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PubMed1986

Interruption of projections from the medial geniculate body to an archi-neostriatal field disrupts the classical conditioning of emotional responses to acoustic stimuli.

We have previously found that the coupling of changes in autonomic activity and emotional behavior to acoustic stimuli through classical fear conditioning survives bilateral ablation of auditory cortex but is disrupted by bilateral lesions of the medial geniculate nucleus or inferior colliculus in rats. Auditory fear conditioning thus appears to be mediated by the relay of acoustic input from the medial geniculate nucleus to subcortical rather than cortical targets. Since the medial geniculate nucleus projects, in addition to auditory cortex, to a striatal field, involving portions of the posterior neostriatum and underlying archistriatum (amygdala), we have sought to determine whether interruption of connections linking the medial geniculate nucleus to this subcortical field also disrupts conditioning. The conditioned emotional response model studied included the measurement of increases in mean arterial pressure and heart rate and the suppression of exploratory activity and drinking by the acoustic conditioned stimulus following delayed classical conditioning, where the footshock unconditioned stimulus appeared at the end of the conditioned stimulus. The peak increase in arterial pressure and the duration of activity and drinking suppression were greater in unoperated animals subjected to delayed conditioning than in pseudoconditioned controls, where the footshock was randomly rather than systematically related to the acoustic stimulus. Increases in heart rate, however, did not differ in conditioned and pseudoconditioned groups. While the arterial pressure and behavioral responses therefore reflect associative conditioning, the heart rate response does not. Rats were prepared with bilateral lesions of the medial geniculate nucleus, bilateral lesions of the striatal field or asymmetrical unilateral lesions destroying the medial geniculate nucleus on one side and the striatal field on the contralateral side. The latter preparation leaves one medial geniculate nucleus and one striatal field intact but disconnected and thus produces a selective auditory deafferentation of the intact striatal field. Control groups included animals with unilateral lesion of the medial geniculate nucleus, with unilateral lesion of the medial geniculate nucleus combined with lesion of the ipsilateral striatal field, unilateral lesion of the medial geniculate combined with lesion of the contralateral anterior neostriatum (a striatal area outside of the medial geniculate nucleus projection field).(ABSTRACT TRUNCATED AT 400 WORDS)

Acoustic Stimulation↗
PubMed1990

The influence of dexamethasone on behaviorally conditioned immunomodulation and plasma corticosterone.

Utilizing a conditioned taste aversion paradigm we have previously shown that rats re-exposed to a saccharin solution previously paired with cyclophosphamide (CY) demonstrate significantly reduced in vitro mitogen-induced spleen cell proliferation and IgM secretion assessed 24 h after saccharin re-exposure. In this report treatment of similarly conditioned rats with dexamethasone (DEX) either before conditioning or before re-exposure abrogated the conditioned modulation of pokeweed mitogen (PWM)-induced spleen cell proliferation. The finding that DEX pretreatment on the conditioning day was as effective in abrogating the conditioned response as DEX treatment prior to the test day does not support pituitary-adrenal mediation of the conditioned immusuppressive effect following re-exposure of conditioned animals to the CS. There was no significant conditioned immunosuppression observed with respect to PHA- and Con A-induced proliferation and the influence of DEX on these parameters could not be assessed. The effect on PWM-induced IgM production was inconclusive since the reduced IgM response among conditioned animals was of only borderline significance.

Animals↗
PubMed2004

Enhancement of antibody production and expression of c-Fos in the insular cortex in response to a conditioned stimulus after a single-trial learning paradigm.

Immune responses can be modulated by Pavlovian conditioning techniques. In this study, to evaluate the conditionability of antibody response via a single-trial conditioning paradigm, we used a protein antigen ovalbumin as an unconditioned stimulus (UCS) that was paired with a novel taste of saccharin in a single-trial learning protocol. A significant enhancement of anti-ovalbumin antibody production was observed in the conditioned rats at Days 15, 20 and 25 after re-exposure to the conditioned stimulus. The pattern of conditioned antibody response is similar to that of antigen-induced antibody response. Furthermore, to identify the involvement of a limbic brain structure in the expression of conditioned antibody response, immediate-early gene c-fos expression was used as a marker of neuronal activation to detect the functional activation in the insular cortex (IC) in response to the conditioned stimulus. The re-exposure of conditioned rats to the conditioned stimulus resulted in a significant increase of c-Fos immunoreactivity in all three areas of the IC including the agranular, dysgranular, and granular areas, suggesting that IC is involved in the neural mechanism of expression of conditioned immune response.

