Effects Of Footshock Research Articles

Distinct acute stressors exert an antagonistic effect on complex grooming during novelty habituation in rats

Grooming is a common readout in multiple rat models of neuropsychiatric diseases. It is usually associated with distress and negative emotionality, but also with emotional de-arousal after stress. These seemingly conflicting interpretations may result from specific grooming sequences appearing at different arousal levels and during distinct phases of the stress response. To further explore this hypothesis, we analyzed how distinct stressors affect grooming syntaxis and kinetics. To that end, we explored the independent and interacting effects of foot shocks, corticosterone (CORT), and novelty on exploratory activity, grooming, and ultrasonic vocalizations (USVs) in an open-field test (OF). Wistar rats were intraperitoneally injected either with vehicle or CORT, placed in a chamber where half of them were foot-shocked and then assessed in the OF. The next day, animals were re-exposed to the shock chamber and then tested in the OF without receiving any treatment. On day 1, foot shocks and –to a less extent CORT– increased freezing and inhibited rearing in the chamber, but only foot shocks increased distress USVs. In the OF, both treatments suppressed complex grooming, with foot-shocks also inhibiting exploration and CORT marginally reducing rearing. On day 2, foot-shocked rats showed conditioned fear when re-exposed to the chamber. When tested in the OF, foot-shocked and CORT-treated animals still showed low levels of complex grooming, with the former group also showing increased distress USVs. In this study, all different stressors inhibited complex grooming, suggesting an inverse association between these grooming subtypes and negative emotionality.

Co-released norepinephrine and galanin act on different timescales to promote stress-induced anxiety-like behavior.

Both the noradrenergic and galaninergic systems have been implicated in stress-related neuropsychiatric disorders, and these two neuromodulators are co-released from the stress-responsive locus coeruleus (LC); however, the individual contributions of LC-derived norepinephrine (NE) and galanin to behavioral stress responses are unclear. Here we aimed to disentangle the functional roles of co-released NE and galanin in stress-induced behavior. We used foot shock, optogenetics, and behavioral pharmacology in wild-type (WT) mice and mice lacking either NE (Dbh-/-) or galanin (GalcKO-Dbh) specifically in noradrenergic neurons to isolate the roles of these co-transmitters in regulating anxiety-like behavior in the elevated zero maze (EZM) either immediately or 24 h following stress. Foot shock and optogenetic LC stimulation produced immediate anxiety-like behavior in WT mice, and the effects of foot shock persisted for 24 h. NE-deficient mice were resistant to the anxiogenic effects of acute stress and optogenetic LC stimulation, while mice lacking noradrenergic-derived galanin displayed typical increases in anxiety-like behavior. However, when tested 24 h after foot shock, both Dbh-/- and GalcKO-Dbh mice lacked normal expression of anxiety-like behavior. Pharmacological rescue of NE, but not galanin, in knockout mice during EZM testing was anxiogenic. In contrast, restoring galanin, but not NE, signaling during foot shock normalized stress-induced anxiety-like behavior 24 h later. These results indicate that NE and noradrenergic-derived galanin play complementary, but distinguishable roles in behavioral responses to stress. NE is required for the expression of acute stress-induced anxiety, while noradrenergic-derived galanin mediates the development of more persistent responses following a stressor.

Foot shock facilitates reward seeking in an experience-dependent manner

Animals organize reward seeking around aversive events. An abundance of research shows that foot shock, as well as a shock-associated cue, can elicit freezing and suppress reward seeking. Yet, there is evidence that experience can flip the effect of foot shock to facilitate reward seeking. Here we examined cue suppression, foot shock suppression and foot shock facilitation of reward seeking in a single behavioural setting. Male Long Evans rats received fear discrimination consisting of danger, uncertainty, and safety cues. Discrimination took place over a baseline of rewarded nose poking. With limited experience (1–2 sessions), all cues and foot shock suppressed reward seeking. With continued experience (10–16 sessions), suppression became specific to shock-associated cues, foot shock briefly suppressed, then facilitated reward seeking. Our results provide a means of assessing positive properties of foot shock, and may provide insight into maladaptive behaviour around aversive events.

