at long latencies after 7-13 days. The responses grew more vigorous and the latencies decreased over subsequent days. Full escape locomotor responses were observed as early as 15 days postlesion. By Postlesion Day 27, all of the animals had completely recovered and gave full escape responses. The mean latency of the escape locomotor response in recovered animals was not significantly different from prelesion control values. In behaviorally recovered animals, retrograde tracing from a point distal to the lesion site stained neurons in the cerebral ganglion. Intracellular dye injections of individual neurons revealed sprouting of new processes. Stimulation of the tail nerve and individual neurons demonstrated synaptic connections between cerebral and pleural ganglia neurons. These results suggest that the observed behavioral recovery was due to pleural ganglia neurons regenerating and forming appropriate synaptic connections in the cerebral ganglion.

Animals↗
PubMed2001

The Mauthner cell and other identified neurons of the brainstem escape network of fish.

This paper reviews the development of our research on the motor consequences of Mauthner cell function and related brainstem neurons. These cells activate fast-start responses such as seen in fishes escaping from predatory attacks. Our goal was to devise a neuroethological theory of fish escape that accurately reconciled the underlying neural function with a correct concept of the motor act. The identified neuron concept of invertebrates greatly influenced the initial studies. Horseradish peroxidase technology allowed us and other workers to identify principal neurons in the brainstem escape system. Digital imaging technology permitted adequate kinematic characterization of the behavior. Resulting experiments showed that Mauthner system demonstrates two general principles of motor organization: (1) the Mauthner cell is a command-like higher order neuron that serially outputs to a lower level central pattern generator; and (2) the Mauthner cell participates in a larger parallel, brainstem escape network. In this network, we showed that the spatio-temporal pattern of activity codes the timing and magnitude of agonist and antagonist trunk muscle contractions during the behavior. Because the approach angle of the stimulus determines these parameters, we were able to discover the overall sensorimotor relationship between stimulus angle and motor output. This relationship is given as a set of descriptive equations written in terms of stimulus angle, magnitude and timing variables of trunk muscle contractions, and resulting escape trajectory. The equations unify the apparent variability of C-start movement patterns into a single, quantitative theory. Recent studies by other workers show how this concept can make accurate predictions about the underlying neural processes, even at the level of the single, identified cell.

Animals↗
PubMed1997

Activity wheel running reduces escape latency and alters brain monoamine levels after footshock.

We examined the effects of chronic activity wheel running on brain monoamines and latency to escape foot shock after prior exposure to uncontrollable, inescapable foot shock. Individually housed young (approximately 50 day) female Sprague-Dawley rats were randomly assigned to standard cages (sedentary) or cages with activity wheels. After 9-12 weeks, animals were matched in pairs on body mass. Activity wheel animals were also matched on running distance. An animal from each matched pair was randomly assigned to controllable or uncontrollable inescapable foot shock followed the next day by a foot shock escape test in a shuttle box. Brain concentrations of norepinephrine (NE), dopamine (DA), dihydroxyphenylacetic acid (DOPAC), 5-hydroxytryptamine (5-HT), and 5-hydroxyindole acetic acid (5-HIAA) were assayed in the locus coeruleus (LC), dorsal raphe (DR), central amygdala (AC), hippocampus (CA1), arcuate nucleus, paraventricular nucleus (PVN), and midbrain central gray. After prior exposure to uncontrollable foot shock, escape latency was reduced by 34% for wheel runners compared with sedentary controls. The shortened escape latency for wheel runners was associated with 61% higher NE concentrations in LC and 44% higher NE concentrations in DR compared with sedentary controls. Sedentary controls, compared with wheel runners, had 31% higher 5-HIAA concentrations in CA1 and 30% higher 5-HIAA concentrations in AC after uncontrollable foot shock and had 28% higher 5-HT and 33% higher 5-HIAA concentrations in AC averaged across both foot shock conditions. There were no group differences in monoamines in the central gray or in plasma prolactin or ACTH concentrations, despite 52% higher DA concentrations in the arcuate nucleus after uncontrollable foot shock and 50% higher DOPAC/DA and 17% higher 5-HIAA/5-HT concentrations in the PVN averaged across both foot shock conditions for sedentary compared with activity wheel animals. The present results extend understanding of the escape-deficit by indicating an attenuating role for circadian physical activity. The altered monoamine levels suggest brain regions for more direct probes of neural activity after wheel running and foot shock.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1994

Memory of rats with amygdala lesions induced 30 days after footshock-motivated escape training reflects degree of original training.

This experiment was conducted to determine whether the amount of preoperative training influences the effects, on retention, of amygdala lesions induced 30 days after escape training. Rats received 1 or 10 footshock-motivated escape training trials; 30 days later, sham or neurotoxic amygdala lesions were induced. Results of an inhibitory avoidance test performed 4 days after surgery indicated that amygdala lesions impaired retention performance; however, increased preoperative training partially attenuated the retention deficit. Increased preoperative training also attenuated the impairing effects of the lesions on retention assessed in a continuous multiple-trial inhibitory avoidance task given 36 days after the original escape training. The finding that amygdala-lesioned rats remembered the escape training suggests that the amygdala is not a critical locus of the changes underlying the long-term retention of footshock-motivated escape training.

