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PubMed1989

Diazepam modulates lateral hypothalamic self-stimulation but not stimulation-escape in rats.

Rats electrically stimulated via chronically implanted lateral hypothalamic (LH) electrodes were assessed with and without diazepam (DZ), for thresholds of stimulation-bound feeding (SBF) and for barpressing rates to administer and to escape from the same current, Six pure-reward rats, who self-stimulated but did not escape LH stimulation, exhibited SBF. Their electrode tips lay in medical forebrain bundle (MFB) and zona inserta along the entire rostral-caudal extent of the ventromedial nucleus of the hypothalamus (VMH). Six reward-escape rats, who self-stimulated and escaped from LH stimulation, did not (with one histologically deviant exception) show SBF. Reward-escape electrode tips were anterior to all the pure-reward placements. They lay in MFB rostral to the VMH up to the level of the bed nucleus of the stria terminalis (with the deviant electrode tip located on the zona inserta/ventral thalamic border). After i.p. injections of DZ, self-stimulation (SS) rates increased for both groups of animals and SBF thresholds decreased. Stimulation-escape (SE) rates, however, remained unchanged by the drug. The results are consistent with the existence of dual substrates: a DZ-sensitive reward system, present in both groups of animals, and a simultaneously stimulated, drug-resistant aversion system which is powerfully engaged in reward-escape animals only.

Animals↗
PubMed1988

Effect of nifedipine on the shuttlebox escape deficit induced by inescapable shock in the rat.

The behavioural effect of subchronic treatment with calcium channel antagonists (nifedipine, verapamil) and with imipramine was assessed in rats subjected to inescapable shock (IS). The effect of subchronic treatment with nifedipine and imipramine on specific [3H]nitrendipine ([3H]NDP) binding was investigated in frontal cortex of naive rats and in rats given IS then tested for shuttlebox escape. The rats showed a severe impairment in escape behaviour after IS. Imipramine and nifedipine significantly reduced FR1 and FR2 escape deficits. Verapamil had no effect. A small but significant increase in the number of [3H]NDP binding sites (Bmax) was seen in rats exposed to the shuttlebox escape test independent of a previous exposure to IS. Imipramine had no influence on Bmax in any of the groups. Nifedipine did not affect [3H]NDP binding in naive rats but decreased Bmax in rats subjected to IS and the shuttlebox escape test. The comparable ability of nifedipine and imipramine to reverse the shuttlebox escape deficit induced by IS argues for a possible antidepressant activity of nifedipine. The biochemical data indicate that cortical [3H]NDP binding sites are not correlated to performance in the shuttlebox escape test.

Animals↗
PubMed1986

Ventral tegmental stimulation modulates centrally induced escape responding.

Electrical stimulation of the ventromedial tegmentum (VT) exerts a dual effect on escape responding, induced by stimulating either the medial hypothalamus (MH) or the dorsal part of the central gray matter (CG), namely a suppressant effect which reduces MH or CG induced escape responses and a facilitating one which increases these same responses. The relative magnitude of these effects appears to depend on both the location of the VT stimulation site and the stimulation intensity applied. Furthermore, VT stimulation is often more effective in suppressing escape responding induced by MH as opposed to CG stimulation. VT stimulation has clear rewarding effects but seems to have also aversive effects. The VT sites whose stimulation induces escape suppression seem to yield less marked aversive effects than those sites whose stimulation induces escape facilitation. Furthermore, a negative correlation was found to exist between the escape rate induced by a combined CG/VT or MH/VT stimulation and the self-stimulation rate yielded by these VT sites. These results suggest that the effects of a VT stimulation on escape responding induced by electrical brain stimulation are somehow related to the rewarding and/or aversive effects of this same VT stimulation.

Animals↗
PubMed1993

Gender differences in escape-avoidance behavior of mice after haloperidol administration.