Effects of footshocks on anxiety-like behavior and mRNA levels of precursor peptides for corticotropin releasing factor and opioids in the forebrain of the rat

Corticotropin releasing factor (CRF) and dynorphin are neuropeptides that are associated with the negative emotional states. Experimental evidence indicates that dynorphin neurons located in the nucleus accumbens and CRF neurons in the bed nucleus of the stria terminalis (BST) and the central nucleus of the amygdala (CeA) mediate anxiety-like behaviors immediately after the stressful experience (24–48h). The present study was done to evaluate if changes in the levels of the mRNA for these peptides in the striatum, BST, and CeA were associated with the long-lasting avoidance of novelty, a measure of an anxiety-like state, in a subset of rats exposed to unpredictable and moderately intense footshocks (5×2s of 1.5mA). Shocked rats with enhanced fear to a novel tone 24h after the footshocks (high responders; HR) displayed long-lasting avoidance in the elevated T-maze whereas shocked rats with low levels of acute fear (low responders; LR) had low levels of avoidance similar to nonshocked rats. An increase in the level of proCRF mRNA was detected in the CeA of the HR compared to LR and nonshocked rats but not in other areas of the brain sampled. In contrast, prodynorphin and proenkephalin mRNA levels in the striatum, BST and CeA were not different between HR, LR and nonshocked rats. This study provides evidence that CRF neurons in the CeA may play a role in the anxiety-like state produced in a subset of rats exposed to footshocks.

Footshock-induced responses in ventral subiculum neurons are mediated by locus coeruleus noradrenergic afferents

The ventral subiculum (vSub) of the hippocampus is critically involved in mediating the forebrain's response to stress, particularly with regard to psychogenic stressors. Stress, in turn, is known to aggravate many psychiatric conditions including schizophrenia, depression, anxiety, and drug abuse. Pathological alterations in hippocampal function have been identified in all these disorders; thus, it is of interest to understand how stress affects this brain region. The vSub receives dense projections from the stress-related locus coeruleus (LC); however, it is not known what role this input plays in signaling stressful stimuli. In this study, the direct LC innervation of the vSub was investigated as a potential mediator of stress responses in this region. To examine responses to an acute stressor, the effect of footshock on single vSub neurons was tested in rats. Footshock inhibited 13%, and activated 48% of neurons in this region. Importantly, responses to footshock were correlated with LC stimulation-evoked responses in single neurons, and LC inactivation blocked these responses. Furthermore, prazosin, an alpha-1 antagonist, reversed footshock-evoked inhibition, revealing an underlying activation. Inactivation of the basolateral amygdala (BLA) did not block phasic footshock-evoked activation; however, it reduced tonic activity in the vSub. These results suggest that the LC NE system plays an important role in mediating stress responses in the vSub. Footshock evokes both inhibition and excitation in the vSub, by activating noradrenergic inputs from the LC. These responses may contribute to stress adaptation; while an imbalance of this system may lead to pathological stress responses in mental disorders.

