Partial reinforcement effects in instrumental escape conditioning

In Experiment I acquisition and extinction of instrumental escape conditioning with rats (N = 64) were studied as a function of reinforcement magnitude under conditions of partial and continuous reinforcement. In Experiment II the effects of partial and continuous reinforcement were studied in rats (N = 96) during acquisition followed by small, medium, and large reductions in reinforcement magnitude. A water-tank escape apparatus was used with temperature as the relevant variable. It was found that (1) with large reinforcement magnitude a continuously reinforced group was superior in acquisition to one that was partially reinforced; there were no differences with small reinforcement; (2) disruptive effects of a nonreinforced trial (a) appear early in learning, (b) are quite strong after each nonreinforced trial, and (c) persist through several succeeding reinforced trials; (3) major competing behaviors persist throughout acquisition for small reinforcement magnitude regardless of schedule, decline with large reinforcement (more so with continuous than with partial), and return to a high level in extinction for all conditions; (4) the partial reinforcement extinction effect occurs after large reinforcement but not after small, and it appears only with large reductions in reinforcement magnitude which approach extinction conditions. Only the first part of the last finding appears to be consistent with the appetitive conditioning literature.     

Intrahippocampal scopolamine impairs both acquisition and consolidation of contextual fear conditioning

Lesions of the dorsal hippocampus have been shown to disrupt both the acquisition and the consolidation of memories associated with contextual fear (fear of the place of conditioning), but do not affect fear conditioning to discrete cues (e.g., a tone). Blockade of central muscarinic cholinergic receptor activation results in selective acquisition deficits of contextual fear conditioning, but reportedly has little effect on consolidation. Here we show for the first time that direct infusion of the muscarinic cholinergic receptor antagonist, scopolamine, into the dorsal hippocampus produces a dose-dependent deficit in both acquisition and consolidation of contextual fear conditioning, while having no impact on simple tone conditioning.     

Olfactory fear conditioning paradigm in rats: Effects of midazolam,propranolol or scopolamine

In rodents, fear conditioned responses are more pronounced toward olfactory stimulus, since olfaction is a dominant sense in these subjects. The present study was outlined to investigate if the association between coffee odor (CS1) and electrical footshock (US) would be an effective model for the study of fear-induced behavior and whether compounds used in humans for emotional-related disorders such as midazolam, propranolol, or scopolamine, applied during the different stages of fear conditioning (acquisition, consolidation and expression), affect the defensive responses to both, the olfactory CS1, and the context (CS2) where the CS1 had been presented (second order conditioning). The results revealed that five pairings between coffee odor (CS1) and electrical footshock (US) were able to elicit consistent defensive responses and a second order conditioning to the context (CS2). Midazolam (0.375–0.5 mg/kg; i.p.) treatment was able to interfere with the CS1–US association and with the consolidation of the aversive information. The propranolol (5–10 mg/kg; i.p.) treatment interfered with the CS1–US association, with the retention of fear memory and with the CS1–CS2 association. Propranolol also attenuated the expression of conditioned fear responses when applied before the CS1 test session. Scopolamine (0.6–1.2 mg/kg; i.p.) treatment impaired the acquisition of CS1–US and CS1–CS2 associations, and also disrupted the expression of conditioned fear responses when injected prior to the CS1 test session. These findings have pointed out the usefulness for the olfactory fear conditioning paradigm to investigate drug effects on the acquisition, consolidation and expression of fear conditioned responses.     

The effects of escape conditioning and shock intensity on responding during inescapable shock

Eight albino rats, conditioned to press a lever to escape shock, continued to lever press during short inescapable shocks presented subsequently. The rate of this behavior was found to be higher for higher shock intensities regardless of the order in which shock values were presented. Relative to the immediately preceding escape rate, responding during inescapable shock was higher following conditioning at higher fixed-ratio escape requirements. Four subjects not conditioned to escape shock pressed the lever very infrequently during inescapable shock and showed little change with changes in shock intensity. The escape conditioning effects suggest that responding during inescapable shock is superstitious escape behavior. The effects of shock intensity on this behavior appear to be similar to reported effects of shock intensity on escape behavior.     

