Mapping the estrous cycle to context-specific extinction memory.

In Pavlovian renewal paradigms, intact female rats have previously failed to exhibit renewal of appetitive behavior after extinction. However, when treated with exogenous estradiol, female rats exhibit robust renewal behavior. The current study aims to investigate whether the estrous cycle can influence renewal of appetitive behaviors and activity in brain areas known to support the renewal effect. We further aimed to examine whether the estrous cycle would similarly affect renewal of two different types of appetitive behaviors. We first establish that rats in the proestrous stage of the estrous cycle during extinction exhibit elevated renewal behavior compared with rats in either metestrous/diestrous stages, and only rats in proestrus during extinction training (but not during the renewal test) exhibit elevated renewal behavior. Furthermore, we show that this estrous cycle dependent effect on renewal only applies to the conditioned approach behavior toward the food delivery site but not the conditioned approach behavior toward the light cue associated with food delivery. Finally, we examined FOS activity within the prelimbic and infralimbic areas of the medial prefrontal cortex, the dorsal and ventral hippocampal formation, the paraventricular nucleus of the thalamus, the nucleus accumbens, and areas of the amygdala. Particularly in the hippocampus and amygdala, FOS expression which corresponded to the behavioral differences between groups was observed. Results from this study suggest that context information processing may vary as a function of endogenous female hormones across the gonadal hormone cycle and that encoding and retrieval of this information is accomplished in a state-specific manner. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Learned together, extinguished apart: reducing fear to complex stimuli.

Pairing a previously neutral conditioned stimulus (CS; e.g., a tone) to an aversive unconditioned stimulus (US; e.g., a footshock) leads to associative learning such that the tone alone comes to elicit a conditioned response (e.g., freezing). We have previously shown that an extinction session that occurs within the reconsolidation window attenuates fear responding and prevents the return of fear in pure tone Pavlovian fear conditioning. Here we sought to examine whether this effect also applies to a more complex fear memory. First, we show that after fear conditioning to the simultaneous presentation of a tone and a light (T+L) coterminating with a shock, the compound memory that ensues is more resistant to fear extinction than simple tone-shock pairings. Next, we demonstrate that the compound memory can be disrupted by interrupting the reconsolidation of the two individual components using a sequential retrieval+extinction paradigm, provided the stronger compound component is retrieved first. These findings provide insight into how compound memories are encoded, and could have important implications for PTSD treatment.

FGF-2-induced functional improvement from neonatal motor cortex injury via corticospinal projections.

The administration of basic fibroblast growth factor (FGF-2) to rats with postnatal 10 (P10) motor cortex (MCx) lesions results in functional improvements accompanied with filling of the previously lesioned area with tissue. In the present experiment, we tested the prediction that FGF-2 induces functional recovery by promoting meaningful reconnection of neurons from the filled region to the periphery. Rats received bilateral MCx lesions on P10 and subcutaneous injections of either vehicle or FGF-2 for 7 days beginning on P11. In adulthood, we evaluated the physiology and anatomy of corticospinal projections using intracortical microstimulation together with recordings of evoked electromyographic (EMG) activity in wrist extensors, and anterogradely tracing projecting axons using biotin dextran amine. We found that activity could be induced in the wrist extensors following stimulation of the filled region with onset delays comparable to undamaged corticospinal tract fibers in 5 out of 7 lesioned, FGF-2 treated rats. Furthermore, in the rats in which EMG activity could be elicited, long descending axons were labeled with projections into the spinal cord comparable to corticospinal tracts from undamaged motor cortex. Our results demonstrate that FGF-2 treatment restores the connectivity of the filled region in neonatal rats. This provides a possible mechanism for FGF-2-induced functional recovery.