Gender differences in the disruptive effects of haloperidol on some reinforced behaviors have been observed in different species. However, the inhibitory action of haloperidol on the acquisition and performance of escape-avoidance behavior has only been investigated in male subjects. The present experiment was designed to investigate possible gender differences in the effects of haloperidol on the initial phase of an escape-avoidance learning task. Male and female mice of the OF1 strain were given a single training session in a shuttle-box. Thirty minutes prior to the behavioral test, mice were injected IP with haloperidol (0.25 mg/kg) or physiological saline (10 ml/kg). Latencies of escape and avoidance responses and the number of nonresponses, escapes, avoidances, pseudoavoidances, crossings during the adaptation period, and crossings during intertrial intervals (ITIs) were evaluated. The disruptive action of haloperidol on the escape-avoidance behavior of the mice was greater in males than in females. The number of nonresponses were higher and the number of escapes lower in treated males than in their female counterparts. These gender differences were not found in control subjects. Activity measures of spontaneous motor behavior (crossings in the adaptation period and during ITIs) did not present gender differences either. Several possible mechanisms responsible for this greater susceptibility of males to the inhibitory effects of haloperidol on escape-avoidance learning are discussed, especially the modulating role of female hormones on dopaminergic activity.

Animals↗
PubMed1986

Step-down-type passive avoidance- and escape-learning method. Suitability for experimental amnesia models.

A method for evaluating passive avoidance- and escape-learning responses simultaneously has been developed for the study of learning and memory in mice. Prolongation of the step-down latency and shortening of the escape latency in the retention test depended on the strength of the voltage of the electric shocks delivered during the training test. Therefore, the step-down latency and escape latency may be good parameters of learning and memory performance. By cycloheximide treatment immediately after training, the step-down latency and escape latency were shortened and prolonged, respectively, in a dose-related manner, and the relationship between the step-down latency and escape latency was significant. Treatment with cycloheximide within 30 min after training caused significant amnesia, but not after more than 60 min. Furthermore, amnesic action of cycloheximide developed 24 hr after the treatment, but not within 4 hr. On the other hand, the step-down latency and/or the escape latency in the training test were changed by pretreatment with diethyldithiocarbamate and scopolamine. Therefore, the amnesic action of these drugs administered before the training should be investigated in detail. The present method, simultaneously estimating passive avoidance- and escape-learning responses, may be useful for the development of experimental amnesia models.

Amnesia↗
PubMed2001

Repeated treatment with imipramine, fluvoxamine and tranylcypromine decreases the number of escape failures by activating dopaminergic systems in a rat learned helplessness test.

Chronic administration of antidepressants has been shown to reduce the number of escape failures in the rat learned helplessness test (LH). In the present study we investigated the role of D1, D2 and D3 receptors in mediating this effect. In our first series of experiments, we demonstrated that SKF38393, D1 receptor agonist, in a dose of 2.5 mg/kg (i.p.) and quinpirole, D2 receptor agonist in a dose of 0.5 mg/kg (i.p.), significantly decreased the number of escape failures in LH, and these were reversed by SCH23390 (0.015 mg/kg), D1 receptor antagonist, and by sulpiride (25 mg/kg), D2 receptor antagonist, respectively. In contrast, 7-OH-DPAT, a D3 receptor agonist, in a dose of 10 mg/kg (i.p.) did not affect the number of escape failures in LH. In a second series of experiments, we showed that eight days of repeated treatment with imipramine (10 mg/kg, p.o.), fluvoxamine (1.25 mg/kg, p.o.) and tranylcypromine (1.25 mg/kg, p.o.) significantly decreased the number of escape failures in LH. The decrease in escape failures seen with use of imipramine and tranylcypromine was reversed by sulpiride in LH, but not by SCH23390. On the other hand, the effect of fluvoxamine was reversed by both SCH23390 and sulpiride. These findings indicate that stimulation of D1 and D2 receptors decreased the number of escape failures in LH, respectively. Thus, D2 and/or D1 receptors are probably involved in the decreased number of escape failures in case of repeated treatment with antidepressants in LH.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed2001

Serotonergic regulation of inhibitory avoidance and one-way escape in the rat elevated T-maze.

