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PubMed2001

Fear conditioning-induced alterations of phospholipase C-beta1a protein level and enzyme activity in rat hippocampal formation and medial frontal cortex.

We investigated the effects of one-trial fear conditioning on phospholipase C-beta1a catalytic activity and protein level in hippocampal formation and medial frontal cortex of untreated control rats and rats prenatally exposed to ethanol. One hour following fear conditioning of untreated control rats, phospholipase C-beta1a protein level was increased in the hippocampal cytosolic fraction and decreased in the hippocampal membrane and cortical cytosolic and cortical membrane fractions. Twenty-four hours after fear conditioning, phospholipase C-beta1a protein level was reduced in the hippocampal cytosolic fraction and elevated in the cortical nuclear fraction; in addition, 24 h after conditioning, phospholipase C-beta1a activity in the cortical cytosolic fraction was increased. Rats that were exposed prenatally to ethanol displayed attenuated contextual fear conditioning, whereas conditioning to the acoustic-conditioned stimulus was not different from controls. In behavioral control (unconditioned) rats, fetal ethanol exposure was associated with reduced phospholipase C-beta1a enzyme activity in the hippocampal nuclear, cortical cytosolic, and cortical membrane fractions and increased phospholipase C-beta1a protein level in the hippocampal membrane and cortical cytosolic fractions. In certain cases, prenatal ethanol exposure modified the relationship between fear conditioning and changes in phospholipase C-beta1a protein level and/or activity. The majority of these effects occurred 1 h, rather than 24 h, after fear conditioning. Multivariate analysis of variance revealed interactions between fear conditioning, subcellular fraction, and prenatal ethanol exposure for measures of phospholipase C-beta1a protein level in hippocampal formation and phospholipase C-beta1a enzyme activity in medial frontal cortex. In the majority of cases, fear conditioning-induced changes in hippocampal phospholipase C-beta1a protein level were augmented in rats prenatally exposed to ethanol. In contrast, fear conditioning-induced changes in cortical phospholipase C-beta1a activity were, often, in opposite directions in prenatal ethanol-exposed compared to diet control rats. We speculate that alterations in subcellular phospholipase C-beta1a catalytic activity and protein level contribute to contextual fear conditioning and that learning deficits observed in rats exposed prenatally to ethanol result, in part, from dysfunctions in phospholipase C-beta1a signal transduction.

Acoustic Stimulation↗
PubMed1989

Cat red nucleus activity preceding movement depends on initiation conditions.

The activity of 98 Red Nucleus neurons was recorded in 3 cats operantly conditioned to perform a ballistic forelimb flexion movement triggered after a brief sound in a simple Reaction Time condition, or Delayed after the same sound in the presence of a tone cue. Fifty-eight task related neurons presented changes of activity in either one or both conditions. Forty-four of them were studied quantitatively and classified in 3 categories: 1) only 16% of the units presented similar changes of firing preceding the triggered or delayed movement; 2) most units (55%) presented different changes of activity in the two conditions: in the Delayed condition, the activation occurred earlier before the movement, and/or the change in magnitude was reduced or the pattern of activity was modified; 3) moreover, for 29% of the units, the change of activity observed before movement in the Reaction Time condition was severely reduced or even absent in the Delayed condition. For some of these neurons a building-up of activity was observed very early in the Reaction Time condition, during the preparatory period, well before the occurrence of the conditioned stimulus. These results show that the Red Nucleus activity preceding a movement is clearly dependent on its initiation conditions. The distinct patterns of unit firing observed in the Reaction Time condition and in the Delayed condition are tentatively related to the different preparation and initiation constraints determined by the behavioral conditions.

Action Potentials↗
PubMed1980

The effects of pipradrol on the acquisitionof responding with conditioned reinforcement: a role for sensory preconditioning.

