Unconditioned Stimulus Onset Research Articles

Pupil dilation tracks divergent learning processes in aware versus unaware Pavlovian conditioning.

Evidence regarding unaware differential fear conditioning in humans is mixed and even less is known about the effects of contingency awareness on appetitive conditioning. Phasic pupil dilation responses (PDR) might be more sensitive for capturing implicit learning than other measures, such as skin conductance responses (SCR). Here, we report data from two delay conditioning experiments utilizing PDR (alongside SCR and subjective assessments) to investigate the role of contingency awareness in aversive and appetitive conditioning. In both experiments, valence of unconditioned stimuli (UCS) was varied within participants by administering aversive (mild electric shocks) and appetitive UCSs (monetary rewards). Preceding visual stimuli (CSs) predicted either the reward, the shock (65% reinforcement), or neither UCS. In Exp. 1, participants were fully instructed about CS-UCS contingencies, whereas in Exp. 2, no such information was given. PDR and SCR demonstrated successful differential conditioning in Exp. 1 and in (learned) aware participants in Exp. 2. In non-instructed participants who remained fully unaware of contingencies (Exp. 2), differential modulation of early PDR (immediately after CS onset) by appetitive cues emerged. Associations with model-derived learning parameters further suggest that early PDR in unaware participants mainly reflect implicit learning of expected outcome value, whereas early PDR in aware (instructed/learned-aware) participants presumably index attentional processes (related to uncertainty/prediction error processing). Similar, but less clear results emerged for later PDR (preceding UCS onset). Our data argue in favor of a dual-process account of associative learning, suggesting that value-related processing can take place irrespective of mechanisms involved in conscious memory formation.

Bed nucleus of the stria terminalis regulates fear to unpredictable threat signals.

The bed nucleus of the stria terminalis (BNST) has been implicated in conditioned fear and anxiety, but the specific factors that engage the BNST in defensive behaviors are unclear. Here we examined whether the BNST mediates freezing to conditioned stimuli (CSs) that poorly predict the onset of aversive unconditioned stimuli (USs) in rats. Reversible inactivation of the BNST selectively reduced freezing to CSs that poorly signaled US onset (e.g., a backward CS that followed the US), but did not eliminate freezing to forward CSs even when they predicted USs of variable intensity. Additionally, backward (but not forward) CSs selectively increased Fos in the ventral BNST and in BNST-projecting neurons in the infralimbic region of the medial prefrontal cortex (mPFC), but not in the hippocampus or amygdala. These data reveal that BNST circuits regulate fear to unpredictable threats, which may be critical to the etiology and expression of anxiety.

Hippocampectomy disrupts trace eye-blink conditioning in rabbits.

The role of the hippocampus (HFC) in trace eye-blink conditioning was evaluated using a 100-ms tone conditioned stimulus (CS), a 300- or 500-ms trace interval, and a 150-ms air puff unconditioned stimulus (UCS). Rabbits received complete hippocampectomy (dorsal & ventral), sham lesions, or neocortical lesions. Hippocampectomy produced differential effects in relation to the trace interval used. With a 300-ms trace interval, HPC-lesioned Ss showed profound resistance to extinction after acquisition. With a 500-ms trace interval, HPC-lesioned Ss did not learn the task (only 22% conditioned responses (CRs) after 25 sessions, whereas controls showed >80% after 10 sessions), and on the few trials in which a CR occurred, most were "nonadaptive" short-latency CRs (i.e., they started during or just after the CS and always terminated prior to UCS onset). The authors conclude that the HPC encodes a temporal relationship between CS and UCS, and when the trace interval is long enough (e.g., 500 ms), that the HPC is necessary for associative learning of the conditioned eye-blink response.

Impaired trace fear conditioning and diminished ERK1/2 phosphorylation in the dorsal hippocampus of adult rats administered alcohol as neonates.