Mild acute stress reactivates memory of a discriminative avoidance task in mice

Previous studies have demonstrated that stress or glucocorticoids impair the retrieval of spatial memory in rodents and declarative memory in humans. However, the effects on memory retrieval of stress introduced a long time after learning have not been well studied. We investigated whether a mild, extrinsic stressor (1-s 0.1 or 0.3 mA foot shock) would reactivate low baseline retrieval of an aversive memory [the plus-maze discriminative avoidance task (PM-DAT)] and if it would be modulated by glucocorticoids. In Experiment 1, male Swiss mice received pre-test foot shock (n = 10 mice/group) 7 days after training and just before testing. A time-retrieval curve for low baseline retrieval for the subsequent experiments was also determined (Experiment 2, n = 10 mice/group). We investigated if pre-test foot shock could modify corticosterone release (Experiment 3, n = 8–9 mice/group) and reinstate retrieval in the PM-DAT (Experiment 4, n = 15 mice/group). The effects of metyrapone (100 mg/kg) on retrieval reinstatement (Experiment 5, n = 15 mice/group) and serum corticosterone enhancement (Experiments 6, n = 7–9 mice/group) induced by foot shock were analyzed. Finally, the effects of foot shock itself on PM-DAT exploration were verified (Experiment 7, n = 10 mice/group). We demonstrated here that foot shock reinstated the retrieval of a low baseline, discriminative avoidance task 30 (but not 7) days after training. This facilitative effect was not dependent on corticosterone secretion because metyrapone abolished the enhancement of corticosterone concentration but did not reverse the stress-induced reinstatement of retrieval.

The effects of footshock and immobilization stress on tyrosine hydroxylase phosphorylation in the rat locus coeruleus and adrenal gland

Tyrosine hydroxylase (TH), the rate-limiting enzyme in catecholamine biosynthesis, is regulated acutely by protein phosphorylation. No studies have systematically investigated the time course of TH phosphorylation in vivo in response to different stressors. We therefore determined the extent of TH phosphorylation at Ser19, Ser31, and Ser40 over a 40-min period in response to footshock or immobilization stress in the rat locus coeruleus and adrenal medulla. There were significant changes in TH phosphorylation in both tissues and the responses to the two stressors differed markedly. With each of the phosphorylation sites immobilization stress caused a much smaller, or less sustained, response than footshock stress. With immobilization stress there was a transient increase in Ser31 phosphorylation in the locus coeruleus and in the adrenal medulla, but there were no effects on Ser19 or Ser40 phosphorylation. With footshock stress there was a substantial decrease in Ser19 phosphorylation over time, a substantial increase in Ser31 phosphorylation over time, but there were no effects on Ser40 phosphorylation. Measuring TH phosphorylation at Ser19, Ser31, and Ser40 over time can therefore be used as a sensitive index to differentiate the effects of different stressors on catecholaminergic cells.

Enduring sensorimotor gating abnormalities following predator exposure or corticotropin-releasing factor in rats: A model for PTSD-like information-processing deficits?

A deficit in prepulse inhibition (PPI) can be one of the clinically observed features of post-traumatic stress disorder (PTSD) that is seen long after the acute traumatic episode has terminated. Thus, reduced PPI may represent an enduring psychophysiological marker of this illness in some patients. PPI is an operational measure of sensorimotor gating and refers to the phenomenon in which a weak stimulus presented immediately before an intense startling stimulus inhibits the magnitude of the subsequent startle response. The effects of stress on PPI have been relatively understudied, and in particular, there is very little information on PPI effects of ethologically relevant psychological stressors. We aimed to develop a paradigm for evaluating stress-induced sensorimotor gating abnormalities by comparing the effects of a purely psychological stressor (predator exposure) to those of a nociceptive physical stressor (footshock) on PPI and baseline startle responses in rats over an extended period of time following stressor presentation. Male Sprague–Dawley rats were exposed (within a protective cage) to ferrets for 5 min or left in their homecage and then tested for PPI immediately, 24 h, 48 h, and 9 days after the exposure. The effects of footshock were evaluated in a separate set of rats. The effects seen with stressor presentation were compared to those elicited by corticotropin-releasing factor (CRF; 0.5 and 3 μg/6 μl, intracerebroventricularly). Finally, the effects of these stressors and CRF administration on plasma corticosterone were measured. PPI was disrupted 24 h after ferret exposure; in contrast, footshock failed to affect PPI at any time. CRF mimicked the predator stress profile, with the lowdose producing a PPI deficit 24 h after infusion. Interestingly, the high dose also produced a PPI deficit 24 h after infusion, but with this dose, the PPI deficit was evident even 9d later. Plasma corticosterone levels were elevated acutely (before PPI deficits emerged) by both stressors and CRF, but returned to normal control levels 24 h later, when PPI deficits were present. Thus, predator exposure produces a delayed disruption of PPI, and stimulation of CRF receptors recapitulates these effects. Contemporaneous HPA axis activation is neither necessary nor sufficient for these PPI deficits. These results indicate that predator exposure, perhaps acting through CRF, may model the delayed-onset and persistent sensorimotor gating abnormalities that have been observed clinically in PTSD, and that further studies using this model may shed insight on the mechanisms of information-processing deficits in this disorder. This article is part of a Special Issue entitled ‘Post-Traumatic Stress Disorder’.