Previous studies have shown that pipradrol enhances the acquisition of responding with conditioned reinforcement. The present experiments replicated this finding and assessed the possible role of nonspecific stimulus change, feeding in the test environment and prior exposure to the conditioned stimulus. The test procedure consisted of three phases: Operant rates of pressing two levers, one of which produced a 3-s tone, were measured in the pre-exposure phase; the tone was paired with food in the four conditioning sessions; and conditioned reinforcement was demonstrated in the test phase by a relative increase in pressing the tone lever. A group (N = 8) receiving food but no tone during the conditioning phase also increased responding on the tone lever in the test phase and this effect was enhanced in a group (N = 8) receiving pipradrol prior to the test. A group (N = 8) receiving neither tones nor pellets during conditioning and pipradrol prior to test failed to show a change in lever bias, ruling out the possibility that pipradrol produced a nonspecific enhancement of responding for stimulus change. It was hypothesized that the conditioned reinforcement effect seen in the food-alone groups resulted from sensory preconditioning. According to this hypothesis, the tone was conditioned to environmental stimuli during the pre-exposure phase; subsequent presentation of pellets resulted in a learned association between environmental stimuli and food, leading to increased responding for the tone in the test phase. The results of two control experiments supported this view. One group (N = 8) received no tone in the pre-exposure phase, pellets alone in the conditioning phase and then pipradrol prior to test. The second group, but under altered environmental stimulus conditions, and then was given pipradrol prior to test. Neither group showed evidence of conditioned reinforcement. It was concluded that pipradrol enhanced acquisition of responding with conditioned reinforcement even if the conditioned reinforceing stimulus was established with sensory preconditioning procedures.

Acoustic Stimulation↗
PubMed1990

On the possible involvement of glutamate receptors in conditioning of behavioural effects of apomorphine.

It was shown previously that behavioural effects of apomorphine (locomotor activation and stereotyped behaviour) can be conditioned when they are associated with well-defined environmental stimuli. In the present study, the hypothesis was tested that glutamatergic mechanisms play an important role either in formation of conditioned responses to apomorphine or in the expression of previously established conditioned responses. For this purpose, two blockers of glutamate receptors were applied, either MK-801 (dizocilpine), a non-competitive, but selective blocker of NMDA-type receptors or MLV-6976, a non-selective blocker of glutamate receptors. MK-801 produced some locomotor activation by itself in a dose-dependent way (0.125-0.50 mg/kg ip). The locomotor activation produced by 0.25 mg/kg could not be conditioned. When rats were conditioned 9 times with 2 mg/kg apomorphine after pretreatment with 0.25 mg/kg of MK-801, this pretreatment did not prevent the development of apomorphine-conditioned locomotor activity or stereotypies which appeared when the rats were treated with saline in presence of the conditioned stimuli. Similar results were obtained when rats were conditioned 7 times with the same dose of apomorphine after pretreatment with 20 mg/kg ip MLV-6976, which drug did not induce any visible alterations in motility by itself. When rats were conditioned 7 times with 2 mg/kg apomorphine alone and tested with MK-801 (0.25 mg/kg) in the presence of the conditioned stimuli, neither locomotor activity nor stereotypies appeared as conditioned responses. When rats were conditioned with the same dose of apomorphine alone and tested with MLV-6976 (20 mg/kg ip), stereotypies did not appear as conditioned responses, but some locomotor activity occurred.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Experimental psychogenic hypertension: blood pressure changes conditioned to painful stimuli (schizokinesis).

1. During habituation in 4 dogs to a new environment and attachment of apparatus, the blood pressure was at first high but fell from about 175 systolic the first day to about 135 on the ninth day. 2. In the first group of dogs used two years previously to form 3 cardiac conditional reflexes to 3 intensities of shock, the blood pressure measured after a 13-month rest was retained and specific to the 3 intensities of shock. In another group of 2 dogs the blood pressure was specific to the excitatory and to the inhibitory signals for pain. 3. The conditioned hypertension was parallel to the conditioned heart rate. 4. The conditioned hypertension was parallel to the motor conditional reflex with certain exceptions: the conditioned hypertension was, like the cardiac conditional reflex, quicker to form and more persistent, thus being present often in the absence of the motor conditional reflex--an evidence of schizokinesis. 5. The conditioned hypertension was retained for a 13-month rest period without intervening training, being present immediately when the dog was brought back into the environment where the stress had been given. 6. Although the conditioned hypertension was retained in the long rest period, it could in one dog be reduced somewhat by repeating the conditional stimulus without the shock (non-reinforcement), a more efficient way of extinction than simple rest. In another dog the hypertension became exaggerated though there was no repetition of the stress, showing evidence of an internal development (autokinesis). 7. The amplitude of the conditioned hypertension varied according to the individual dog from about 130 average control to limits of 150 to 225 (conditioned hypertension) in the separate dogs.