Analysis of Variance↗
PubMed2005

Age-related deficits in the retention of memories for cued fear conditioning are reversed by galantamine treatment.

Aging has diverse effects on different behaviors and underlying neural systems. This study utilized fear conditioning to determine if aged mice have deficits in the acquisition and/or retention of memories for contextual or cued fear conditioning, and to determine if galantamine, an acetylcholinesterase (AChE) inhibitor and allosteric modulator of nicotinic acetylcholinergic receptors, would alter acquisition and/or retention of fear conditioning memories in young (2-3 months) and aged (19-20 months) C57BL/6 mice. Mice were trained with two white-noise CS (85 dB, 30 s)-footshock US (0.57 mA, 2 s) presentations. In the initial study, separate groups were tested 24, 48, or 96 h post-training. All mice were retested 1 week after the initial test. Aged mice were impaired in freezing to the CS for the 48 and 96 h train-test intervals, but not the 24-h interval. When retested 1 week after the initial test, freezing to the CS was significantly lower for all train-test intervals. No age-related deficits were found in contextual fear conditioning. In the second study, 2 mg/kg galantamine was administered to young and aged mice before fear conditioning and conditioned fear was assessed 48 h later. No age-related deficits in cued fear conditioning were seen in galantamine-treated aged mice. Thus, aged C57BL/6 mice are impaired in the long-term retention of auditory cued fear conditioning, but not the acquisition of auditory cued or contextual fear conditioning. This retention deficit for cued fear conditioning is ameliorated by treatment with the AChE inhibitor galantamine.

Acoustic Stimulation↗
PubMed2005

Stress differentially modulates fear conditioning in healthy men and women.

BACKGROUND: Stress and stress hormones modulate emotional learning in rats and might have similar effects in humans. Theoretic accounts of posttraumatic stress disorder (PTSD), for example, implicate the stress-induced modulation of fear conditioning in the development of intrusive emotional reactions. The present study examined the impact of acute stress and cortisol (CORT) on classically conditioned fear in men and women. METHODS: Ninety-four healthy undergraduates were exposed to a mild stressor (or control condition) while subjective anxiety and glucocorticoid stress responses (salivary CORT) were measured. One hour later, all participants participated in a differential fear conditioning procedure while conditioned skin conductance responses (SCR) were recorded. RESULTS: Exposure to the stressor increased subjective anxiety and elevated CORT levels. In men, stress exposure facilitated fear conditioning; whereas in women, stress appeared to inhibit fear conditioning. The impact of stress on differential conditioning in men was associated with increased CORT levels. CONCLUSIONS: Consistent with animal models, these results demonstrate that stress exposure can modulate classical conditioning in humans, possibly via hormonal mechanisms. The enhancing effects of stress on the formation of conditioned fear might provide a useful model for the formation of pathological emotional reactions, such as those found in PTSD.

Adolescent↗
PubMed2005

Dose response effects of lithium chloride on conditioned place aversions and locomotor activity in rats.

