Trade-offs between feeding and shock avoidance in goldfish (Carassius auratus)

Previous work showed that goldfish learn to avoid a region of an aquarium where they receive a discrete shock to the flank. This avoidance is reduced if another fish is present next to the shock zone, suggesting fish trade-off avoidance against a tendency to associate [Dunlop, R., Millsopp, S., Laming, P., 2006. Avoidance learning in goldfish (Carassius auratus) and trout (Oncorhynchus mykiss) and implications for pain perception. App. Anim. Behav. Sci. 97 (2–4), 255–271]. Only shock intensity was adjusted in those experiments, here we report results where a requirement for food was also altered.Fish were trained to feed at a region of the aquarium where subsequently they would receive a discrete shock to the flank. One experimental group had different shock intensities applied, whereas in the other group shock intensity was consistent but food deprivation was varied.We show the number of feeding attempts and time spent in the feeding/shock zone decreased with increased shock intensity and with increased food deprivation the number and the duration of feeding attempts increased as did escape responses as this zone was entered. These data suggest that goldfish balance their need for food against avoidance of an acute noxious stimulus.     

Stressors produce a concurrent decrease and increase in reflex amplitude in rats treated with naloxone

The effect of inescapable foot-shock on the tail-flick response and on the startle response to brief shocks and brief tones was studied in rats. In the first experiment, 25 minutes of inescapable foot shock (stressor) produced a significant increase in tail-flick latency which was antagonized by the opioid antagonist naloxone (2.0 mg/kg). In the second experiment, the startle response to an electric shock to the tail was significantly diminished by the stressor, and this effect was not significantly reduced by naloxone. However, the size of the startle response to a brief tone was significantly increased in rats treated with naloxone. Thus, rats injected with naloxone had a decreased startle to shock but an increased startle to tone following inescapable foot shock. Finally, tones which preceded shocks by one second produced a facilitation of the startle response to the shocks in tests that followed exposure to the stressor. This facilitation was not affected significantly by naloxone. These results indicate that the changes in the startle response following the stressor were not mediated exclusively by endogenous opioids.     

Differences in inhibitory avoidance,cortisol and brain gene expression in TL and AB zebrafish

Recently, we established an inhibitory avoidance paradigm in Tupfel Long‐Fin (TL) zebrafish. Here, we compared task performance of TL fish and fish from the AB strain; another widely used strain and shown to differ genetically and behaviourally from TL fish. Whole‐body cortisol and telencephalic gene expression related to stress, anxiety and fear were measured before and 2 h post‐task. Inhibitory avoidance was assessed in a 3‐day paradigm: fish learn to avoid swimming from a white to a black compartment where a 3V‐shock is given: day 1 (first shock), day 2 (second shock) and day 3 (no shock, sampling). Tupfel Long‐Fin fish rapidly learned to avoid the black compartment and showed an increase in avoidance‐related spatial behaviour in the white compartment across days. In contrast, AB fish showed no inhibitory avoidance learning. AB fish had higher basal cortisol levels and expression levels of stress‐axis related genes than TL fish. Tupfel Long‐Fin fish showed post‐task learning‐related changes in cortisol and gene expression levels, but these responses were not seen in AB fish. We conclude that AB fish show higher cortisol levels and no inhibitory avoidance than TL fish. The differential learning responses of these Danio strains may unmask genetically defined risks for stress‐related disorders.     

Effects of apomorphine on the expression of learned helplessness behavior

Dopaminergic system and its D1 as well as D2 receptors are involved in the modulation of emotional behavior. This experiment investigated the role of dopaminergic activity in the inescapable stress-induced learned helplessness, a widely used depression animal model, by using the pharmacological manipulation through the apomorphine (APO), an agonist for D1 and D2 receptors, and sulpiride (SUL), a selective D2 antagonist. Male Sprague Dawley rats were used and tested in a shuttle box. In the day-1 session, the rats received a 10-trial (1 min/trial) inescapable stressor: a 3 sec conditioned stimulus (CS; 75 db sound and 250 lux red light) followed by a 10 sec unconditioned stimulus (UCS; electrical foot shock, 0.5 mA). In the day-2 session, a 15-trial active avoidance test, 3 sec CS followed by UCS, was performed 30 min after the administration of APO (0, 0.05, 0.5, 1, and 5 mg/kg, i.p.). The number of failures was counted and the UCS was stopped when the rats did not escape after 15 sec UCS. The results showed that APO at the dosage of 0.5 mg/kg had a tendency to enhance the avoidance behavior. In contrast, the treatment of higher dose of APO, 1 and 5 mg/kg, reduced the number of escape but increased the number of failure. Pretreatment of SUL (5 mg/kg, i.p.), 10 min before 1 mg/kg of APO, significantly enhanced the failure behavior. The present data suggest that the activity of D2 receptor may be associated with the adaptive or protective role in the prevention of escape deficits after exposure to inescapable stress. However, the excessive stimulation of D1 receptor may participate in the failure of coping behavior leading to learned helplessness and therefore in the pathophysiological mechanisms underling the development of depression.     