Animals↗
PubMed2002

Role of benzodiazepine and serotonergic mechanisms in conditioned freezing and antinociception using electrical stimulation of the dorsal periaqueductal gray as unconditioned stimulus in rats.

RATIONALE: The dorsal periaqueductal gray matter (dPAG) has been implicated in the modulation of defensive behavior. Electrical stimulation of this structure can be used as an unconditioned stimulus to produce a conditioned fear reaction expressed by freezing, antinociception, and autonomic responses. OBJECTIVES: This study investigated the influence of benzodiazepine, serotonergic, and opioid mechanisms on these conditioned responses. METHODS: Animals implanted with an electrode and a guide cannula into the dPAG were submitted to two conditioning sessions. Each session consisted of ten pairings of the light in a distinctive chamber (CS) with the electrical stimulation of this structure at the escape threshold. On the next day, each animal was exposed only to the CS (testing) and the duration of freezing, number of rearing and grooming episodes were recorded for 5 min. Before and after the testing session, animals were submitted to the tail-flick test. Fifteen minutes before the exposure to the CS, animals received injections into the dPAG of midazolam (a positive modulator of benzodiazepine sites), alpha-methyl-5-hydroxytryptamine (alpha-Me-5-HT; an agonist of 5-HT(2) receptors), naltrexone (an opioid antagonist), or vehicle. RESULTS: Conditioning with dPAG electrical stimulation caused significant increases in the time of freezing and conditioned antinociception. Injections of midazolam into the dPAG significantly inhibited freezing behavior and antinociception due to conditioning. Injections of alpha-Me-5-HT inhibited the effects of conditioning on freezing without affecting conditioned antinociception. Injections of naltrexone (13 nmol/0.2 micro l) did not change any of the conditioned responses studied. CONCLUSIONS: (1) Conditioned freezing and antinociception are modulated by benzodiazepine mechanisms into dPAG. (2) 5-HT(2) receptors seem to regulate conditioned freezing behavior. However, conditioned antinociception was not affected by 13 nmol naltrexone. (3) Opioid mechanisms do not seem to be involved in the conditioned responses using electrical stimulation of the dPAG as unconditioned stimulus. Further studies with other opioid and 5-HT(2) receptor antagonists are still needed to confirm the conclusions drawn from the present work.

Animals↗
PubMed2001

Conditioned antinociception and freezing using electrical stimulation of the dorsal periaqueductal gray or inferior colliculus as unconditioned stimulus are differentially regulated by 5-HT2A receptors in rats.

RATIONALE: Electrical stimulation of the dorsal periaqueductal gray matter (dPAG) and the inferior colliculus (IC) has been used as an aversive unconditioned stimulus. However, studies on the behavioral, sensorial and autonomic components of the conditioned fear elaborated in the midbrain tectum are lacking. OBJECTIVES: This study was undertaken to investigate the nature of the aversiveness of stimulation of the dPAG and IC as well as the modulation by 5-HT mechanisms of the fear conditioned responses to these stimulations. METHODS: Animals chronically implanted with an electrode glued to a guide cannula into the dPAG or the IC were submitted to one, two or three sessions of conditioning. Each session consisted of ten pairings of the light in a distinctive chamber (CS) with the electrical stimulation of one of these regions at the escape threshold determined previously. Control groups were submitted to the same procedure, except for the conditioning sessions in which the conditioned stimuli were presented alone in one case and performed in a different context in the other. On the next day, each animal was exposed only to the CS (testing) and the duration of freezing, number of rearings, grooming, bouts of micturition and fecal boli were recorded for 5 min. Before and after the testing session, the animals were submitted to the tail-flick test. RESULTS: The data showed that the conditioning with electrical stimulation of the dPAG and the IC caused significant increases in the time of freezing, defecation and micturition, and significant reductions in the number of rearings and grooming. On the other hand, only the conditioning with electrical stimulation of the dPAG produced significant conditioned antinociception. Microinjections of methysergide, a non-specific antagonist of 5-HT receptors, or ketanserin, an antagonist of 5-HT2A receptors, into the dPAG before testing significantly inhibited the antinociception without affecting any of the behavioral or autonomic conditioned responses. CONCLUSIONS: 1) Conditioned freezing may be produced using the electrical stimulation of the dPAG or IC as unconditioned stimuli, 2) only the pairing of CS plus dPAG but not with IC stimulation, produces significant conditioned antinociception, 3) blockade of 5-HT2A receptors inhibits conditioned antinociception but not the conditioned defensive behavior using the electrical stimulation of the dPAG as unconditioned stimulus.