The present study examined the multi-variable locomotor activity effects of lithium chloride (LiCl) treatment in male rats. Of interest was a determination of which variables might show a dose-response relationship in LiCl-induced conditioned place aversions. Automated open-fields were partitioned into two chambers distinct in tactile and visual cues. A control group [n=8] received saline (NaCl; 0.15 M) paired with both chambers while three LiCl groups (0.15 M; 32 mg/kg [n=7], 95 mg/kg [n=7], 127 mg/kg [n=7]) received LiCl paired with the normally preferred chamber and saline paired with the non-preferred chamber. During extinction trials, rats were allowed to choose between the two chambers to provide an index of conditioned place aversions. Locomotor activity and its distribution within the chambers were also assessed during both conditioning and extinction trials. Dose-dependent decreases occurred in all measures of locomotor activity following LiCl administration during conditioning. During extinction trials, place aversions developed in animals conditioned with LiCl. LiCl-treated rats spent significantly less time in the LiCl-paired chamber relative to controls but not in a dose-dependent manner. Animals that had been conditioned with 95 or 127 but not 32 mg/kg LiCl, displayed significantly more vertical activity in the LiCl-paired chamber than controls during extinction trials. These findings indicate that, in addition to producing dose-dependent unconditioned effects on locomotor activity, LiCl also produces dose-dependent conditioned effects on vertical activity. These conditioned rearing response effects provide a valid measure of the conditioned avoidance response that provides evidence for dose-dependent LiCl-induced conditioned place aversions.

Animals↗
PubMed2004

Lesions in the bed nucleus of the stria terminalis disrupt corticosterone and freezing responses elicited by a contextual but not by a specific cue-conditioned fear stimulus.

The bed nucleus of the stria terminalis (BNST) is believed to be a critical relay between the central nucleus of the amygdala (CE) and the paraventricular nucleus of the hypothalamus in the control of hypothalamic-pituitary-adrenal (HPA) responses elicited by conditioned fear stimuli. If correct, lesions of CE or BNST should block expression of HPA responses elicited by either a specific conditioned fear cue or a conditioned context. To test this, rats were subjected to cued (tone) or contextual classical fear conditioning. Two days later, electrolytic or sham lesions were placed in CE or BNST. After 5 days, the rats were tested for both behavioral (freezing) and neuroendocrine (corticosterone) responses to tone or contextual cues. CE lesions attenuated conditioned freezing and corticosterone responses to both tone and context. In contrast, BNST lesions attenuated these responses to contextual but not tone stimuli. These results suggest CE is indeed an essential output of the amygdala for the expression of conditioned fear responses, including HPA responses, regardless of the nature of the conditioned stimulus. However, because lesions of BNST only affected behavioral and endocrine responses to contextual stimuli, the results do not support the notion that BNST is critical for HPA responses elicited by conditioned fear stimuli in general. Instead, the BNST may be essential specifically for contextual conditioned fear responses, including both behavioral and HPA responses, by virtue of its connections with the hippocampus, a structure essential to contextual conditioning. The results are also not consistent with the hypothesis that BNST is only involved in unconditioned aspects of fear and anxiety.

Animals↗
PubMed2006

Behavioral, central monoaminergic and hypothalamo-pituitary-adrenal axis correlates of fear-conditioned analgesia in rats.

Fear-conditioned analgesia is an important survival response which is expressed upon re-exposure to a context previously paired with a noxious stimulus. The aim of the present study was to characterize further the behavioral, monoaminergic and hypothalamo-pituitary-adrenal axis alterations associated with expression of fear-conditioned analgesia. Rats which had received footshock conditioning 24 h earlier, exhibited reduced formalin-evoked nociceptive behavior upon re-exposure to the footshock chamber, compared with non-footshocked formalin-treated rats. Intra-plantar injection of formalin reduced the duration of contextually-induced freezing and 20-40 kHz ultrasound emission. Intra-plantar injection of formalin to non-footshocked, non-conditioned rats did not induce ultrasonic vocalizations. Intra-plantar injection of formalin to footshock-conditioned rats, significantly increased tissue levels of 3,4-dihydroxyphenylacetic acid and the 3,4-dihydroxyphenylacetic acid:dopamine ratio in the periaqueductal gray and reduced levels of dopamine in the thalamus, compared with saline-treated footshocked controls. Non-footshocked, non-conditioned rats were capable of mounting a robust formalin-evoked increase in plasma corticosterone levels. Moreover, plasma corticosterone levels were significantly higher in saline-treated, footshock conditioned rats compared with saline-treated non-footshocked rats and levels did not differ between saline- and formalin-treated footshock conditioned rats. Assessment of the effects of the intra-plantar injection procedure revealed an attenuation of short-term extinction of contextually-induced freezing in rats anesthetized for intra-plantar injection of saline compared with non-anesthetized, non-injected rats as well as discrete effects on monoamines, their metabolites and plasma corticosterone levels. These data extend behavioral characterization of the phenomenon of fear-conditioned analgesia and suggest that measurement of ultrasound emission may be used as an ethologically relevant index of the defense response during fear-conditioned analgesia. Ultrasonic vocalization may also be a useful behavioral output to aid separation of nociception and aversion. The data provide evidence for discrete alterations in dopaminergic activity in the periaqueductal gray and thalamus and for altered hypothalamo-pituitary-adrenal axis activity following expression of defensive behavior.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2004