It has been proposed that distinct 5-HT pathways modulate different types of anxiety. Activation of the ascending dorsal raphe (DR)-5-HT pathway, innervating the amygdala and frontal cortex, would facilitate learned defensive behaviors. On the other hand, activation of the DR-periventricular 5-HT pathway, which innervates the dorsal periaqueductal gray matter (DPAG), would inhibit innate flight or fight reactions. Dysfunction of these pathways has been suggested to relate to generalized anxiety disorder (GAD) and panic disorder (PD) in humans, respectively. The elevated T-maze has been developed to separate conditioned (inhibitory avoidance) from unconditioned (escape) defensive responses in the same rat. Pharmacological validation of this model has shown that the GAD-effective serotonergic anxiolytic buspirone or the putative anxiolytic ritanserin selectively impaired inhibitory avoidance while leaving one-way escape unchanged. Chronic injection of the 5-HT/noradrenaline reuptake inhibitor imipramine impaired inhibitory avoidance and prolonged escape, an effect that may be related to the therapeutic action of this drug on both GAD and PD. Like imipramine, intra-DPAG injection of the 5-HT(1A) agonist 8-OH-DPAT impaired both inhibitory avoidance and one-way escape. Intra-DPAG administration of the 5-HT(2A/2C) agonist DOI prolonged escape, without affecting inhibitory avoidance. The reversible inactivation of the DRN by muscimol impaired inhibitory avoidance, while facilitating escape from the open arm. Taken together, these results suggest that 5-HT exerts differential control on inhibitory avoidance and escape response in the elevated T-maze, mobilizing different types of 5-HT receptors in key structures implicated in fear/anxiety.

Animals↗
PubMed1999

Escape-related behaviours in an unstable elevated and exposed environment. I. A new behavioural model of extreme anxiety.

The aim of this study was to validate a new behavioural test for extreme anxiety, designed to elicit unconditioned escape from animals on an unstable, elevated and exposed plus maze. The animals were also run on a standard elevated plus maze, so that well-validated anxiety measures could be compared with the animals' propensity to escape. The first experiment compared the behavioural repertoire of three rat strains; more escape behaviours were elicited from the Sprague Dawleys (SDs) and dark agouti (DAs) than from the hooded listers (HLs) on the unstable maze. Similarly, the SDs and DAs exhibited higher anxiety profiles than the HLs on the standard plus maze. There was a clear correlation, therefore, between the propensity to escape and well-validated anxiety measures. A further group of rats [HLs] was tested on both the unstable and standard plus mazes (Experiment 2) and principal components analyses carried out on all behavioural measures. The extracted factors identified separate and independent factors relating to escape-linked behaviours on the unstable plus maze and anxiety on the standard plus maze. The escape-linked behaviours exhibited on the unstable plus maze appear to reflect a different type of anxiety from that exhibited on the standard plus maze. The bias towards escape behaviours shown by some rats on the unstable plus maze may mimic the chronically hyper-aroused, persistent 'fight/flight' state exhibited by certain categories of anxiety patients, and hence provide a behavioural model of extreme anxiety.

Animals↗
PubMed1993

Dissociation of interference with the speed and accuracy of escape produced by inescapable shock.

Benzodiazepines and naltrexone administered before inescapable shock block behavioral consequences of the inescapable shock such as poor shuttle box escape, reduced activity in reaction to shock, reduced social interaction, and so on. Anxiogenic beta-carboline derivatives such as FG-7142 can produce these effects by themselves. In the present study, neither diazepam nor naltrexone had any effect on the interference with Y-maze choice escape accuracy produced by inescapable shock even though they both eliminated the reduction in Y-maze escape response speed produced by inescapable shock. Analogously, FG-1742 did not lead to a reduction in Y-maze choice escape response accuracy even though it did slow escape responding. These data imply that inescapable shock interferes with escape choice learning and escape response speed by different mechanisms, the former not involving fear-anxiety processes.