Neuronal cell adhesion molecule deletion induces a cognitive and behavioral phenotype reflective of impulsivity

Cell adhesion molecules, such as neuronal cell adhesion molecule (Nr-CAM), mediate cell-cell interactions in both the developing and mature nervous system. Neuronal cell adhesion molecule is believed to play a critical role in cell adhesion and migration, axonal growth, guidance, target recognition and synapse formation. Here, wild-type, heterozygous and Nr-CAM null mice were assessed on a battery of five learning tasks (Lashley maze, odor discrimination, passive avoidance, spatial water maze and fear conditioning) previously developed to characterize the general learning abilities of laboratory mice. Additionally, all animals were tested on 10 measures of sensory/motor function, emotionality and stress reactivity. We report that the Nr-CAM deletion had no impact on four of the learning tasks (fear conditioning, spatial water maze, Lashley maze and odor discrimination). However, Nr-CAM null mice exhibited impaired performance on a task that required animals to suppress movement (passive avoidance). Although Nr-CAM mutants expressed normal levels of general activity and body weights, they did exhibit an increased propensity to enter stressful areas of novel environments (the center of an open field and the lighted side of a dark/light box), exhibited higher sensitivity to pain (hot plate) and were more sensitive to the aversive effects of foot shock (shock-induced freezing). This behavioral phenotype suggests that Nr-CAM does not play a central role in the regulation of general cognitive abilities but may have a critical function in regulating impulsivity and possibly an animal's susceptibility to drug abuse and addiction.

Footshock-induced sensitization of the acoustic startle response in two strains of mice

It has been shown before that unconditioned footshocks can augment the acoustic startle response in rats. In the present study, male mice of two strains, C57Bl/6N and BALB/c, were compared with regard to footshock-induced sensitization of the acoustic startle response. Presentation of footshocks did not affect the acoustic startle response in C57Bl/6N mice, while in contrast, footshock-induced sensitization was apparent in the BALB/c strain. Shocked C57Bl/6N mice, but not BALB/c mice, displayed robust conditioning to the startle context when re-tested the next day. These findings indicate that mice may exhibit footshock-induced sensitization of the acoustic startle response, but that the effects of footshocks on the acoustic startle are strain- and time-dependent.

Alpha-2 Adrenergic Receptor Agonists Block Stress-Induced Reinstatement of Cocaine Seeking

The alpha-2 adrenergic receptor agonists, clonidine, lofexidine and guanabenz, blocked stress- but not cocaine-induced reinstatement of cocaine seeking at doses that suppressed footshock-induced release of noradrenaline in prefrontal cortex and amygdala. Rats were trained to self-administer cocaine (0.5 mg/kg/infusion, i.v; 10-12 days) and, after a drug-free period (7-13 days), were returned to the self-administration chambers for daily extinction and reinstatement test sessions. Both intermittent footshock (15 min, 0.6 mA) and cocaine priming (20 mg/kg, i.p.) reinstated extinguished drug seeking. Pretreatment with either clonidine (20, or 40 microg/kg, i.p.) or lofexidine (50, 100, 150, or 200 microg/kg, i.p.) attenuated footshock- but not cocaine-induced reinstatement of cocaine seeking. Guanabenz (640 microg/kg, i.p.), an alpha-2 agonist with low affinity for imidazoline type-1 receptors, also attenuated footshock- but not cocaine-induced reinstatement of cocaine seeking. The results point to an important role for NE systems in the effects of footshock on relapse to cocaine seeking.