Influence of chronic corticosterone and glucocorticoid receptor antagonism in the amygdala on fear conditioning.

Glucocorticoid receptor activation within the basolateral amygdala (BLA) during fear conditioning may mediate enhancement in rats chronically exposed to stress levels of corticosterone. Male Sprague-Dawley rats received corticosterone (400 microg/ml) in their drinking water (days 1-21), a manipulation that was previously shown to cause hippocampal CA3 dendritic retraction. Subsequently, rats were adapted to the fear conditioning chamber (day 22), then trained (day 23), and tested for conditioned fear to context and tone (day 25). Training consisted of two tone (20s) and footshock (500 ms, 0.25 mA) pairings. In Experiment 1, muscimol (4.4 nmol/0.5 microl/side), a GABAergic agonist, was microinfused to temporarily inactivate the BLA during training. Rats given chronic corticosterone showed enhanced freezing to context, but not tone, compared to vehicle-supplemented rats. Moreover, BLA inactivation impaired contextual and tone conditioning, regardless of corticosterone treatment. In Experiment 2, RU486 (0, 0.3, and 3.0 ng/0.2 microl/side) was infused on training day to antagonize glucocorticoid receptors in the BLA. Corticosterone treatment enhanced fear conditioning to context and tone when analyzed together, but not separately. Moreover, RU486 (3.0 ng/side) selectively exacerbated freezing to context in chronic corticosterone-exposed rats only, but failed to alter tone conditioning. Serum corticosterone levels were negatively correlated with contextual, not tone, conditioning. Altogether, these suggest that chronic corticosterone influences fear conditioning differently than chronic stress as shown previously. Moreover, chronic exposure to corticosteroids alters BLA functioning in a non-linear fashion and that contextual conditioning is influenced more than tone conditioning by chronic corticosterone and BLA glucocorticoid receptor stimulation.

Amygdala↗
PubMed2004

Evidence for Pavlovian conditioning of cocaine-induced responses linked to emotional behavioral effects.

The pairing of cocaine treatments with a specific test environment typically leads to cocaine-conditioned drug effects. In this study, we first pre-exposed rats 10 times to an open-field environment to establish an habituation asymptote in locomotor activity prior to the initiation of cocaine treatments. Two groups (N=10) equated for locomotion, grooming, central zone penetrations and rearing behavior were used. One group received five pairings of cocaine (10.0 mg/kg) and the second group five pairings of saline injections with placements in the open-field environment. Subsequently, both groups received a saline test to detect possible cocaine-conditioned behavioral effects. During the cocaine treatment phase, cocaine enhanced locomotion and central zone penetrations but decreased rearing and grooming. On the conditioning test, the cocaine group exhibited enhanced central zone penetrations and decreased grooming as compared to the saline group. There were no group differences in locomotion or rearing. When within group comparisons were performed between behavioral responses on the pre-conditioning test vs. the conditioning test, the saline group scores were essentially unchanged. In contrast, the cocaine group exhibited higher central zone penetrations and decreased grooming without changes in locomotion or rearing. In that a cocaine conditioning test can also be viewed as a cocaine withdrawal test, two additional experiments were conducted using an unpaired conditioning protocol to test for withdrawal effects without conditioning. These results indicated that the central zone and grooming effects observed in the conditioning protocol were not withdrawal effects. Altogether, these findings provide support for Pavlovian conditioning of cocaine-induced changes in emotion-related behavioral responses.

Animals↗
PubMed2005

Effects of pre- or post-training entorhinal cortex AP5 injection on fear conditioning.