Shuttlebox avoidance in rhesus monkeys: effects on plasma cortisol and beta-endorphin

Groups of monkeys either extensively pretrained to avoid shocks in a shuttlebox or with minimal prior experience were compared for plasma cortisol and beta-endorphin levels immediately following: (1) an exposure to the box with no shock, (2) the box providing repeated inescapable shocks or (3) a re-exposure to the box, again with no shock presentation. Mere exposure to the unfamiliar box elevated plasma cortisol just as much as exposure + shock did when inexperienced monkeys were tested. However, animals with a history of previously successful shock avoidance showed smaller elevations when exposed to the box alone, than they did when inescapable shock was received. Plasma beta-endorphin levels following shuttlebox exposure showed only a sporadic pattern of elevations in either inexperienced or pretrained monkeys. However, levels of beta-endorphin as determined under control conditions in the home cage were lower in pretrained animals, as were plasma levels of cortisol. The results indicate that behavioral factors may effect plasma cortisol and beta-endorphin following both acute and chronic shuttlebox experience.     

Neurodevelopmental disruption of cortico-striatal function caused by degeneration of habenula neurons

Background

The habenula plays an important role on cognitive and affective functions by regulating monoamines transmission such as the dopamine and serotonin, such that its dysfunction is thought to underlie a number of psychiatric conditions. Given that the monoamine systems are highly vulnerable to neurodevelopmental insults, damages in the habenula during early neurodevelopment may cause devastating effects on the wide-spread brain areas targeted by monoamine innervations.

Methodology/Principal Findings

Using a battery of behavioral, anatomical, and biochemical assays, we examined the impacts of neonatal damage in the habenula on neurodevelopmental sequelae of the prefrontal cortex (PFC) and nucleus accumbens (NAcc) and associated behavioral deficits in rodents. Neonatal lesion of the medial and lateral habenula by ibotenic acid produced an assortment of behavioral manifestations consisting of hyper-locomotion, impulsivity, and attention deficit, with hyper-locomotion and impulsivity being observed only in the juvenile period, whereas attention deficit was sustained up until adulthood. Moreover, these behavioral alterations were also improved by amphetamine. Our study further revealed that impulsivity and attention deficit were associated with disruption of PFC volume and dopamine (DA) receptor expression, respectively. In contrast, hyper-locomotion was associated with decreased DA transporter expression in the NAcc. We also found that neonatal administration of nicotine into the habenula of neonatal brains produced selective lesion of the medial habenula. Behavioral deficits with neonatal nicotine administration were similar to those caused by ibotenic acid lesion of both medial and lateral habenula during the juvenile period, whereas they were different in adulthood.

Conclusions/Significance

Because of similarity between behavioral and brain alterations caused by neonatal insults in the habenula and the symptoms and suggested neuropathology in attention deficit/hyperactivity disorder (ADHD), these results suggest that neurodevelopmental deficits in the habenula and the consequent cortico-striatal dysfunctions may be involved in the pathogenesis and pathophysiology of ADHD.     

Adult-born hippocampal neurons promote cognitive flexibility in mice

The hippocampus is involved in segregating memories, an ability that utilizes the neural process of pattern separation and allows for cognitive flexibility. We evaluated a proposed role for adult hippocampal neurogenesis in cognitive flexibility using variants of the active place avoidance task and two independent methods of ablating adult-born neurons, focal X-irradiation of the hippocampus, and genetic ablation of glial fibrillary acidic protein positive neural progenitor cells, in mice. We found that ablation of adult neurogenesis did not impair the ability to learn the initial location of a shock zone. However, when conflict was introduced by switching the location of the shock zone to the opposite side of the room, irradiated and transgenic mice entered the new shock zone location significantly more than their respective controls. This impairment was associated with increased upregulation of the immediate early gene Arc in the dorsal dentate gyrus, suggesting a role for adult neurogenesis in modulating network excitability and/or synaptic plasticity. Additional experiments revealed that irradiated mice were also impaired in learning to avoid a rotating shock zone when it was added to an initially learned stationary shock zone, but were unimpaired in learning the identical simultaneous task variant if it was their initial experience with place avoidance. Impaired avoidance could not be attributed to a deficit in extinction or an inability to learn a new shock zone location in a different environment. Together these results demonstrate that adult neurogenesis contributes to cognitive flexibility when it requires changing a learned response to a stimulus-evoked memory. ? 2012 Wiley Periodicals, Inc.     