Animals↗
PubMed1985

Development of hypoglycemia and hyperglycemia as a function of number of trials in insulin conditioning.

A neutral environment paired with insulin injections can develop the capacity to elicit glycemic changes. However, both conditioned hypoglycemia and conditioned hyperglycemia have been reported under apparently similar circumstances. The present study examined conditioned glycemic changes as a function of the number of conditioning trials and the novelty of the conditioning environment. Adult, male Wistar rats were injected with either insulin or physiological saline every second day, in either a novel or a familiar environment. On the test day, all rats were injected with saline and blood was collected 20 minutes later for determination of glucose levels. In rats given insulin in the novel environment, conditioned hypoglycemia was observed after two trials but was replaced by conditioned hyperglycemia after five trials. No conditioning at all occurred in the familiar environment. The two conditioned responses observed were interpreted as reflecting two unconditioned responses brought about by insulin--a hypoglycemic response to the central detection of insulin, and a hyperglycemic response to the detection of (insulin-induced) hypoglycemia. Taken in conjunction with previous experiments in which both conditioned response patterns have occurred, the present results suggest that the homeostatic response of hyperglycemia can become strong enough to overcome the initial conditioned response of hypoglycemia, but that its establishment depends on the use of a novel conditioned stimulus and a larger number of conditioning trials.

Animals↗
PubMed2006

Conditioned locomotion induced by unilateral intrastriatal administration of apomorphine: D(2) receptor activation is critical but not the expression of the unconditioned response.

The present study examined the role of D(1) and D(2) receptors in the conditioning of apomorphine-induced locomotor behavior. A Pavlovian conditioning protocol was used in which rats received 5 daily intrastriatal apomorphine treatments paired or unpaired to an open-field environment followed, 2 days later, by a saline test for conditioning. In the conditioning induction phase, the intrastriatal apomorphine treatment increased locomotor activity expressed as an increased number of sectional crossings and rearings. In the conditioning test, the apomorphine-paired group had significantly higher locomotor activity than the unpaired and vehicle groups, consistent with the development of a conditioned locomotor response. The concomitant blockade of D(1) and D(2) receptors with D(1) (SCH23390) and D(2) (sulpiride) antagonists prevented the apomorphine-induced behavioral response during the induction phase and in the conditioning test. Pretreatment with the D(1) antagonist SCH 23390 also blocked the apomorphine-induced behavioral response during the induction phase but did not block the apomorphine conditioned response. Pretreatment with the selective D(2) antagonist sulpiride blocked the apomorphine behavioral response during the induction phase and in the conditioning test. Altogether, these results indicate that antagonism of either the D(1) or D(2) receptors in the dorsal striatum can block apomorphine-induced locomotor activation but that D(2) but not D(1) antagonism can prevent the development of the apomorphine conditioned response. Altogether, these findings indicate a key role for the D(2) receptor site in the mediation of apomorphine conditioned behavior; and, in addition, that apomorphine conditioned locomotor response can develop without the expression of the locomotor stimulant response during the induction phase of conditioning.

Animals↗
PubMed2005

The conditioned enhancement of neutrophil activity is catecholamine dependent.