Utilizing a rat model of fetal alcohol spectrum disorder (FASD), ethanol was administered over postnatal days (PD) 4 to 9. As adults, control and ethanol rats underwent trace fear conditioning (TFC), in which a tone conditioned stimulus (CS) and footshock unconditioned stimulus (US) were repeatedly paired, though the two stimuli never overlapped in time. Following training in Experiment 1, conditioned fear (freezing) to the tone CS was dose-dependently reduced in ethanol rats relative to controls. Experiment 2 was designed to test whether the TFC deficit varied based on the duration of the trace interval (TI; time from CS offset to US onset). Holding the time separating CS onset from US onset constant at 20 sec, control and ethanol rats were trained with a 5 or 15 sec tone CS, followed 15 or 5 sec later, respectively, by the US. Conditioned fear to the tone CS was significantly reduced in high dose ethanol rats trained with the 15 sec TI only. Acquisition and consolidation of trace fear memories relies on forebrain N-methyl-d-aspartate receptor (NMDAR) signaling, including the downstream phosphorylation of extracellular signal-regulated kinase 1/2 (pERK1/2). Separate rats were trained with the 5 or 15 sec TI and then sacrificed 1 hr later. Significant reductions in pERK1/2-positive neurons were seen in areas CA1 and CA3 of the dorsal hippocampus (DH) following training at both TIs in ethanol rats. The disruption of DH learning-dependent plasticity appears tied to freezing behavior in ethanol rats, but only when the training stimuli are separated by more than 5 sec.

Towards a unified model of pavlovian conditioning: short review of trace conditioning models.

There are three basic paradigms of classical conditioning: delay, trace and context conditioning where presentation of a conditioned stimulus (CS) or a context typically predicts an unconditioned stimulus (US). In delay conditioning CS and US normally coterminate, whereas in trace conditioning an interval of time exists between CS termination and US onset. The modeling of trace conditioning is a rather difficult computational problem and is a challenge to the behavior and connectionist approaches mainly due to a time gap between CS and US. To account for trace conditioning, Pavlov (Conditioned reflexes: an investigation of the physiological activity of the cerebral cortex, Oxford University Press, London, 1927) postulated the existence of a stimulus "trace" in the nervous system. Meanwhile, there exist many other options for solving this association problem. There are several excellent reviews of computational models of classical conditioning but none has thus far been devoted to trace conditioning. Eight representative models of trace conditioning aimed at building a prospective model are being reviewed below in a brief form. As a result, one of them, comprising the most important features of its predecessors, can be suggested as a real candidate for a unified model of trace conditioning.