Animals↗
PubMed2003

Self-organized queuing and scale-free behavior in real escape panic.

Numerical investigations of escape panic of confined pedestrians have revealed interesting dynamical features such as pedestrian arch formation around an exit, disruptive interference, self-organized queuing, and scale-free behavior. However, these predictions have remained unverified because escape panic experiments with real systems are difficult to perform. For mice escaping out of a water pool, we found that for a critical sampling rate the escape behavior exhibits the predicted features even at short observation times. The mice escaped via an exit in bursts of different sizes that obey exponential and (truncated) power-law distributions depending on exit width. Oversampling or undersampling the mouse escape rate prevents the observation of the predicted features. Real systems are normally subject to unavoidable constraints arising from occupancy rate, pedestrian exhaustion, and nonrigidity of pedestrian bodies. The effect of these constraints on the dynamics of real escape panic is also studied.

Animals↗
PubMed2005

Development of the escape response in teleost fishes: do ontogenetic changes enable improved performance?

Teleost fishes typically first encounter the environment as free-swimming embryos or larvae. Larvae are morphologically distinct from adults, and major anatomical structures are unformed. Thus, larvae undergo a series of dramatic morphological changes until they reach adult morphology (but are reproductively immature) and are considered juveniles. Free-swimming embryos and larvae are able to perform a C-start, an effective escape response that is used evade predators. However, escape response performance improves during early development: as young fish grow, they swim faster (length-specific maximum velocity increases) and perform the escape more rapidly (time to complete the behavior decreases). These improvements cease when fish become juveniles, although absolute swimming velocity (m s(-1)) continues to increase. We use studies of escape behavior and ontogeny in California halibut (Paralichthys californicus), rainbow trout (Oncorhynchus mykiss), and razorback suckers (Xyrauchen texanus) to test the hypothesis that specific morphological changes improve escape performance. We suggest that formation of the caudal fin improves energy transfer to the water and therefore increases thrust production and swimming velocity. In addition, changes to the axial skeleton during the larval period produce increased axial stiffness, which in turn allows the production of a more rapid and effective escape response. Because escape performance improves as adult morphology develops, fish that enter the environment in an advanced stage of development (i.e., those with direct development) should have a greater ability to evade predators than do fish that enter the environment at an early stage of development (i.e., those with indirect development).

Acceleration↗
PubMed2006

Escape responses in juvenile Atlantic cod Gadus morhua L.: the effects of turbidity and predator speed.

We examined the effect of turbidity (0.5-14 beam attenuation m(-1)) and predator attack speed (150 and 296 cm s(-1)) on escape responses of juvenile cod Gadus morhua in the laboratory. We triggered escape responses using a predator model and measured escape timing, direction and locomotor performance. We also measured responsiveness and estimated the likelihood of fish escaping the ;predator attack' (putative escape success, PES). Turbidity affected both PES and the type of escape response used by the fish, but these effects depended on predator speed. PES for the fast predator attack declined from 73% in clear water to 21% in highly turbid water, due to decreased responsiveness and poorly timed escapes. Intermediate turbidity enhanced PES and responsiveness to the slow predator attack. Locomotor performance was reduced by turbidity, whereas predator speed had the opposite effect. Our results suggest that both predator attack speed and turbidity have important roles in determining the vulnerability of fish attacked by piscivorous predators.

Animals↗
PubMed1975

Extrinsic modulation of crayfish escape behaviour.

