Incubation of food craving in rats: A review

Incubation of food craving is an abstinence-dependent increase in responding for reward-paired cues. Incubation of craving was first reported for rats responding for cocaine-paired cues, and later generalized to several drugs of abuse and for food. Incubation of drug and food craving has been reported in clinical studies as well. Incubation of food craving by rats has been reported for standard chow as well as for high fat and sucrose reinforcers. Parametric and other evaluations of the incubation of food craving reveal manipulations that reduce incubation, including environmental enrichment and pharmacological manipulation of dopamine, glutamate, and endogenous opiates. Several brain regions are likely involved in the effect, including mesolimbic terminals and the central nucleus of the amygdala. Further study of the incubation of food craving could facilitate development of treatments for cravings that precede relapse characteristic of drug and food addictions.     

"Scared stiff": catatonia as an evolutionary-based fear response

Catatonia, long viewed as a motor disorder, may be better understood as a fear response, akin to the animal defense strategy tonic immobility (after G. G. Gallup & J. D. Maser, 1977). This proposal, consistent with K. L. Kahlbaum's (1874/1973) original conception, is based on similarities between catatonia and tonic immobility ("death feint") as well as evidence that catatonia is associated with anxiety and agitated depression and responds dramatically to benzodiazepines. It is argued that catatonia originally derived from ancestral encounters with carnivores whose predatory instincts were triggered by movement but is now inappropriately expressed in very different modern threat situations. Found in a wide range of psychiatric and serious medical conditions, catatonia may represent a common "end state" response to feelings of imminent doom and can serve as a template to understand other psychiatric disorders.     

Effects of fear on exploratory behaviour in rats

It has been suggested that mild fear may evoke rather than inhibit exploratory responses in rats. The relationship between conditioned fear and exploratory behaviour was analysed in three experiments and there was no evidence that mild fear increased exploration. Conditioned fear was found to be under relatively precise stimulus control and its magnitude was related to the intensities and durations of the unconditioned stimulus, inescapable electric shock.     

Learned fear of "unseen" faces after Pavlovian, observational, and instructed fear

This study compared fear learning acquired through direct experience (Pavlovian conditioning) and fear learning acquired without direct experience via either observation or verbal instruction. We examined whether these three types of learning yielded differential responses to conditioned stimuli (CS+) that were presented unmasked (available to explicit awareness) or masked (not available to explicit awareness). In the Pavlovian group, the CS+ was paired with a mild shock, whereas the observational-learning group learned through observing the emotional expression of a confederate receiving shocks paired with the CS+. The instructed-learning group was told that the CS+ predicted a shock. The three groups demonstrated similar levels of learning as measured by the skin conductance response to unmasked stimuli. As in previous studies, participants also displayed a significant learning response to masked stimuli following Pavlovian conditioning. However, whereas the observational-learning group also showed this effect, the instructed-learning group did not.     

Social transmission of Pavlovian fear: fear-conditioning by-proxy in related female rats

Pairing a previously neutral conditioned stimulus (CS; e.g., a tone) to an aversive unconditioned stimulus (US; e.g., a foot-shock) leads to associative learning such that the tone alone will elicit a conditioned response (e.g., freezing). Individuals can also acquire fear from a social context, such as through observing the fear expression of a conspecific. In the current study, we examined the influence of kinship/familiarity on social transmission of fear in female rats. Rats were housed in triads with either sisters or non-related females. One rat from each cage was fear conditioned to a tone CS+ shock US. On day two, the conditioned rat was returned to the chamber accompanied by one of her cage mates. Both rats were allowed to behave freely, while the tone was played in the absence of the foot-shock. The previously untrained rat is referred to as the fear-conditioned by-proxy (FCbP) animal, as she would freeze based on observations of her cage-mate’s response rather than due to direct personal experience with the foot-shock. The third rat served as a cage-mate control. The third day, long-term memory tests to the CS were performed. Consistent with our previous application of this paradigm in male rats (Bruchey et al. in Behav Brain Res 214(1):80–84, 2010), our results revealed that social interactions between the fear conditioned and FCbP rats on day two contribute to freezing displayed by the FCbP rats on day three. In this experiment, prosocial behavior occurring at the termination of the cue on day two was significantly greater between sisters than their non-sister counterparts, and this behavior resulted in increased freezing on day three. Our results suggest that familiarity and/or kinship influences the social transmission of fear in female rats.     

Polyaminergic agents modulate contextual fear extinction in rats

Polyamines, such as spermidine and spermine, have been reported to improve memory retention through the activation of N-methyl-d-aspartate receptors (NMDAr). However whether polyamine agonists and antagonists alter extinction remains unclear. In the current study, we investigated whether spermidine and polyamine antagonists that selectively block the NR2B subunit at the NMDAr alter the extinction of contextual conditioned fear in male Wistar rats. The bilateral intra-hippocampal administration of exogenous spermidine (2 nmol/site) immediately after, but not 6 h after extinction training, facilitated the extinction of fear conditioning. The injection of the NMDAr antagonists arcaine (0.2 nmol/site), ifenprodil (20 nmol/site) and traxoprodil (0.2 nmol/site), disrupted fear extinction and, at doses that had no effect per se, reversed the facilitatory effect of spermidine on fear extinction. These results suggest that exogenous and endogenous polyamines facilitate the extinction of contextual conditioned fear through activation of NR2B subunit-containing NMDAr in the hippocampus. Since extinction-based exposure therapy is widely used as treatment for a number of anxiety-related disorders, including phobias and post-traumatic stress, the currently reported facilitation of extinction by polyaminergic agents suggest these compounds as putative candidates for drug development.