Fear conditioning is one of the most studied paradigms to assess the neural basis of emotional memory. The circuitry involves NMDA receptor activation in the amygdala and, in the case of contextual conditioning, in the hippocampus. Entorhinal cortex is one of the major input/output structures to the hippocampus and also projects to the amygdala, both through glutamatergic transmission. Other learning tasks involving hippocampus and amygdala, such as inhibitory avoidance, require entorhinal cortex during acquisition and consolidation. However, the involvement of NMDA receptors mediated transmission in entorhinal cortex in fear conditioning acquisition and consolidation is not clear. To investigate that issue, rats were trained in fear conditioning to both contextual and tone conditioned stimulus. Immediately before, immediately, 30 or 90 min after training they received NMDA antagonist AP5 or saline injections bilaterally in the entorhinal cortex (AP-6.8 mm, L +/-5.0 mm DV-6.8 mm). Contextual fear conditioning was measured 24 h after training, and tone fear conditioning 48 h after training. AP5 injections selectively impaired contextual fear conditioning only when injected pre-training. Post-training injections had no effect. These findings suggest that entorhinal cortex NMDA receptors are necessary for acquisition, but not for consolidation, of contextual fear conditioning. On the other hand, both acquisition and consolidation of tone fear conditioning seem to be independent of NMDA receptors in the entorhinal cortex.

2-Amino-5-phosphonovalerate↗
PubMed2006

Ketamine administration disturbs behavioural and distributed neural correlates of fear conditioning in the rat.

The neurotransmitter glutamate and its associated receptors perform an important role in the brain circuitry underlying normal fear processing. The glutamate NMDA receptor, in particular, is necessary for the acquisition and recollection of conditioned-fear responses. Here the authors examine how acute blockage of the NMDA receptor with sub-anaesthetic doses of ketamine affects behavioural assays of fear-conditioned stress (e.g. freezing) and cFos expression in a network of brain areas that have previously been implicated in fear processing. Fear-conditioned rats displayed significantly more freezing behaviour than non-conditioned controls. In fear-conditioned rats that also received ketamine, this conditioning effect was largely neutralised. Fear conditioning also led to increased cFos expression in various areas central to fear processing, including the basolateral nucleus of the amygdala, the paraventricular nucleus of the hypothalamus and the anterior cingulate. Ketamine abolished such increases in cFos expression in most brain areas investigated. The present study therefore demonstrates that systemic ketamine administration in rats interferes with fear conditioning on a behavioural level and in a network of brain regions associated with fear and anxiety. The combination of ketamine and fear conditioning may therefore provide a useful model of abnormal fear processing, as observed in certain psychiatric conditions.

Analysis of Variance↗
PubMed1998

Acoustic transmission in the dentate nucleus. I. Patterns of activity to click and hiss; II. Changes in activity and excitability after conditioning.

Recordings were made from 95 units of the dentate nucleus of naive cats to determine if patterns of response to 70 dB clicks could be distinguished from those to another acoustic stimulus (a hiss) of approximately equal sound pressure level. Further studies of an additional 309 units were conducted to determine if unit excitability and the response to clicks changed after Pavlovian conditioning in which blink responses were elicited by the clicks as conditioned stimuli. Over 50% of units tested before conditioning responded to click or hiss with increased activity, and 8% responded in the first 4-8 ms after the onset of the rapidly rising click. Cross-correlation of the respective 160 ms poststimulus histogram averages of mean activity showed dissimilar patterns of response to clicks and hisses (Pearson product-moment correlation coefficient + 0.02). Thus the averaged population responses distinguished these stimuli. In addition, individual cells were found in each behavioral state that responded selectively to either click or hiss. After conditioning with click as the conditioned stimulus, the number of units responding in the first 4-8 ms to click increased to 23%. The mean magnitude of activity 4-8 ms after presenting the click increased after conditioning but not after sensitization produced by backward pairing of the stimuli used for conditioning. After backward pairing only 6% of the units responded in the first 4-8 ms to click. The changes in activity after conditioning were accompanied by increases in neural excitability to intracellularly applied depolarizing current. In contrast with the changes in activity, the increases in neural excitability were also found after backward pairing. We conclude that short as well as long latency acoustic transmissions to click change in the dentate nucleus after conditioning, that changes in response to click are expressed in 4-8 ms responsive cells, and that many of these cells have different patterns of spike activity in response to click and hiss. The findings support the hypothesis that the dentate nucleus can play a significant role in short as well as long latency, adaptive acoustic transmission that can enhance the response to an acoustic signal used as a Pavlovian conditioned stimulus.