Instructed fear learning,extinction, and recall: additive effects of cognitive information on emotional learning of fear

The effects of instruction on learning of fear and safety are rarely studied. We aimed to examine the effects of cognitive information and experience on fear learning. Fourty healthy participants, randomly assigned to three groups, went through fear conditioning, extinction learning, and extinction recall with two conditioned stimuli (CS+). Information was presented about the presence or absence of conditioned stimulus–unconditioned stimulus (CS–US) contingency at different stages of the experiment. Information about the CS–US contingency prior to fear conditioning enhanced fear response and reduced extinction recall. Information about the absence of CS–US contingency promoted extinction learning and recall, while omission of this information prior to recall resulted in fear renewal. These findings indicate that contingency information can facilitate fear expression during fear learning, and can facilitate extinction learning and recall. Information seems to function as an element of the larger context in which conditioning occurs.     

Limbic networks and associative learning: I. Entorhinal contributions to instrumental conditioning

The hippocampal formation is a highly delineated brain structure that is believed to play a prominent role in learning and memory. The present experiment evaluated the contributions of medial and lateral perforant path input to bar press-conditioning under (a) continuous and (b) differential reinforcement of low rates of responding (DRL) schedules, and (c) shuttlebox avoidance conditioning. Bilateral deafferentation of either pathway had no effect on the acquisition of bar press responses or on performance under the DRL schedule. Deafferentation of the medial pathway facilitated acquisition of avoidance responses in a manner much like the effects seen in hippocampectomized animals. It is suggested that the medial perforant path participates in the expression of correlated patterns of neuronal discharge known to develop within the hippocampus and that this “model” serves to modulate the temporal characteristics of simple conditioned reflexes. Loss of the modulatory influence of the model may affect acquisition and extinction rates. Contributions of other hippocampal circuits are discussed in relation to established deficits. Preliminary results of this experiment were presented at the second annual convention of the American Psychological Society, Dallas, Texas, June 1990.     

Limbic networks and associative learning: I. Entorhinal contributions to instrumental conditioning

The hippocampal formation is a highly delineated brain structure that is believed to play a prominent role in learning and memory. The present experiment evaluated the contributions of medial and lateral perforant path input to bar press-conditioning under (a) continuous and (b) differential reinforcement of low rates of responding (DRL) schedules, and (c) shuttlebox avoidance conditioning. Bilateral deafferentation of either pathway had no effect on the acquisition of bar press responses or on performance under the DRL schedule. Deafferentation of the medial pathway facilitated acquisition of avoidance responses in a manner much like the effects seen in hippocampectomized animals. It is suggested that the medial perforant path participates in the expression of correlated patterns of neuronal discharge known to develop within the hippocampus and that this “model” serves to modulate the temporal characteristics of simple conditioned reflexes. Loss of the modulatory influence of the model may affect acquisition and extinction rates. Contributions of other hippocampal circuits are discussed in relation to established deficits. Preliminary results of this experiment were presented at the second annual convention of the American Psychological Society, Dallas, Texas, June 1990.     

Role of fear in mediating shuttle escape learning deficit produced by inescapable shock

The relation between the shuttlebox escape deficit produced by prior inescapable shock (IS) and fear during shuttlebox testing as assessed by freezing was investigated in rats. IS rats learned to escape poorly and were more fearful than either escapably shocked subjects or controls, both before and after receiving shock in the shuttlebox. However, fear and poor escape performance did not covary with the manipulation of variables designed to modulate the amount of fear and the occurrence of the escape deficit. A 72-hr interval between IS and testing eliminated the escape deficit but did not reduce preshock freezing. Diazepam before testing reduced both preshock and postshock fear in the shuttlebox but had no effect on the escape deficit. Naltrexone had no effect on fear but eliminated the escape deficit. This independence of outcomes suggests that the shuttlebox escape deficit is not caused by high levels of fear in IS subjects.     