Stress and relapse to drug seeking in rats: studies on the generality of the effect.

Intermittent footshock reinstates drug-taking behavior in rats, but not behaviors previously maintained by food reinforcers. Here we tested further the generality of this phenomenon by determining whether restraint and food deprivation stressors would reinstate heroin seeking, whether the environment in which footshock is given modulates footshock-induced reinstatement, and whether footshock would reinstate operant responding previously maintained by brain stimulation reward (BSR). Groups of rats were trained to self-administer for 10 days either heroin (0.05-0.1 mg/kg/infusion, IV, three 3-h sessions/day) or brain stimulation into the septal area (trains of monopolar cathodal pulses of 100 micros for 500 ms, one 60-min session/day). After extinction of the heroin-reinforced behavior (10-13 days), the rats were tested for reinstatement after exposure to food deprivation (1 and 21 h), restraint given outside the self-administration environment (5, 15 and 30 min), or intermittent footshock (0.8 mA, 15 min) given in the self-administration environment or in a novel (non-drug) environment. For BSR-trained rats, the effect of footshock on reinstatement after extinction (6-10 days) was compared with that induced by noncontingent brain stimulation (three or six discrete stimulations at the start of the test sessions). Food deprivation reinstated heroin seeking. Footshock reliably reinstated heroin seeking when given in the drug environment, but not when given in a non-drug environment. Similarly, restraint given outside the self-administration environment failed to reinstate heroin seeking. In addition, footshock was as effective as priming brain stimulation in reinstating operant responding previously maintained by BSR. The effect of footshock on reinstatement of heroin seeking generalizes to food deprivation, and appears to be dependent on the environment in which the stressor is given. The data with BSR indicate that the phenomenon of footshock-induced reinstatement is not selective for drug reinforcers.

Injection of corticotropin-releasing hormone into the locus coeruleus or foot shock increases neuronal fos expression

Previous research suggests that corticotropin-releasing hormone can act in the locus coeruleus to increase the firing of locus coeruleus neurons and elicit physiological responses resembling those associated with stress. The present study used immunocytochemical detection of Fos as a measure of neuronal activation to identify brain areas that were activated by bilateral injections of corticotropin-releasing hormone into the locus coeruleus of rats. Injection of corticotropin-releasing hormone into the locus coeruleus increased the expression of Fos in the locus coeruleus as compared with injection of vehicle into the locus coeruleus or injection of corticotropin-releasing hormone into neighbouring pontine sites. The pattern of Fos expression throughout the brain after injections of corticotropin-releasing hormone into the locus coeruleus was generally consistent with the anatomical organization of efferent projections arising from the locus coeruleus; increased Fos expression was observed in many brain areas including the ventral lateral septum, septohypothalamic nucleus, bed nucleus of the stria terminalis, the central amygdaloid nucleus, the dorsomedial nuclei of the hypothalamus, and the thalamic paraventricular and rhomboid nuclei. Foot shock also increased Fos expression in the locus coeruleus and the other brain regions that expressed Fos after corticotropin-releasing hormone injections into the locus coeruleus. A few brain regions, most notably the hypothalamic paraventricular nucleus, expressed Fos in response to foot shock but not corticotropin-releasing hormone. These results indicate that local injection of corticotropin-releasing hormone into the locus coeruleus stimulates the activity of the locus coeruleus neurons. However, the pattern of Fos expression throughout the brain evoked by injection of corticotropin-releasing hormone into the locus coeruleus does not fully replicate the effects of foot shock.