Neutrophil activity was elevated in the conditioned mice for the first time through an established conditioned training process. Catecholamines were proved to be important in the regulation of this conditioned innate immunity. In the study, the camphor odor (as the conditioned stimulus, CS) and poly I: C (as the unconditioned stimulus, US) was used to conditionally elevate the activity of the splenic neutrophils. The mechanism(s) responsible for the conditioned enhancement of neutrophil activity was further investigated using the neurochemical blocking assay and immunohistochemical analysis. Results showed that the neutrophil activity was significantly enhanced through the conditioned training process; both reserpine and 6-hydroxydopamine (6-OHDA) significantly blocked this conditioned innate immunity at the conditioned recall stage. Dexamethasone (Dex), however, showed no effect on the conditioned neutrophil response. Tyrosine hydroxylase (TH)-positive cells significantly increased in the locus coeruleus (LC), hypothalamus, and cortex but not in the spleen of the conditioned animals. These results indicate that during the conditioned recall stage, the brain signals the splenic neutrophils via the sympathetic nervous system (SNS) by releasing the peripheral catecholamines in spleen. The activation of the SNS, on the other hand, is also under the influence of catecholamines released in the LC. The hypothalamic pituitary (HP) axis, on the other hand, plays no role in the regulation of the conditioned neutrophil response.

Adrenergic Agents↗
PubMed2005

N-methyl-D-aspartate receptors play important roles in acquisition and expression of the eyeblink conditioned response in glutamate receptor subunit delta2 mutant mice.

Classical eyeblink conditioning has been known to depend critically on the cerebellum. Apparently consistent with this, glutamate receptor subunit delta2 null mutant mice, which have serious morphological and functional deficiencies in the cerebellar cortex, are severely impaired in delay paradigm. However, these mutant mice successfully learn in trace paradigm, even in '0-trace paradigm,' in which the unconditioned stimulus starts just after the conditioned stimulus terminates. Our previous studies revealed that the hippocampus and the muscarinic acetylcholine receptors play crucial roles in 0-trace paradigm in glutamate receptor subunit delta2 null mutant mice unlike in wild-type mice, suggesting a large contribution of the forebrain to 0-trace conditioning in this type of mutant mice. In the present study, we investigated the role of N-methyl-D-aspartate receptors in 0-trace eyeblink conditioning in glutamate receptor subunit delta2 null mutant mice. Mice were injected intraperitoneally with the noncompetitive N-methyl-d-aspartate receptor antagonist (+)MK-801 (0.1mg/kg) or saline, and conditioned with 350-ms tone conditioned stimulus followed by 100-ms periorbital shock unconditioned stimulus. Glutamate receptor subunit delta2 null mutant mice that received (+)MK-801 injection exhibited a severe impairment in acquisition of the conditioned response, compared with the saline-injected glutamate receptor subunit delta2 null mutant mice. In contrast, wild-type mice were not impaired in acquisition of 0-trace conditioned response by (+)MK-801 injection. After the injection solution was changed from (+)MK-801 to saline, glutamate receptor subunit delta2 null mutant mice showed a rapid and partial recovery of performance of the conditioned response. On the other hand, when the injection solution was changed from saline to (+)MK-801, glutamate receptor subunit delta2 null mutant mice showed a marked impairment in expression of the pre-acquired conditioned response, whereas impairment of the expression was small in wild-type mice. Injection of (+)MK-801 had no significant effects on spontaneous eyeblink frequency or startle eyeblink frequency to the tone conditioned stimulus in either glutamate receptor subunit delta2 null mutant mice or wild-type mice. These results suggest that N-methyl-D-aspartate receptors play critical roles both in acquisition and expression of the conditioned response in 0-trace eyeblink conditioning in glutamate receptor subunit delta2 null mutant mice.

Animals↗
PubMed2006

Involvement of medial prefrontal cortex neurons in behavioral and cardiovascular responses to contextual fear conditioning.