Naloxone and Pavlovian fear conditioning

Previous research has shown that pretreating rats with the opiate antagonist naloxone increases the freezing that follows painful electric shock. Three experiments, using freezing behavior as a dependent variable, were carried out to determine whether the drug might cause this effect by enhancing fear conditioning. Two of the studies employed a differential context fear-conditioning paradigm. Naloxone did not affect freezing behavior during the preshock adaptation period. In Experiment 1, naloxone was found to increase resistance to extinction in the S+ context. In Experiment 2, naloxone was found to increase freezing in the S+ context. This effect was dependent upon administering naloxone during training but not dependent on administering it during testing. The third study employed a generalization paradigm. It was found that naloxone's effect on postshock freezing was dependent on the place of testing; as the contextual cues of the test chamber were changed from those of the conditioning chamber, the effect of naloxone on freezing was reduced. The results of these experiments lend strong support to the hypothesis that naloxone increases freezing by enhancing the conditioning of fear to contextual stimuli associated with shock.     

Genetic background differences and nonassociative effects in mouse trace fear conditioning

Fear conditioning, including variants such as delay and trace conditioning that depend on different neural systems, is widely used to behaviorally characterize genetically altered mice. We present data from three strains of mice, C57/BL6 (C57), 129/SvlmJ (129), and a hybrid strain of the two (F(1) hybrids), trained on various versions of a trace fear-conditioning protocol. The initial version was taken from the literature but included unpaired control groups to assess nonassociative effects on test performance. We observed high levels of nonassociative freezing in both contextual and cued test conditions. In particular, nonassociative freezing in unpaired control groups was equivalent to freezing shown by paired groups in the tests for trace conditioning. A number of pilot studies resulted in a new protocol that yielded strong context conditioning and low levels of nonassociative freezing in all mouse strains. During the trace-CS test in this protocol, freezing in unpaired controls remained low in all strains, and both the C57s and F(1) hybrids showed reliable associative trace fear conditioning. Trace conditioning, however, was not obtained in the 129 mice. Our findings indicate that caution is warranted in interpreting mouse fear-conditioning studies that lack control conditions to address nonassociative effects. They also reveal a final set of parameters that are important for minimizing such nonassociative effects and demonstrate strain differences across performance in mouse contextual and trace fear conditioning.     

Contiguity and contingency in instrumental conditioning

There have been several attempts to construct molar theories of conditioning on the empirical basis that response-reinforcement contingency is important in determining conditioning. Such theories claim to explain behavior in terms of molar level processes which transcend the molecular level and, therefore, are not reducible to molecular processes or their interaction. These molar theories are critically examined and found to be seriously flawed because they fail to account for the effects of delaying reinforcement (degree of contiguity). Observed molar level relations, such as the matching law, do not require a molar theory, but may be more usefully considered as a product of molecular processes.     

Lack of phenotype for LTP and fear conditioning learning in calpain 1 knock-out mice

We previously proposed the hypothesis that calpain activation played an important role in long-term potentiation (LTP) of synaptic transmission in hippocampus. Two forms of calpain are predominant in brain tissues, calpain 1 (mu-calpain), activated by micromolar calcium concentration and calpain 2 (m-calpain), activated by millimolar calcium concentration in vitro. In the present study, we tested the role of calpain 1 in LTP and in learning and memory using calpain 1 knock-out mice. Changes in learning and memory were assessed using both context and tone fear conditioning. No differences in freezing responses were observed between the knock-out and the wild-type animals during the acquisition phase of the training, eliminating the possibility that the knock-out animals could be differentially affected by the foot shock. Likewise, no differences in freezing responses elicited by either the context or the tone were observed during the retention phase. No differences in short-term potentiation (STP) or LTP were observed in hippocampal slices from the knock-out and matched wild-type mice. Several interpretations might explain these negative results. First, it is conceivable that calpain 2 plays a more dominant role in neurons, and that calpain 1 makes a minor contribution as opposed to its suspected predominant role in the hematopoietic system. Alternatively, it is conceivable that some as yet unknown compensatory mechanisms take effect, and that calpain 2 or another calpain isoform substitutes for the missing calpain 1.