Stress-induced increase in brain neuroactive steroids: Antagonism by abecarnil

Acute foot shock stress elicits a selective and time-dependent increase of neuroactive steroid (pregnenolone, progesterone, allotetrahydrodeoxycorticosterone) concentrations in rat brain cortex, accompanied by a marked increase of plasma corticosterone. The brain cortical neuroactive steroid levels peaked between 10 and 30 min poststress and returned to control values by 2 h. Abecarnil (0.3 mg/kg, IP), a beta-carboline derivative with anxiolytic properties, completely antagonized the effect of foot shock on brain cortical neuroactive steroids. A single administration of the anxiogenic beta-carboline FG 7142 (15 mg/kg, IP), in contrast, mimicked the effect of foot shock. These data support the hypothesis for the existence of a functional relationhip between brain neuroactive steroid concentrations and GABA A receptor function/emotional state of the animal.

Left and right 6-hydroxydopamine lesions of the medial prefrontal cortex differentially alter subcortical dopamine utilization and the behavioral response to stress

The effects of left and right prefrontal cortical dopamine (DA) depletion on circling behavior, stress-escape behavior and subcortical DA function were examined in rats exhibiting left or right turning biases. 6-Hydroxydopamine lesions of the medial prefrontal cortex (PFC) caused significant DA depletions when assessed in separate studies at 3 days and 3–4 weeks. However, depletions were smaller at 3–4 weeks and there was a significant increase in DA concentration on the left side following right lesions. Significant increases in striatal DA content were observed following lesions of either side at 3–4 weeks, but not at 3 days. No changes in DA concentration were observed in the nucleus accumbens septi (NAS). Left circling rats significantly increased their circling behavior following right sided lesions and showed disrupted footshock-escape behavior following left sided lesions. Performance of the footshock-escape task exerted an effect on striatal and NAS DA utilization as indicated by the ratio of 3,4-dihydroxyphenylacetic acid (DOPAC) to DA. The effects of footshock on NAS DA utilization were greater following left PFC lesions as compared to the right lesion and sham conditions. These lesion effects were also greater in left- than in right-turning animals. The data indicate that an intrinsic asymmetry in brain DA systems interacts with left and right PFC lesions to differentially determine subcortical DA function and behaviors that it subserves.

Effects of footshock-, psychological- and forced swimming-stress on the learning and memory processes: involvement of opioidergic pathways.

Modulation of learning and memory acquisition, retention and retrieval in the one trial passive avoidance learning task in mice by three inescapable stresses, i.e., footshock (FS), psychological (PSY) and forced swimming (SW) were investigated. Pre-, post-training and pre-test FS-stress (2 mA, 0.2 Hz, 1 sec for 30 min) and pre-training PSY-stress (communication box, 5 min) resulted in enhanced test latencies. On the contrary, SW-stress (20 degrees C, 5 min) immediately or 1 hr after training impaired retention latencies that tended to recover after 2 hr post-training SW-stress, suggesting that at least 2 hr are required to consolidate newly acquired information. In contrast, pre-stress naloxone (Nx), which did not affect FS- and PSY-stress induced facilitatory effects, returned to control levels the impaired retention latencies induced by SW-stress. Taken collectively, these results imply the involvement of an opioid-dependent mechanism in the modulation of memory by SW-stress and non-opioid in the case of FS- and PSY-stress. Furthermore, they suggest that different mechanisms are involved in stress-induced memory modifications and the production of stress-induced analgesia (SIA) since in the latter, FS and PSY but not SW stress produce Nx-sensitive antinociception.