Amygdala↗
PubMed1979

Escape performance after inescapable shock in selectively bred lines of mice: response maintenance and catecholamine activity.

The effects of inescapable shock on subsequent escape performance and shock-elicited activity were examined in six lines of mice selectively bred for differences in general locomotor activity. The line differences in locomotor activity were found to be unrelated to the differences observed on shock-elicited activity. However, escape performance following exposure to inescapable shock was predictable from the levels of shock-elicited activity. Those lines that displayed the greatest decline in motor activity during shock likewise displayed the most pronounced escape deficits. The line differences in escape performance induced by inescapable shock could be mimicked by treatment with a tyrosine hydroxylase inhibitor, alpha-methyl-p-tyrosine. As predicted, the lines that displayed the least interference after tyrosine hydroxylase inhibition exhibited the smallest reduction in levels of catecholamines. The effects on escape performance following inescapable shock are interpreted in terms of the role of response maintenance deficits produced by catecholamine depletion.

Animals↗
PubMed1979

Catecholamine depletion in mice upon reexposure to stress: mediation of the escape deficits produced by inescapable shock.

Immediately following exposure to 60 inescapable shocks, Swiss-Webster mice had significantly reduced hypothalamic norepinephrine (NE). Within 24 hr NE levels returned to control values. Reexposure to as few as 10 shocks 24 hr after initial stress exposure resulted in a significant decline of hypothalamic NE. Moreover, at this interval after inescapable shock, escape performance was severely disrupted, with a large proportion of mice exhibiting numerous failures to escape shock. Increasing brain dopamine (DA) and NE by L-dopa treatment prior to inescapable shock prevented the escape deficits. Conversely, pairing five inescapable shocks with NE depletion by FLA-63, or both DA and NE depletion by alpha-methyl-p-tyrosine, disrupted escape performance 24 hr later. Residual drug effects, state dependence, or sustained amine turnover could not account for the behavioral changes observed. Data are discussed in terms of catecholamine mediation of escape performance through variations in response maintenance abilities. Furthermore, it is suggested that the long-term effects of inescapable shock may be due to sensitization effects or conditioned amine depletion.

Animals↗
PubMed2002

Natural selection of tumor variants in the generation of "tumor escape" phenotypes.

The idea that tumors must "escape" from immune recognition contains the implicit assumption that tumors can be destroyed by immune responses either spontaneously or as the result of immunotherapeutic intervention. Simply put, there is no need for tumor escape without immunological pressure. Here, we review evidence supporting the immune escape hypothesis and critically explore the mechanisms that may allow such escape to occur. We discuss the idea that the central engine for generating immunoresistant tumor cell variants is the genomic instability and dysregulation that is characteristic of the transformed genome. "Natural selection" of heterogeneous tumor cells results in the survival and proliferation of variants that happen to possess genetic and epigenetic traits that facilitate their growth and immune evasion. Tumor escape variants are likely to emerge after treatment with increasingly effective immunotherapies.

Animals↗
PubMedDate not supplied

A field study of the effects of incline on the escape locomotion of a bipedal lizard, Callisaurus draconoides.

We analyzed footprints on the surface of a sand dune to estimate maximal running speeds and the incidence of bipedality in nature, as well as to investigate the effects of incline on the escape locomotion of the lizard Callisaurus draconoides. Previous laboratory tests predicted that inclines would negatively affect sprinting performance in C. draconoides. Although physiologists commonly assume that escape locomotion will be near maximal capacity, we found that only 11% of all strides were greater than 90% of maximal speed of C. draconoides. Escape paths averaged 10 m in length and were generally straight. Approximately 30% of the strides taken by C. draconoides were bipedal, and this value was three times greater than previously found for the closely related species Uma scoparia. The modal value of bipedal stride lengths was greater than that for quadrupedal strides. Inclines negatively affected velocity of only the first meter of C. draconoides escape paths. The location of nearest cover had better predictive value for the initial orientation of C. draconoides escapes than incline. On steep slopes (>15 degrees), C. draconoides avoided running directly downhill and uphill and primarily ran horizontally, whereas on shallow slopes, lizards exhibited approximately equal amounts of horizontal, direct uphill, and direct downhill running.

Animals↗
PubMedDate not supplied

Hindlimb asymmetry reduces escape performance in the lizard Psammodromus algirus.

Locomotor performance of lizards and its relationship to the ecology and morphology of the forms concerned has been well studied recently. Asymmetry of limbs might make the body unstable and make performance less effective. However, their effects on terrestrial locomotion remain almost unexplored. In this article, the escape performance of the lizard Psammodromus algirus running at high speed was related to hindlimb morphology and fluctuating asymmetry levels. Femur length was significantly shorter than crus length. However, absolute fluctuating asymmetry in femur length was significantly larger than in crus length. Asymmetry was not related to body or limb size, thus larger individuals or those with longer limbs did not have significantly greater fluctuating asymmetry. Neither body size nor the length of the limbs (femur or crus) were significantly related to any of the variables describing escape performance. However, escape performance was affected by femur-length fluctuating asymmetry, which resulted in significantly reduced overall escape speeds. In contrast, asymmetry in crus length did not affect escape performance. We discuss the possible basis of these alterations of locomotion, the relevance of reduced performance for the ecology of this species, and how individuals may compensate for the costs of asymmetry.

Adaptation, Physiological↗