Teleost cerebellum and heart rate conditioning

Event Abstract Back to Event Teleost cerebellum and heart rate conditioning Isabel Martin Monzon1*, Antonia Gomez1, Cosme Salas1 and Fernando Rodriguez1 1 University of Seville, Laboratorio de Psicobiologia, Spain A growing number of studies suggest that the cerebellum of mammals participates not only in the conditioning of simple motor responses but also in emotional learning. Although neuroanatomical and neurophysiological data indicate that the organization of the cerebellum is notably well conserved in vertebrates, little is actually known about the cerebellum contribution to processes besides the motor domain in non-mammals. In this study the participation of the teleost fish cerebellum in emotional learning was studied by analysing the effects of lesions of the corpus cerebelli, proposed as homologous to the vermis of mammals, on delay and trace heart rate conditioning in goldfish. A light was used as conditioned stimulus (CS) and a shock as unconditioned stimulus (US). In the delay procedure the CS was 8 sec in duration and both stimuli coterminated; in the trace procedure, the CS was 1 sec long and a trace of 7sec was introduced between the end of the CS and the onset of the US. The results showed that with paired CS-US presentations the sham and the telencephalon ablated fish rapidly increased the percentage of conditioned bradycardia in both procedures, and decreased quickly during the following extinction training to pseudoconditioned animals level. The results also showed that these goldfish accurately timed their heart rate responses to the duration of the trace interval, showing maximal bradycardiac responses close to the US onset. In contrast, the goldfish with cerebellar lesions failed to acquire the conditioned bradycardia. As in vermis ablated mammals, no deficit was observed neither in the reflex response to the US nor in the autonomic orientation response to the CS in the fish with corpus cerebelli or with telencephalon ablation. These data indicate that the involvement of the teleost cerebellum in fear conditioning is strikingly similar to mammals and suggest that the emotional function of the cerebellum may have evolved early in vertebrate evolution. Conference: 41st European Brain and Behaviour Society Meeting, Rhodes Island, Greece, 13 Sep - 18 Sep, 2009. Presentation Type: Poster Presentation Topic: Poster presentations Citation: Martin Monzon I, Gomez A, Salas C and Rodriguez F (2009). Teleost cerebellum and heart rate conditioning. Conference Abstract: 41st European Brain and Behaviour Society Meeting. doi: 10.3389/conf.neuro.08.2009.09.224 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 11 Jun 2009; Published Online: 11 Jun 2009. * Correspondence: Isabel Martin Monzon, University of Seville, Laboratorio de Psicobiologia, Seville, Spain, isabelmartin@us.es Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Isabel Martin Monzon Antonia Gomez Cosme Salas Fernando Rodriguez Google Isabel Martin Monzon Antonia Gomez Cosme Salas Fernando Rodriguez Google Scholar Isabel Martin Monzon Antonia Gomez Cosme Salas Fernando Rodriguez PubMed Isabel Martin Monzon Antonia Gomez Cosme Salas Fernando Rodriguez Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

The cerebellum: An incomplete multilayer perceptron?

Experimental studies have demonstrated the involvement of the cerebellum in showing classical conditioning paradigms including acquisition, extinction, savings, and spontaneous recovery of the conditioned eyelid response in rabbits. A few experimental studies suggest that the cerebellum is also able to show negative patterning (exclusive or) given that a sufficiently large interval between the conditioned stimulus onset and the unconditioned stimulus onset is provided. In this study, we use a detailed simulation of the cerebellum to shed light on the mechanisms underlying the computation of the exclusive or function. The results suggest that the timing of the conditioned response and the computation of the negative patterning paradigm are mutually exclusive.

Dynamic neural activity recorded from human amygdala during fear conditioning using magnetoencephalography

Magnetoencephalography (MEG) was used to record the dynamics of amygdala neuronal population activity during fear conditioning in human participants. Activation during conditioning training was compared to habituation and extinction sessions. Conditioned stimuli (CS) were visually presented geometric figures, and unconditioned stimuli (US) were aversive white-noise bursts. The CS+ was paired with the US on 50% of presentations and the CS− was never paired. The precise temporal resolution of MEG allowed us to address the issue of whether the amygdala responds to the onset or offset of the CS+, and/or the expectation of the initiation or offset of the an omitted auditory US. Fear conditioning elicited differential amygdala activation for the unpaired CS+ compared to the CS−, extinction and habituation. This was especially robust in the right hemisphere at CS onset. The strongest peaks of amygdala activity occurred at an average of 270 ms in the right and 306 ms in the left hemisphere following unpaired CS+ onset, and following offset at 21 ms in the left and 161 ms in the right (corresponding to an interval of 108 ms and 248 ms after the anticipated onset of the US, respectively). However, the earliest peaks in this epoch preceded US onset in most subjects. Thus, the activity dynamics suggest that the amygdala both differentially responds to stimuli and anticipates the arrival of stimuli based on prior learning of contingencies. The amygdala also shows stimulus omission-related activation that could potentially provide feedback about experienced stimulus contingencies to modify future responding during learning and extinction.

Endogenous cannabinoid signaling through the CB1 receptor is essential for cerebellum-dependent discrete motor learning.