Amygdaloid noradrenaline is involved in the sensitization of the acoustic startle response in rats

The present study examined the role of noradrenaline (NA) in the central nucleus of the amygdala (cA) in the sensitization of the acoustic startle response (ASR) in rats. In the first experiment, local microinjections of 0, 0.5, 1, 2 nmol of the α 2-adrenergic antagonist yohimbine into the cA increased the magnitude of the ASR in a dose-dependent way. In the second experiment, foot shocks were applied to increase the ASR amplitude (sensitization). Local microinjections of 0, 4, 8, 16 nmol of the α 2-adrenergic agonist ST-91 into the cA dose dependently decreased the sensitizing effects of foot shocks on the amplitude of the ASR. It is conjectured that yohimbine increases and ST-91 decreases local NA release by acting at presynaptic autoreceptors. The present data suggest that the release of NA in the cA is involved in the mediation of the sensitizing effects of foot shocks on the ASR.

The effect of eye-like schema on shuttling activity of wild house mice (Mus musculus domesticus): Context-dependent threatening aspects of the eyespot patterns

The effects of footshock and various light-spot models on the shuttling activity of mice were examined in a passive avoidance situation. It was found that mild footshocks elicited initial exploration followed by an increased tendency to escape from the compartment in which the shocks were administered. An encounter with models, consisting of various numbers of small yellow lights, without footshock did not cause significant differences in shuttling activity. But if the models were paired with footshock, a tendency to explore during the first trial, high readiness to escape, and avoidance learning were found. These were characterized by a temporary increase in number of gate crossings, a decrease in the time spent in the shocked compartment, and a considerable increase in latency to enter the shocked compartment. The most effective model had two horizontally arranged yellow lights, which may share some characteristics with eye-like patterns.

A chronic high-salt diet fails to enhance blood pressure reactivity to a tone associated with footshock in SHR, BHR, and WKY rats

Both the human and animal literatures suggest that reactivity to stress is enhanced in the presence of a positive family history of hypertension. There is also some suggestive evidence, though not as strong, that a high-salt diet will enhance reactivity to stress, at least in a subpopulation of individuals. In the present study, rats withzero (Wistar-Kyoto, or WKY), one (borderline hypertensive, or BHR), or two (spontaneously hypertensive, or SHR) hypertensive parents were placed on a normal or high (8% in chow)-salt diet for 8 weeks starting at 8 weeks of age. After 6 weeks on the appropriate diet, rats were stressed daily for 5 days. Each session consisted of 28 foot shock trials preceded by a tone. On the following week, animals were instrumented with femoral artery catheters. After a 2-day recovery period, they were again subjected to the experimental paradigm, during which blood pressure was continuously monitored. Differences were found with respect to blood pressure reactivity and family history: SHR were the most reactive to the tone associated with foot shock. However, no effects of salt on reactivity were observed, despite an effect of this manipulation on basal blood pressure. The effect of foot shock itself was also studied, and revealed that BHR showed a blood pressure reactivity response intermediate between SHR and WKY. Once again, no effects of the salt manipulation were seen. In conclusion, while the data support a relationship between family history of hypertension and reactivity to stress, they do not support a relationship between salt intake and reactivity to stress. Studies that do suggest such a relationship appear to have in common the use of stressors that would be expected to evoke active coping.

Learned helplessness inducing foot shock can exacerbate morphine responsiveness

Exposure to inescapable tail shock or foot shock has been shown to produce effects on a number of learning tasks. Tail-shock exposure is also known to influence nociception and morphine reactivity. The present series of experiments investigated the effects of foot shock known to induce learned helplessness effects in our laboratory on the subsequent reactivity to morphine. A first set of experiments investigated the hypoalgesic response to a 4 mg/kg dose morphine over 4 consecutive days following exposure to foot shock. Experiment 1A did not reveal an effect of foot shock on morphine-induced hypoalgesia when testing was conducted in a novel context. In Experiment 1B, we observed an increased hypoalgesic response to morphine when testing was conducted in the shock context. The findings of Experiment 1B were replicated in Experiment 2 and extended to assess the contribution of conditioned fear hypoalgesia to these effects. The possible mechanisms responsible for these findings are discussed.