To explore the ventral medial prefrontal cortex (vMPFC) involvement in behavioral and autonomic fear-conditioned responses to context, vMPFC synaptic transmission was temporarily inhibited by bilateral microinjections of 200 nL of the nonselective synapse blocker CoCl(2) (1 mM). Behavioral activity (freezing, motor activity and rearing) as well as evoked cardiovascular responses (arterial pressure and heart rate) was analyzed. Rats were pre-exposed to the footshock chamber (context) and shock stimulus was used unconditioned stimulus. During re-exposure to context, conditioned rats spent 80% of the session in freezing while non-conditioned rats (no shock group) spent less than 15% of the session time in freezing. Conditioned rats had significantly lower activity scores than non-conditioned animals. Exposure to context increased mean arterial pressure (MAP) and heart rate (HR) of both groups. MAP and HR of the conditioned animals were markedly increased and remained at a high and stable level, whereas MAP and HR increases in non-conditioned animals were less pronounced and declined during the session. CoCl(2) microinjected in the vMPFC significantly reduced freezing and attenuated MAP and HR increase of the conditioned group. Cobalt-induced vMPFC inhibition also significantly reduced MAP and HR increase observed in non-conditioned animals, without any behavioral changes. The effect of vMPFC acute ablation on MAP and HR did not seem to be specific to the fear response because they were also evident in non-conditioned animals. The results indicate that vMPFC integrity is crucial for expression of fear-conditioned responses to context, such as freezing and cardiovascular changes, suggesting that fear-conditioned responses to context involve cortical processing prior to amygdalar output. They also indicate a cardiovascular response observed during re-exposure of non-conditioned rats to the context is completely dependent on vMPFC integrity.

Analysis of Variance↗
PubMed1999

Amygdaloid D1 dopamine receptor involvement in Pavlovian fear conditioning.

The amygdala has long been implicated in conditioned fear. The mesencephalic dopaminergic system provides a rich innervation to the amygdala [J.H. Fallon, P. Ciofi, Distribution of monoamines within the amygdala, in: J.P. Aggleton (Ed.), The Amygdala: Neurobiological Aspects of Emotion, Memory and Mental Dysfunction, Wiley, New York, 1992, pp. 97-114; L.J. Freedman, M.D. Cassell, Distribution of dopaminergic fibers in the central division of the extended amygdala of the rat. Brain Research 633 (1994) 243-252; E. Asan, The catecholaminergic innervation of the rat amygdala. Advances in Anatomy Embryology and Cell Biology 142 (1996) 1-107]. Specific activation of the mesoamygdaloid dopaminergic system has been reported to occur in response to conditioned fear-arousing stimuli [M.L. Coco, C.M. Kuhn, T.D. Ely, C.D. Kilts, Selective activation of mesoamygdaloid dopamine neurons by conditioned stress: attenuation by diazepam. Brain Research 590 (1992) 39-47] suggesting that dopamine release in the amygdala may contribute to the acquisition and/or expression of conditioned fear. Using a 2x2 factorial design, Experiment 1A investigated the effects of bilateral intra-amygdaloid infusions of the selective D1 receptor antagonist, SCH 23390 (2.0 microgram 0.5 microliter-1 side-1), on the acquisition and expression of Pavlovian conditioned fear measured by freezing to acoustic and background contextual stimuli. Infusions of SCH 23390 prior to acquisition training, prior to retention testing or prior to both significantly attenuated conditioned freezing during retention testing. Experiment 1B investigated the dose-dependent effects of pre-training infusions of SCH 23390 (0.5, 1.0 and 2.0 microgram) on conditioned fear. Pre-training infusions of SCH 23390 dose-dependently attenuated conditioned freezing during retention testing. Experiment 2A investigated the effects of bilateral infusions of the selective D1 receptor agonist, SKF 82958 (2.0 microgram 0.5 microliter-1 side-1) on the acquisition and expression of conditioned fear. Infusions of SKF 82958 prior to training facilitated conditioned freezing during retention testing. Experiment 2B investigated the dose-dependent effects of pre-training infusions of SKF 82958 (1.0, 2.0 and 4.0 microgram) on conditioned fear. Pre-training infusions of SKF 82958 dose-dependently facilitated conditioned freezing during retention testing. In conclusion, these results suggest that dopamine transmission within the amygdala contributes to the acquisition and expression of Pavlovian fear conditioning.

Amygdala↗
PubMed2000

Involvement of cerebral cortical structures in the classical conditioning of eyelid responses in rabbits.