Acoustic Stimulation↗
PubMed1999

Identification of differently timed motor components of conditioned blink responses.

Electromyographic recordings were made from the orbicularis oculi muscles of cats in order to identify differently timed motor components of conditioned eye blink responses (CRs). Conditioning was established rapidly by pairing electrical stimulation of the hypothalamus (HS) with a click conditioned stimulus (CS) and a glabella tap unconditioned stimulus (US). Analysis of the EMG responses disclosed five different motor components of the CR that could be distinguished and characterized according to their latencies of occurrence. Four were associated with an increase in EMG activity elicited by the CS (16-48 ms, alpha(1); 48-80 ms, alpha(2); 80 to 120 ms, beta; >/=120 ms, gamma), and one was associated with a decrease in activity (16 to 60 ms, alpha(i)). Analysis of the amplitudes of the different components of the CR during the course of conditioning and extinction disclosed that short latency, alpha(1) components of the CRs were acquired and extinguished in a manner equivalent to longer latency components of the CRs. The observations supported the hypothesis that short and long latency components of blink responses represented comparable rather than substantially different forms of Pavlovian conditioning. The alpha(2) response was present before conditioning began, and increased with other components after conditioning. The alpha(i) response component was also observed prior to conditioning, and represents a previously undetected, inhibitory consequence of presenting weak (70 dB) acoustic stimuli. It could play a role in conditioned inhibition, latent inhibition and blocking as well as suppression of the conditioned motor response during extinction.

Adaptation, Physiological↗
PubMed2003

Prior exposure to a single stress session facilitates subsequent contextual fear conditioning in rats. Evidence for a role of corticosterone.

Previous studies showed that exposure of rats to chronic restraint stress for 21 days enhances subsequent contextual fear conditioning. Since recent evidence suggest that this effect is not dependent on stress-induced neurodegenerative processes, but to elevated training-elicited glucocorticoid release in chronically stressed animals, we aimed to explore here whether a single exposure to restraint stress, which is not expected to induce neuronal damage, would also affect contextual fear conditioning. We also questioned whether post-training corticosterone levels might be associated with any potential effect of stress on fear conditioning. Adult male Wistar rats were exposed to acute restraint stress for 2 h and, two days later, trained in the contextual fear conditioning task, under training conditions involving either moderate (0.4 mA shock) or high (1 mA shock) stress levels. The results showed that acute stress enhanced conditioned freezing at both training conditions, although data from the 1 mA shock intensity experiment only approached significance. Stressed animals were shown to display higher post-training corticosterone levels. Furthermore, the facilitating effect of prior stress was not evident when animals were trained in the hippocampal-independent auditory-cued conditioning task. Therefore, these findings support the idea that stress experiences preceding exposure to new types of stressors facilitate the development of contextual fear conditioning. They also indicate that not only repeated, but also a single exposure to aversive stimulation is sufficient to facilitate context-dependent fear conditioning, and suggest that increased glucocorticoid release at training might be implicated in the mechanisms mediating the memory facilitating effects induced by prior stress experiences.

Acoustic Stimulation↗
PubMed2002

Fasting stress exacerbates classical conditioned histamine release in guinea pigs.