Monoamine Receptors in an Animal Model of Affective Disorder

After a relatively mild course of uncontrollable shocks, two distinct groups of rats can be defined in terms of their performance in learning to escape from a controllable stressor. Response-deficient (RD) rats do not learn to terminate the controllable stressor, whereas nondeficient (ND) rats learn this response as readily as do untreated control rats. The current studies were designed to determine the neurochemical correlates of the behavioral differences between these groups of rats. The major findings concerned postsynaptic beta-adrenergic effects in the hippocampus of RD rats. These included an up-regulation of beta-adrenergic receptors and, in parallel experiments, an increase in the sensitivity of adenylyl cyclase to stimulation by norepinephrine. There was no difference in brain levels of catecholamines between the three groups of rats. A statistically significant increase in levels of 5-hydroxytryptamine was noted in the hippocampus and hypothalamus of RD rats as compared to levels in ND rats, but no significant differences were measured between groups of rats in terms of S1 or S2 serotonergic receptor binding. These results implicate both beta-adrenergic and serotonergic mechanisms in the behavioral deficit caused by uncontrollable shock.     

Characterization of radiation-induced performance decrement using a two-lever shock-avoidance task

Rats were trained to perform a task involving responses on two levers. Responding on an avoidance lever delayed the onset of electrical footshock for 20 sec and responding on a warning lever turned on a light for 60 sec. When the light was on, the task on the avoidance lever was changed from unsignaled shock avoidance to signaled shock avoidance by preceding the shocks with 5-sec warning tones. The animals preferred the signaled avoidance condition. After 100 Gy of 60Co irradiation, the animals were less able to avoid shock, an effect from which the animals recovered somewhat over 90 min. The response rate on the avoidance lever remained at or above control rates, while the response rate on the warning lever showed an initial increase, followed by a decrease below baseline. The increase in responding on the avoidance lever occurred in bursts just after presentation of the shocks. The data suggest that under these experimental conditions a subject will not respond appropriately to avoid shock or acquire cues that can facilitate the avoidance of shock. The effects, however, do not reflect an inability to perform the required movements but instead appear to reflect some characteristic of the task associated with a particular lever.     

Acute exposure to offshore produced water has an effect on stress- and secondary stress responses in three-spined stickleback Gasterosteus aculeatus

Pollution is one of today's greatest problems, and the release of contaminants into the environment can cause adverse changes in vitally important biological pathways. In this study, we exposed three-spined stickleback Gasterosteus aculeatus to produced water (PW), i.e. wastewater from offshore petroleum production. PW contains substances such as alkylphenols (APs) and aromatic hydrocarbons (PAHs) known to induce toxicant stress and endocrine disruption in a variety of organisms. Following exposure to PW, a standardized confinement treatment was applied as a second stressor (PW-stress), testing how fish already under stress from the pollutant would respond to an additional stressor. The endpoint for analysis was a combination of blood levels of cortisol and glucose, in addition to transcribed levels of a set of genes related to toxicant stress, endocrine disruption and general stress. The findings of this study indicate that low doses of PW do not induce vitellogenin in immature female stickleback, but do cause an upregulation of cytochrome (CYP1A) and UDP-glucuronsyltransferase (UDP-GT), two biomarkers related to toxicant stress. However, when the second stressor was applied, both genes were downregulated, indicating that the confinement exposure had a suppressive effect on the expression of toxicant biomarkers (CYP1A and UDP-GT). Further, two of the stress related genes, heat shock protein 90 (HSP90) and stress-induced phosphoprotein (STIP), were upregulated in both PW- and PW-stress-treatment, but not in the water control confinement treatment, indicating that PW posed as a larger stress-factor than confinement for these genes. The confinement stressor caused an increased level of glucose in both control and PW-treated fish, indicating hyperglycemia, a commonly reported stress response in fish.     