The classical conditioning of the eyelid motor system in alert behaving rabbits has been used to study the expression of Fos in the hippocampus, and in the occipital, parietal, piriform and temporal cortices. Animals were classically conditioned with both delay and trace conditioning paradigms. As conditioned stimulus, both short and long (20 and 100 ms) tones (600 Hz, 90 dB) or short, weak (20 ms, 1kg/cm(2)) air puffs were used. The unconditioned stimulus was always a long, strong (100 ms, 3 kg/cm(2)) air puff that started 250-270 ms after the onset of the conditioned stimulus. The expression of Fos was significantly increased after both delayed and trace conditioning in the hippocampus, and in the parietal and piriform cortices contralateral to the unconditioned stimulus presentation side, compared with equivalent ipsilateral structures in conditioned animals, or with Fos production in the same contralateral structures in pseudo-conditioned and control animals. Fos expression in some cortical sites was specific to tone versus air puff stimuli when used as conditioned stimulus. Thus, Fos expression was significantly increased in the contralateral temporal lobe when tones were used as conditioned stimulus, for both delayed and trace conditioning paradigms, but not when animals were conditioned to short, weak air puffs. The present results indicate a specific Fos activation in several cerebral cortical structures during associative eyelid conditioning.

Animals↗
PubMed1999

Acquired resistance to acoustic trauma by sound conditioning is primarily mediated by changes restricted to the cochlea, not by systemic responses.

Hearing loss caused by intense sound exposure can be significantly reduced by pre-exposing subjects to moderate-level acoustic stimuli. This phenomenon occurs in a variety of mammals. We investigated whether sound conditioning provides acquired resistance to acoustic trauma through local mechanisms selectively in the conditioned ears or if systemic mechanisms are involved that would yield contralateral protection in unconditioned ears. Guinea pigs (group I) in which one external ear canal was occluded were exposed to conditioning sound (2-20 kHz, 85 dB SPL, 5 h/day, 10 days). After removing the occlusion, the animals were then subjected bilaterally to intense noise (2-20 kHz, 110 dB SPL, 5 h) 5 days after the last conditioning exposure. Animals without ear canal occlusion were also exposed to the intense sound without conditioning (group II) or following the same conditioning exposure (group III). Intense sound exposure caused significantly greater permanent ABR threshold shifts at all frequencies tested (4, 8, 12, 16 and 20 kHz) in group II than in group III. In group I, the occluded ears showed significantly greater threshold shifts at all frequencies compared to the unoccluded ears. The threshold shifts in the occluded ears in group I were identical to those observed in group II; and the shifts in unoccluded ears in group I were identical to those in group III. Protective effects provided by sound conditioning were almost the same in group III and in the unoccluded ears in group I. The extent of hair cell damage supported the physiological findings. These results indicate that acquired resistance to acoustic trauma provided by sound conditioning is restricted to the cochlea exposed to conditioning sound, suggesting that conditioning protection is mediated primarily by the changes that occur locally within the conditioned cochlea. This animal model, with unilateral external ear canal occlusion during sound conditioning, is useful for studies of the mechanisms of conditioning protection.

Acoustic Stimulation↗
PubMed1995

Disruptive effects of posttraining perirhinal cortex lesions on conditioned fear: contributions of contextual cues.

Lesions placed in the rostral perirhinal cortex (rPRh) after fear conditioning interfere with the expression of conditioned fear responses elicited by auditory and visual conditioned stimuli when these stimuli are presented in a context that differs from the conditioning context. The present study examined whether lesions of the rPRh have similar effects when animals are tested in the conditioning context. Two days after male rats received classical fear conditioning, involving the pairing of an auditory conditioned stimulus (CS) with footshock, bilateral electrolytic lesions were produced in the rPRh. Five days later conditioned freezing behavior was measured during a 60-s exposure to the CS in a novel context and then 1 hr later in the conditioning context. There were 3 major findings. First, rPRh-lesioned animals froze significantly less than controls to the CS in the novel context, thus confirming previously reported findings. Second, rPRh-lesioned animals also froze less than controls to the CS in the conditioning context, but froze significantly more to the CS in the conditioning than in the novel context, suggesting that at least part of the deficit in the novel context is due to the absence of contextual cues. Third, animals with rPRh lesions froze significantly less than controls to the conditioning context itself. This latter finding suggests that rPRh lesions interfere with contextual processing and that the improvement of performance in the conditioning context might have been even greater had lesioned animals been able to fully process contextual cues.(ABSTRACT TRUNCATED AT 250 WORDS)

Acoustic Stimulation↗
PubMed1997

Patients with cerebellar lesions cannot acquire but are able to retain conditioned eyeblink reflexes.