Cannabinoids exert their psychomotor actions through the CB1 cannabinoid receptor in the brain. Genetic deletion of CB1 in mice causes various symptoms, including changes in locomotor activity, increased ring catalepsy, supraspinal hypoalgesia, and impaired memory extinction. Although the cerebellar cortex contains the highest level of CB1, severe cerebellum-related functional deficits have not been reported in CB1 knock-out mice. To clarify the roles of CB1 in cerebellar function, we subjected CB1 knock-out mice to a delay version of classical eyeblink conditioning. This paradigm is a test for cerebellum-dependent discrete motor learning, in which conditioned stimulus (CS) (352 ms tone) and unconditioned stimulus (US) (100 ms periorbital electrical shock) are coterminated. We found that delay eyeblink conditioning performance was severely impaired in CB1 knock-out mice. In contrast, they exhibited normal performance in a trace version of eyeblink conditioning with 500 ms stimulus-free interval intervened between the CS offset and the US onset. This paradigm is a test for hippocampus-dependent associative learning. Sensitivity of CB1 knock-out mice to CS or US was normal, suggesting that impaired delay eyeblink conditioning is attributable to defects in association of responses to CS and US. We also found that intraperitoneal injection of the CB1 antagonist SR141716A [N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-3-pyrazole carboxamide] to wild-type mice caused severe impairment in acquisition but not extinction of delay eyeblink conditioning. SR141716A treatment had no effect on trace eyeblink conditioning with a 500 or 750 ms trace interval. These results indicate that endogenous cannabinoid signaling through CB1 is essential for cerebellum-dependent discrete motor learning, especially for its acquisition.

The C50m response: Conditioned magnetocerebral activity recorded from the human brain

Recent advances in neuroimaging technology now permit a precise determination of the dynamics of specific neural activity underlying human associative learning. We used magnetoencephalography (MEG) to characterize the dynamics of conditioned responses (CRs) within auditory cortex during habituation, delay and trace conditioning training, and delay conditioning extinction. Conditioned stimuli (CS) were visually presented geometric figures, and unconditioned stimuli (US) were aversive noise bursts. CS+ stimuli were paired with the US on 50% of presentations: CS− stimuli were never paired with the US. Auditory cortex was activated following the paired CS+ at an average of 49–62 ms following US onset. Our data support the presence of a differential conditioned response (C50m) in auditory cortex following the unpaired CS+ at an average of 30–61 ms after US omission. The current source strength of the auditory C50m was subsequently quantified for the unpaired CS+ and CS− during training, the unpaired CS+ during extinction, and habituation. During delay and trace training, the C50m was stronger for the unpaired CS+ than for the CS−, and was also stronger for the unpaired CS+ during training compared to both habituation and extinction. This is the first description of magnetocerebral conditioning in normal human auditory cortex. The C50m activity in auditory cortex elicited by visual stimuli constitutes a direct observation of associative neural plasticity within the human auditory cortex.

Nicotine enhances trace cued fear conditioning but not delay cued fear conditioning in C57BL/6 mice

Nicotine facilitates hippocampus-dependent contextual but not hippocampus-independent cued delay fear conditioning. To test if the effects of nicotine are specific to contextual fear conditioning or would extend to another hippocampus-dependent version of fear conditioning, we compared the effects of nicotine on cued delay and cued trace fear conditioning in male and female C57BL/6 mice. Unlike cued delay fear conditioning, cued trace fear conditioning is hippocampus dependent. Thus, if nicotine enhances hippocampus-dependent fear conditioning, nicotine should enhance trace fear conditioning. For both trace and delay conditioning, five 30 s, 85 dB white noise conditioned stimuli (CS) were paired with five 2 s, 0.5 mA footshock unconditioned stimuli (US). In the trace paradigm, a 30-s period was inserted between CS offset and US onset. The CS and US co-terminated in the delay paradigm. Testing occurred 24 h later. The data indicate that nicotine (given on training and testing day) enhances trace but not delay cued fear conditioning. No sex differences were found. For delay cued fear conditioning a high level of freezing to the CS was found. Thus, a second experiment examined if the lack of enhancement of delay cued fear conditioning by nicotine was due to a ceiling effect. The CS duration was decreased to 15 s and only one CS–US pairing was used for delay and trace cued fear conditioning. Although overall levels of freezing to the cue were lower in the second experiment, nicotine still enhanced trace fear conditioning but did not enhance delay fear conditioning. Taken together, the results of the present experiments suggest that nicotine enhances hippocampus-dependent versions of fear conditioning.