Tyrosine prevents behavioral and neurochemical correlates of an acute stress in rats

Exposure of rats to an acute, uncontrollable stressor can increase brain norepinephrine (NE) turnover and decrease locomotor and exploratory behavior. We examined the ability of exogenous tyrosine, NE's amino acid precursor, to protect rats from developing these neurochemical and behavioral changes when stressed.Animals pretreated with saline or tyrosine (200 mg/kg, i.p.) were subjected to tail shock (15 v, 2 mA, 5 sec/30 sec) or to no shock during a 60-min period. Exposure to shock depleted NE and increased its turnover [as indicated by altered NE and 3-methoxy-4-hydroxy-phenylethylene-glycol sulfate levels (MHPG-SO₄)] within the locus coeruleus, the hippocampus and the hypothalamus. Behavioral deficits were observed using measures of locomotion, standing on hind legs, and hole-poking in an open-field apparatus. Animals given tyrosine before shock displayed neither shock-induced NE depletion nor the deficits in locomotion and hole-poking; brain MHPG-SO₄ levels tended to be greater than after shock alone. These observations suggest that the stress caused NE to be released from some neurons more rapidly than it could be restored by synthesis or reuptake, thereby impairing noradrenergic transmission and NE-dependent exploratory behaviors. Tyrosine administration presumably enhanced the transmitter's synthesis in stressed animals, thereby preventing both the neurochemical and the behavioral deficits.     

Predators' toxin burdens influence their strategic decisions to eat toxic prey

Toxic prey advertise their unprofitability to predators via conspicuous aposematic coloration [1]. It is widely accepted that avoidance learning by naive predators is fundamental in generating selection for aposematism [2, 3] and mimicry [4, 5] (where species share the same aposematic coloration), and consequently this cognitive process underpins current evolutionary theory [5, 6]. However, this is an oversimplistic view of predator cognition and decision making. We show that predators that have learned to avoid chemically defended prey continue to attack defended individuals at levels determined by their current toxin burden. European starlings learned to discriminate between sequentially presented defended and undefended mealworms with different color signals. Once birds had learned to avoid the defended prey at a stable asymptotic level, we experimentally increased their toxin burdens, which reduced the number of defended prey that they ingested in the subsequent trial. This was due to the birds making strategic decisions to ingest defended prey on the basis of their visual signals. Birds are clearly able to learn about the nutritional benefits and defensive costs of eating defended prey, and they regulate their intake according to their current physiological state. This raises new perspectives on the evolution of aposematism, mimicry, and defense chemistry.     

Cleaner wrasses Labroides dimidiatus are more cooperative in the presence of an audience

Humans may help others even in?situations where the recipient will not reciprocate [1-5]. In some cases, such behavior can be explained by the helpers increasing their image score, which will increase the probability that bystanders will help them in the future [5-7]. For other animals, the notion that many interactions take place in an environment containing an audience of eavesdropping bystanders has also been proposed to have important consequences for social behavior, including levels of cooperation [8]. However, experimental evidence is currently restricted to the demonstration that cleaner fish Labroides dimidiatus can learn to solve a foraging task [9]. The cleaners learned to feed against their preference on artificial clients if that allowed them to access additional artificial clients, which would translate into cooperatively eating ectoparasites rather than cheating by eating client mucus under natural conditions [10]. Here we show that cleaners immediately increase current levels of cooperation in the presence of?bystander client reef fish. Furthermore, we find that bystanders respond to any occurrence of cleaners cheating their current client with avoidance. In conclusion, the results demonstrate, for the first time, that image scoring by an audience indeed leads to increased levels of cooperation in a nonhuman animal.     

Intracerebroventricular injection of streptozotocin in rats produces both oxidative stress in the brain and cognitive impairment