The purpose of these experiments was to examine the role of the human cerebellum in the acquisition and retention of conditioned reflexes. Normal human subjects and patients with cerebellar lesions were tested for their capacity to acquire, retain and express conditioned eyeblink responses. In acquisition tests, subjects were trained in a delay classical conditioning paradigm using a tone conditioned stimulus and a midline forehead tap as an unconditioned stimulus. While normal subjects developed anticipatory eyeblinks to the tone in one session, patients with cerebellar lesions failed to acquire conditioned responses in four consecutive training sessions. The conditioning deficit was bilateral even in patients with a unilateral cerebellar pathology. The same groups of subjects were tested for the presence of eyeblinks to a visual threat. In these experiments, both normal subjects and patients with cerebellar lesions exhibited a high level of responding when they saw an object approaching their face. These eyeblinks to the visual threat are probably naturally acquired conditioned responses because they extinguish in normal subjects if they are not reinforced by the unconditioned cutaneous stimulus. In addition, the stimulus of seeing an approaching object blocks the acquisition of classically conditioned eyeblinks to a new conditioned stimulus in normal subjects. These data imply that patients with cerebellar lesions who cannot acquire new classically conditioned responses are able to retain and express conditioned eyeblinks which were acquired before the onset of the pathology. Consequently, cerebellum-dependent neural substrates which are involved in learning new conditioned reflexes do not seem to be required for the storage of naturally learned conditioned responses.

Adult↗
PubMed2002

Conditioned hyperkinesia induced by cocaine in mice is dose-dependent but not correlated with the unconditioned response or the contextually-sensitized response.

The aims of the study were to test whether drug dose is positively related to the magnitude of the conditioned response following sensitization to the behavioural effects of cocaine and to investigate the relationship between the conditioned response and cocaine-induced sensitization. Male mice (C57BL/6J) were first injected over seven successive days with either saline or cocaine at 2.5, 5, 10 or 20 mg/kg s.c., in the testing room. On the test day, 24 h after the last injection, mice from all conditions were challenged with saline in the testing room to test for conditioned cocaine effects. Mice were video-recorded and various behaviours were later scored using a time-sampling technique. Cocaine-elicited orofacial stereotypy was significantly sensitized at the two highest doses and dose-dependently conditioned at the three highest doses. Cocaine-increased locomotion was sensitized at the three highest doses and significantly conditioned at 10 and 20mg/kg. Cocaine-increased sniffing did not change over pretreatment at any dose, and was conditioned only at 10 mg/kg. Cocaine-decreased immobility also did not change over pretreatment at any dose, but was conditioned at 10 and 20mg/kg. Concomitantly, rearing was reduced by cocaine at 10 and 20mg/kg, without sensitization being induced, and it was reduced under saline challenge after 5 mg/kg cocaine, while cocaine-decreased grooming was sensitized at the three highest doses and conditioned at 10 and 20 mg/kg cocaine. There was a positive relation between the size of the conditioned response for orofacial stereotypy and the magnitude of the unconditioned stimulus (the doses), a result conforming to the Pavlovian account of the placebo effect. This could also be concluded from considering the behaviour patterns as components of a unique placebo effect (hyperkinetic syndrome), since orofacial stereotypy, very apparent at 20 mg/kg cocaine, interfered at that dose with the full-blown expression of locomotion and sniffing, both yielding (approximately) inverted U-shaped dose-effect curves. However, no correlation was found between the magnitude of the conditioned response and the amplitude of sensitization (the difference between the initial unconditioned non-sensitized response and the last unconditioned sensitized response), a finding which indicates that conditioned responding does not participate in the generation of the sensitized effects, contrary to the 'excitatory conditioning model of contextual sensitization'.

Animals↗