Timing of conditioned responses utilizing electrical stimulation in the region of the interpositus nucleus as a CS

A large body of evidence indicates that the cerebellum is essential for the acquisition, retention, and expression of the standard delay conditioned eyeblink response and that the basic memory trace appears to be established in the anterior interpositus nucleus (IP). Adaptive timing of the conditioned response (CR) is a prominent feature of classical conditioning-the CR peaks at the time of onset of the unconditioned stimulus (US) over a wide range of CS-US interstimulus intervals (ISI). A key issue is whether this timing is established by the cerebellar circuitry or prior to the cerebellum. In this study timing of conditioned eyeblink responses established via electrical stimulation of the interpositus nucleus as a conditioned stimulus (CS) was analyzed prior to and following modification of the CS-US interval in well-trained rabbits. Consistent with previous results, learning under these conditions is very rapid and robust. The CR peak eyeblink latencies are initially timed to the US onset and adjust accordingly to lengthening or shortening of the CS-US interval, just as with peripheral CSs. The acquisition of conditioned eyeblink responses by direct electrical stimulation of the IP as a CS thus retains temporal flexibility following shifts in the CS-US delay, as found in standard classical eyeblink conditioning procedures.

Neural substrates mediating human delay and trace fear conditioning.

Previous functional magnetic resonance imaging (fMRI) studies with human subjects have explored the neural substrates involved in forming associations in Pavlovian fear conditioning. Most of these studies used delay procedures, in which the conditioned stimulus (CS) and unconditioned stimulus (UCS) coterminate. Less is known about brain regions that support trace conditioning, a procedure in which an interval of time (trace interval) elapses between CS termination and UCS onset. Previous work suggests significant overlap in the neural circuitry supporting delay and trace fear conditioning, although trace conditioning requires recruitment of additional brain regions. In the present event-related fMRI study, skin conductance and continuous measures of UCS expectancy were recorded concurrently with whole-brain blood oxygenation level-dependent (BOLD) imaging during direct comparison of delay and trace discrimination learning. Significant activation was observed within the visual cortex for all CSs. Anterior cingulate and medial thalamic activity reflected associative learning common to both delay and trace procedures. Activations within the supplementary motor area (SMA), frontal operculum, middle frontal gyri, and inferior parietal lobule were specifically associated with trace interval processing. The hippocampus displayed BOLD signal increases early in training during all conditions; however, differences were observed in hippocampal response magnitude related to the accuracy of predicting UCS presentations. These results demonstrate overlapping patterns of activation within the anterior cingulate, medial thalamus, and visual cortex during delay and trace procedures, with additional recruitment of the hippocampus, SMA, frontal operculum, middle frontal gyrus, and inferior parietal lobule during trace conditioning. These data suggest that the hippocampus codes temporal information during trace conditioning, whereas brain regions supporting working memory processes maintain the CS-UCS representation during the trace interval.

Impairment of eyeblink conditioning in GluRdelta2-mutant mice depends on the temporal overlap between conditioned and unconditioned stimuli.