Recent reports suggest the involvement of free radicals in the pathophysiology of Alzheimer's disease [AD]. Streptozotocin [STZ] injection in the brain is known to cause cognitive impairment in rats and is likened to sporadic AD in humans. Though STZ is known to cause impairment in glucose and energy metabolism, it is not known whether this is associated with free radical generation. The present study was designed to investigate if the changes in learning and memory by intracerebroventricular administration of STZ are associated with changes in the markers of oxidative stress. Adult male Wistar rats [330-340 g] were injected with intracerebroventricular STZ [3 mg/kg] bilaterally stereotaxically under ketamine anesthesia [70 mg/kg]. The rats were treated with STZ twice, on day 1 and on day 3. The learning and memory behavior was analyzed using passive avoidance paradigms, elevated plus maze and the closed field activity test while the parameters of oxidative stress assessed were malondialdehyde [MDA] and glutathione. The behavioral tests were performed on day 17, 18 and 19. The rats developed significant deficits in learning, memory and cognitive behavior, indicated by deficits in passive avoidance paradigm and elevated plus maze as compared to sham rats. On day 21, the rats were sacrificed under ether anesthesia and the brains were analyzed for biochemical studies. There was a development of oxidative stress in the brain as indicated by significant elevations in malondialdehyde [MDA] levels and decreased levels of glutathione. The study demonstrates that intracerebroventricular STZ may be appropriate model for investigations of antioxidants as potential treatment in Alzheimer's dementia.     

Differential effects of chronic escapable versus inescapable stress on male syrian hamster (Mesocricetus auratus) reproductive behavior

Stress decreases sexual activity, but it is uncertain which aspects of stress are detrimental to reproduction. This study used an escapable/inescapable stress paradigm to attempt to dissociate physical from psychological components of stress, and assess each component's impact on reproductive behavior in the male Syrian hamster (Mesocricetus auratus). Two experiments were completed using this protocol where two animals receive the same physical stressor (an electric footshock) but differ in the psychological aspect of control. One group (executive) could terminate the shock for themselves as well as a second group (yoked) by pressing a bar. Experiment 1 demonstrated a significant increase in plasma glucocorticoids at the end of a single 90-min stress session with no difference in glucocorticoid levels between the executive and yoked groups at any time point. Experiment 2 quantified male reproductive behavior prior to and immediately following 12 days of escapable or inescapable stress in executive, yoked, and no-stress control hamsters (n = 12/group). Repeated-measures analysis of variance revealed a number of significant changes in reproductive behavior before and after stress in the three treatment groups. The most striking difference was a decrease in hit rate observed only in the animals that could not control their stress (yoked group). Hit rate in the executive males that received the exact same physical stressor but could terminate the shock by pressing a bar was nearly identical to control animals that never received any foot shock. Therefore, we conclude that coping or control can ameliorate the negative effects of stress on male reproductive behavior.     

Genetic dissection of the zebrafish habenula, a possible switching board for selection of behavioral strategy to cope with fear and anxiety

The habenula is a part of an evolutionarily highly conserved conduction pathway within the limbic system that connects telencephalic nuclei to the brain stem nuclei such as interpeduncular nucleus(IPN), the ventral tegmental area (VTA), and the raphe.In mammals, the medial habenula receives inputs from the septohippocampal system, and relaying such information to the IPN. In contrast, the lateral habenula receives inputs from the ventral pallidum, a part of the basal ganglia. The physical adjunction of these two habenular nuclei suggests that the habenula may act as an intersection of the neural circuits for controlling emotion and behavior. We have recently elucidated that zebrafish has the equivalent structure as the mammalian habenula. The transgenic zebrafish, in which the neural signal transmission from the lateral subnucleus of the dorsal habenula to the dorsal IPN was selectively impaired, showed extremely enhanced levels of freezing response to presentation of the conditioned aversive stimulus. Our observation supports that the habenula may act as the multimodal switching board for controlling emotional behaviors and/or memory inexperience dependent manners.     

Can embryonic skipper frogs (<Emphasis Type="Italic">Euphlyctis cyanophlyctis</Emphasis>) learn to recognise kairomones in the absence of a nervous system?

In this study, we used larval Euphlyctis cyanophlyctis to determine the predator recognition mechanism. We conducted a series of experiments to determine if larval E. cyanophlyctis have the innate ability to recognise predatory odour (kairomones) as a threat or if they learn to do so during ontogeny. In the case of learning, we wanted to determine the developmental window during which learning is accomplished. Further, we tested the antipredator response of predator-naïve as well as predator-experienced tadpoles to chemical cues of different origins in order to assess if they exhibit differential responses. Our results clearly indicate that predator-naïve tadpoles of E. cyanophlyctis do not reduce their activity against predatory cues of dragonfly nymphs, suggesting that they lack the innate ability to recognise kairomones. However, they could learn to do so when trained to perceive kairomones simultaneously along with alarm cues. Surprisingly, larval E. cyanophlyctis could learn to recognise kairomones through association during embryonic stages even before the development of a nervous system. Although larval E. cyanophlyctis lack the innate ability to recognise kairomones, they were able to recognise conspecific alarm cues on the first encounter, indicating that they have the innate ability to recognise alarm cues as a potential threat.     