To clarify the contribution of stress to classical conditioning-associated asthmatic responses, the effect of fasting stress on conditioned histamine release was investigated in a guinea pig model of asthma. The animals were randomly divided into 2 groups for Experiment 1 and 2, and received a conditioning procedure in which ovalbumin (OA) as an unconditioned stimulus (US) and dimethylsulfide (DMS, sulfur smelling) as a conditioned stimulus (CS) were simultaneously inhaled after fasting for 16 h. Then, one group was given food as a reward for respiratory distress, and the other group was denied it for more than 3 h, while being placed in front of the feeding group. After this procedure was repeated 5 times, the plasma histamine levels in response to the CS were measured in half of each group in Experiment 1, and the respiratory resistance (Rrs) was assessed similarly in the other half of each group in Experiment 2. The same experiments were again performed after exchanging assignments of feeding group or fasting group in both experiments. The control groups in both experiments received the CS and the US 10 times separately in a random order under 16 h fasting conditions and were provided food after the exposures. After these pseudo-conditioning presentations, the plasma histamine levels or the Rrs in response to the CS were measured. In Experiment 1, the plasma histamine levels in the fasting stress group after the first conditioning sessions were significantly higher than those of the other groups. This difference was not observed when the groups were exchanged. In Experiment 2, the fasting stress group showed higher values in the Rrs compared to the other groups, irrespective of the first or second conditionings; however, they were not significant. The present study indicates that fasting stress after the conditioning procedures exacerbates the following conditioned histamine release, although the stress effect on bronchoconstriction was not confirmed.

Animals↗
PubMed1997

Classical conditioning.

Evidence has amassed from research in humans indicating that the cerebellar circuitry serving as the substrate for eyeblink classical conditioning is similar to that in nonhuman primates. In patients with bilateral cerebellar lesions or neurodegenerative cerebellar disease, few conditioned eyeblink responses are produced with either the ipsilesional or the contralesional eye. Cerebellar patients with lateralized lesions, like rabbits with experimentally produced unilateral cerebellar lesions, produce relatively normal conditioned responses (CRs) with the contralesional eye and few or no CRs with the ipsilesional eye. Age-related deficits in eyeblink classical conditioning appear in humans and rabbits in middle age. In normal aging in many species, including humans, there is Purkinje cell loss in cerebellar cortex. In rabbits, the Purkinje cell number correlates highly with the rate of learning, regardless of age. Positron emission tomography imaging of normal young adults during eyeblink conditioning reveals changes in activity in the cerebellum. Timed interval tapping, a task that assesses cerebellar function, also predicts performance on eyeblink conditioning. In dual-task conditions involving simultaneous performance of eyeblink conditioning and timed interval tapping, eyeblink conditioning is impaired. Investigations of patients with lesions or neurodegenerative disease not involving the cerebellum demonstrate that acquisition of CRs is possible, although prolonged in the case of hippocampal cholinergic disruption. Evidence to date suggests that the human analogue of the rabbit interpositus nucleus, the globose nucleus, is essential for the production of the conditioned eyeblink response and that cerebellar cortical Purkinje cells play a role in normal acquisition.

Aging↗
PubMed2000

DBA/2J mice develop stronger lithium chloride-induced conditioned taste and place aversions than C57BL/6J mice.

Genetic differences in lithium-induced conditioned aversion were examined using both place- and taste-conditioning procedures. In the place-conditioning procedure, adult male C57BL/6J (B6) and DBA/2J (D2) mice were exposed to a differential conditioning procedure in which each mouse received four 30-min pairings of a distinctive floor cue immediately after IP injections of either 0.75, 1.5, or 3. 0 mEq/kg LiCl. A different floor cue was paired with saline injections. A separate group of control mice received saline injections paired with both floor types. Subsequent floor preference testing revealed greater conditioned aversion in D2 mice compared to B6 mice in groups receiving 3.0 mEq/kg LiCl. Lower LiCl doses did not produce conditioning in either strain. In a conditioned taste-aversion procedure, fluid-restricted mice received four trials in which access to 0.2 M NaCl solution was followed by IP injection of either 0.75, 1.5, 3.0, or 6.0 mEq/kg LiCl. D2 mice showed stronger conditioned taste aversion than B6 mice at all doses, suggesting that taste conditioning may be a more sensitive index of aversive drug sensitivity than place conditioning. These findings are not well explained by strain differences in general learning ability or by strain differences in stimulus salience or innate preference. Rather, these data appear more consistent with previous studies showing strain differences in lithium pharmacokinetics and in general sensitivity to aversive events.

Animals↗