Mice lacking the glutamate receptor subunit delta2 (GluRdelta2) are deficient in cerebellar long-term depression (LTD) at the parallel fibre-Purkinje cell synapses. We conducted delay and trace eyeblink conditioning with these mice, using various temporal intervals between the conditioned stimulus (CS) and unconditioned stimulus (US). During trace conditioning in which a stimulus-free trace interval (TI) of 250, 100 or 50 ms intervened between the 352-ms tone CS and 100-ms US, GluRdelta2-mutant mice learned as successfully as wild-type mice. Even in the paradigm with TI = 0 ms, in which the end of CS and onset of US are simultaneous, there was no difference between the GluRdelta2-mutant and wild-type mice in their acquisition of a conditioned response. However, in the delay paradigm in which the 452-ms CS overlapped temporally with the coterminating 100-ms US, GluRdelta2-mutant mice exhibited severe learning impairment. The present study together with our previous work [Kishimoto, Y., Kawahara, S., Suzuki, M., Mori, H., Mishina, M. & Kirino, Y. (2001) Eur. J. Neurosci., 13, 1249-1254], indicates that cerebellar LTD-independent learning is possible in paradigms without temporal overlap between the CS and US. On the other hand, GluRdelta2 and cerebellar LTD are essential for learning when there is CS-US temporal overlap, suggesting that the cerebellar neural substrates underlying eyeblink conditioning may change, depending on the temporal overlap of the CS and US.

Rabbit classical eyeblink conditioning is altered by brief cerebellar cortical stimulation

A pair of studies examined how cortical intracerebellar stimulation (ICS) affects eyeblink conditioning in the rabbit. Rabbits were implanted with chronic bipolar stimulating electrodes in the cell body layers of cerebellar lobule H-VI. Brief (40 ms) trains of intracranial stimulation (100 Hz, 250 μA) were delivered during training trials [forward pairings of a tone-conditioned stimulus (CS) with an air puff unconditioned stimulus (US)]. In Experiment 1, the onset of ICS varied randomly within sessions. US-onset-coincident ICS proved detrimental to the maintenance of conditioning [measured as the percentage of trials on which conditioned responses (CRs) were made] compared to ICS that ended 60 ms before US onset. Based on these findings, a second experiment compared a group trained with ICS consistently delivered at US onset to groups trained with ICS consistently delivered either at CS onset or between the two stimuli, as well as to unstimulated control subjects. Animals receiving CS- or US-coincident ICS learned slowest, whereas animals receiving middle stimulation learned more quickly than all other groups. In both Experiments 1 and 2, highly trained animals produced blinks in direct response to the stimulation. These data are discussed in terms of a new hypothesis concerning interactions between cerebellar cortex and the deep cerebellar nuclei during eyeblink conditioning — a rebound from inhibition hypothesis.

A model of hippocampal activity in trace conditioning: where's the trace?

The hippocampus is generally thought to play a modulating role in the timing of conditioned responses in classical trace conditioning. One hypothesis is that the hippocampus stores a memory trace of the conditioned stimulus (CS) during the stimulus-free period. Cellular recordings, however, do not show any obvious CS storage. This article examines this issue by using a biologically plausible model of the CA3 region of the hippocampus. Simulations of the model reproduce both behavioral and physiological experimental data. On the basis of neural codes that develop in the model, the authors hypothesize that the hippocampus functions as a time-indexed encoding device for the CS and not as a CS storage buffer. Specifically, the CS initiates a sequence of neural activity during the trace interval that only indirectly represents the CS. The model yields 2 predictions: Some cells will increase in activity only during the trace interval, and some unconditioned stimulus (US)-coding cells will shift in time and fire before US onset.

Short-lasting conditioned stimulus applied to the middle cerebellar peduncle elicits delayed conditioned eye blink responses in the decerebrate ferret.