Extrinsic systems were shown to control the excitability of the neurones which mediate tail-flip escape in the crayfish. Restraint suppresses the escape mediated by giant fibres and some, but not all, categories of non-giant mediated escape; autotomy of claws increases the excitability of non-giant mediated escape without affecting the lateral giant reflex. The effects of restraint on the lateral giant reflex result from inhibition rather than reduced facilitation. The inhibition descends from thoracic and higher levels, and the lateral giant escape command neurone appears to be its primary target. Inhibition may serve to shift the control of escape behaviour from short latency 'reflex' systems to more flexible 'voluntary' ones which can produce responses at times most opportune for successful escape.

Action Potentials↗
PubMed1988

Characteristics of coping behavior of rats exposed to a long-term hardly escapable aversive stimulus: a possible depression model.

The purpose of the present study was to induce a state of depression including both the elements of behavioral despair and chronic stress. Therefore, this study was performed under the hypothesis that a long-term exposure of rats to the experimental situation of difficult to escape from foot-shock in a Skinner box might produce animals with a state of depression containing both the elements. Male Wistar strain rats were trained to press a lever to escape from foot-shock under a fixed ratio (FR) schedule. After the training, rats were exposed daily to a schedule consisting of 20 trials (the early 10 trials, FR 5; the later 10 trials, FR 20) once a day. The exposure resulted in reduction of the number of lever presses and successful escape in FR 20. Only the animals whose number of escapes, reduced to under 20% in FR 20 were treated with psychotropic drugs once a day for 4 days. The results showed that the reduced number of escapes was most improved by antidepressants (imipramine or mianserin), but not by haloperidol and methamphetamine. Although subchronic treatment with chlordiazepoxide partially recovered the reduced escape, the efficiency of lever pressing to escape from foot-shock was lower than that with the antidepressants. The results of the present study suggest that the behavioral suppression observed in this study might include characteristics similar to a state of depression.

Adaptation, Psychological↗
PubMed2004

Compensation of escape direction in unilaterally cercus-ablated crickets, Gryllus bimaculatus, is associated with the distance walked during recovery period.

In response to an air puff stimulus, intact crickets, Gryllus bimaculatus, make an escape almost 180 degrees opposite to the stimulus source. In order to verify our previous hypothesis that a self-stimulation of the wind-sensory system is necessary for a compensational recovery of the escape direction (behavioral compensation) in unilaterally cercus-ablated crickets, we investigated the relationship between the conditions of rearing after a unilateral cercal ablation and the degree of behavioral compensation. A unilaterally cercus-ablated cricket reared in a large cage to permit free locomotion showed a significantly higher degree of recovery of escape direction compared with those reared under restrained conditions in a small glass vial. However, the degree of behavioral compensation in a cricket reared alone in a large cage was smaller than that of crickets reared in a cage of the same size with 5-6 other cercus-ablated crickets. Mutual stimulation possibly increased the extent of locomotion of crickets reared in a group and improved the degree of compensational recovery of the escape direction. To ascertain this, the distance a cricket moved during the recovery period was associated with the degree of compensational change of the escape direction. The result suggests that the degree of compensation of the escape direction clearly depended on the distance walked by the crickets. The compensation seemed not to be caused by other factors such as chemical ones in the case of group rearing because forced locomotion induced by touch stimulation on the body surface was solely effective in improving the escape direction.

Air Movements↗
PubMed1995

Effects of anterolateral spinal lesions on escape responses of rats to hindpaw stimulation.