虚拟视觉刺激引起幼年斑马鱼捕食行为放弃的研究

目的 当动物重复某种行为以逃避危险或获取奖励而无法成功时，会产生放弃。放弃是一种常见且基本的行为，在小鼠等模式动物中已经被广泛研究，但是其部分神经机制仍未被阐明。幼年斑马鱼适合进行全脑光学成像，是神经科学领域的重要模式生物。已经有研究者通过持续电击等消极刺激诱发斑马鱼放弃行为，然而奖励刺激能否引起斑马鱼放弃尚无报道。本文对奖励刺激引起的斑马鱼放弃行为进行了探究。方法 通过给予斑马鱼虚拟的食物视觉刺激，检验斑马鱼对虚拟食物的捕食情况，比较斑马鱼捕食频率和单次捕食时长随时间的变化。结果 虚拟的食物视觉刺激可以引起斑马鱼的捕食行为，接受25 min虚拟刺激后，8日龄以上斑马鱼的捕食频率和单次捕食时长均出现显著下降。结论 此研究丰富了斑马鱼放弃行为的研究范式，实验结果表明，缺失真实奖励的虚拟食物刺激可以诱导斑马鱼放弃捕食行为，这将进一步加深对动物放弃行为的理解，推动对其神经机制的研究。     

Running Reduces Uncontrollable Stress-Evoked Serotonin and Potentiates Stress-Evoked Dopamine Concentrations in the Rat Dorsal Striatum

Accumulating evidence from both the human and animal literature indicates that exercise reduces the negative consequences of stress. The neurobiological etiology for this stress protection, however, is not completely understood. Our lab reported that voluntary wheel running protects rats from expressing depression-like instrumental learning deficits on the shuttle box escape task after exposure to unpredictable and inescapable tail shocks (uncontrollable stress). Impaired escape behavior is a result of stress-sensitized serotonin (5-HT) neuron activity in the dorsal raphe (DRN) and subsequent excessive release of 5-HT into the dorsal striatum following exposure to a comparatively mild stressor. However, the possible mechanisms by which exercise prevents stress-induced escape deficits are not well characterized. The purpose of this experiment was to test the hypothesis that exercise blunts the stress-evoked release of 5-HT in the dorsal striatum. Changes to dopamine (DA) levels were also examined, since striatal DA signaling is critical for instrumental learning and can be influenced by changes to 5-HT activity. Adult male F344 rats, housed with or without running wheels for 6 weeks, were either exposed to tail shock or remained undisturbed in laboratory cages. Twenty-four hours later, microdialysis was performed in the medial (DMS) and lateral (DLS) dorsal striatum to collect extracellular 5-HT and DA before, during, and following 2 mild foot shocks. We report wheel running prevents foot shock-induced elevation of extracellular 5-HT and potentiates DA concentrations in both the DMS and DLS approximately 24 h following exposure to uncontrollable stress. These data may provide a possible mechanism by which exercise prevents depression-like instrumental learning deficits following exposure to acute stress.     

Stress-induced reductions of sensory reactivity in female rats depend on ovarian hormones and the application of a painful stressor

The current experiments occurred in the context of disputes in the literature concerning whether inescapable stress causes differential changes in sensory reactivity, which could lead to differences in many learning procedures. We tested rats for differences in sensitivity and responsivity to acoustic stimuli through the use of the acoustic startle response (ASR) 2 h after stressor exposure and ambulatory activity 24 h later in the open field. Stressed females showed reduced responsivity to acoustic stimuli with no apparent shift in stimulus sensitivity. Males did not show differences in either reactivity index following stressor exposure. Reduced responsivity did not occur if females had been OVX (OVX alone did not effect stimulus responsivity or sensitivity). All groups that experienced tailshock stress also had reduced open field activity 24 h later. Restraint for 2 h did not reduce stimulus responsivity in the ASR or open field activity in female rats. Acute reductions in ASRs after a painful stressor appear to be a feature specific to females, with an apparent role of ovarian hormones as a modulator of the effect. Possible hormone and/or immunological mechanisms of these sex-specific effects are discussed. Understanding the mechanisms of this stressor-induced reduction in sensory reactivity could advance our knowledge of how individual differences in ovarian hormone levels influence the physical and psychological processes by which females acutely respond and later recover from traumatic events.