In delay eye blink conditioning, the conditioned stimulus (CS) ends at the time of the unconditioned stimulus (US). If the CS duration is decreased, there will be a 'trace' period with no ongoing CS before the onset of the US. During this period some neural activity has to continue after the CS offset to: (i) permit association between the CS and the US; and (ii) elicit a conditioned response appearing after the CS offset. In this study we test the role of the cerebellum in maintaining CS activity required for eliciting a conditioned response after the CS offset. Decerebrate ferrets were trained in a delay conditioning paradigm with an electrical stimulation of the forelimb as CS and of the periorbital area as US. The conditioned responses in the upper eyelid were monitored with electromyographical techniques. In well-trained animals, test CSs of short duration down to 0.2 ms were applied to the forelimb or the middle cerebellar peduncle, while the interstimulus interval between CS onset and US onset was kept constant at 300 ms. Test CSs of short duration applied to the forelimb elicited conditioned responses. More importantly, also a short-lasting CS to the middle cerebellar peduncle could elicit conditioned responses. The results indicate that precerebellar CS pathways are not required for maintaining the neural activity that elicits conditioned responses after the CS offset. It is suggested that neurons maintaining such activity are located in the cerebellum, either the cortex alone or the cortex and the deep nuclei.

Conditioned inhibition of autonomic Pavlovian conditioning in humans

The present study aimed to demonstrate conditioned inhibition of Pavlovian conditioning of autonomic responses in humans. Subjects ( N=21) were presented initially with four geometric shapes (A, B, C and D). An electric shock served as the unconditioned stimulus (US) during acquisition. Conditional stimuli lasted for 8 s and US onset coincided with CS offset. Subjects were trained with A-US, C-US, and AC-US pairings and AB alone and B alone presentations. The subsequent summation test consisted of C-US pairings and CB alone and CD alone presentations. Conditioning was evident in self-reported US expectancy and first and second interval electrodermal responses. Evidence for conditioned inhibition during the summation test was found in US expectancy and second interval electrodermal responses.

One-trial simultaneous and backward excitatory fear conditioning in rats: Lick suppression, freezing, and rearing to CS compounds and their elements

Three experiments with rat subjects sought to enhance one-trial excitatory simultaneous and backward fear conditioning by using a two-element compound conditioned stimulus (CS) instead of only a single element. During conditioning, experimental groups received a 4-sec CS either coextensively with a 1-mA grid-shock unconditioned stimulus (US) or immediately after US termination. In subsequent tests, CSs evoked more lick suppression and freezing in these groups than in various controls. Compound CSs evoked more lick suppression and freezing than did CS elements, but did so equally for experimental and control groups. Therefore, the use of compounds did not enhance conditioning. Unexpectedly, an explicitly unpaired control in which CS followed US termination by 3 min tended to show more CS-evoked suppression and freezing than did a control in which CS preceded US onset by 3 min. This result raises the possibility that associations between the CS and the training context might engender responding to backward-paired CSs.

Avoidance and classical conditioning of leg flexion in dogs

This study of leg flexion conditioning in dogs, which were trained under both avoidance and classical contingencies consecutively, confirmed and extended the results from the Wahlsten and Cole study (In Classical Conditioning II: Current Research and Theory, Appleton Century-Crofts, New York, 1972). Briefly, dogs were trained to asymptotic behavioral levels under either avoidance or classical contingencies with a CS-US interval of either three (3) or five (5) seconds where the unconditioned stimulus (US) was shock to the foreleg and the conditioned stimulus (CS) was 1000 Hz tone. The dogs were then switched to the other contingency (without any modification in the stimulus situation other than the shock contingency) and trained to asymptotic behavioral levels. The CS remained on for the entire CS-US period and terminated with the end of the scheduled interval. Under the classical contingency, the US occurred as scheduled on every trial regardless of the dog's behavior. Under the avoidance contingency, the US was prevented from occurring if the subject responded with a criterion leg lift during the CS-US interval. The only feedback to the dog of a successful performance was the leg lift itself. The results indicated that there were two different conditioned responses produced, one just after CS onset under the avoidance contingency, and one just before US onset under the classical contingency for both CS-US intervals. The findings were interpreted as supporting a single-factor informational view of learning and a neural model was presented