In order to determine the effects of spinal cord lesions on nociceptive sensitivity of rodents, methods were developed to assess the speed of operant escape responses to electrocutaneous stimulation (ES). ES was delivered across the dorsal and ventral surfaces of either hindpaw, producing a current path through deep tissues. In order to guide establishment of a range of stimulus intensities for this manner of stimulation, a preliminary human psychophysical experiment was conducted with stimulation between the dorsal and ventral surfaces of a finger. For the human subjects, detection thresholds averaged 0.13 mA, and thresholds for a sharp (but nonpainful) sensation were 0.42 mA. Levels of stimulation between these thresholds for detection and a sharp quality elicited sensations of tingle or itch. Thresholds for reports of pain averaged 0.67 mA. On the basis of these results, intensities of ES ranging from 0.05 to 1.0 mA were presented to the feet of rats that were trained to perform an escape response with one forelimb. Thresholds for escape averaged slightly less than 0.1 mA; responding was consistent at 0.4 mA; and response probability and speed were maximal at approximately 0.8 mA. Thus, the rats responded aversively at intensities below those rated as sharp or painful by the human subjects, but the speed of escape reached a plateau at intensities that were above pain threshold for the human subjects. Unilateral thoracic lesions of the lateral spinal column of rats produced a contralateral hypalgesia. Escape thresholds were elevated, and the speed of escape responses to all intensities was reduced. This effect depended upon interruption of axons in the middle and anterior portions of one lateral column, corresponding to the location of long ascending pathways for nociception, including the spinothalamic tract. The speed of escape responding increased over 20 weeks of postoperative testing of animals with the largest lesions. This confirms results obtained previously from monkeys (by means of a similar paradigm), and corresponds to clinical reports of humans who have received spinal lesions for control of intractable pain. Thus, the location and organization of nociceptive pathways in the spinal cord of rodents appear to be similar to those of primates, and similar adaptations occur following interruption of these pathways.

Adult↗
PubMed2003

Mutations in deadly seven/notch1a reveal developmental plasticity in the escape response circuit.

The relatively simple neural circuit driving the escape response in zebrafish offers an excellent opportunity to study properties of neural circuit formation. The hindbrain Mauthner cell is an essential component of this circuit. Mutations in the zebrafish deadly seven/notch1a (des) gene result in supernumerary Mauthner cells. We addressed whether and how these extra cells are incorporated into the escape-response circuit. Calcium imaging revealed that all Mauthner cells in desb420 mutants were active during an elicited escape response. However, the kinematic performance of the escape response in mutant larvae was very similar to wild-type fish. Analysis of the relationship between Mauthner axon collaterals and spinal neurons revealed that there was a decrease in the number of axon collaterals per Mauthner axon in mutant larvae compared with wild-type larvae, indicative of a decrease in the number of synapses formed with target spinal neurons. Moreover, we show that Mauthner axons projecting on the same side of the nervous system have primarily nonoverlapping collaterals. These data support the hypothesis that excess Mauthner cells are incorporated into the escape-response circuit, but they divide their target territory to maintain a normal response, thus demonstrating plasticity in the formation of the escape-response circuit. Such plasticity may be key to the evolution of the startle responses in mammals, which use larger populations of neurons in circuits similar to those in the fish escape response.

Animals↗
PubMed1996

Interactions between the neural networks for escape and swimming in goldfish.

Interactions between neural networks for different motor behaviors occur frequently in nature; however, there are few vertebrate models for studying these interactions. One potentially useful model involves the interactions between escape and swimming behaviors in fish. Fish can produce escape bends while swimming, using some of the same axial muscles for both behaviors. Here we study the interactions between escape and swimming in a paralyzed goldfish preparation in which we can activate the networks for both behaviors. Fictive swimming was elicited by electrical stimulation in the midbrain locomotor region. During the swimming, we fired a single action potential in the reticulospinal Mauthner (M) cell, which initiates the escape behavior (Zottoli, 1977). Firing the M cell overrode the swimming motor output to produce an output appropriate for escape regardless of the phase of swimming at which it was fired. The M cell also could reset the swimming rhythm dramatically in a way that led to a smooth transition from an escape bend to one side into subsequent swimming. Both the override and reset supported predictions based on previous studies of the organization of the M-cell network. They apparently allow for a well coordinated motor output when a fish must produce an escape while swimming. The potent effects of one action potential in a single, identifiable reticulospinal neuron make this an attractive model system for future studies of the cellular basis of interactions between descending pathways and spinal rhythm-generating networks.

Animals↗