Parent-Led Exposure Therapy: A Pilot Study of a Brief Behavioral Treatment for Anxiety in Young Children

Despite prevalence rates as high as 9.4%, few studies have examined the applicability of cognitive-behavioral therapy for treatment of anxiety disorders in very young children (i.e., below the age of 7 years). The present study examined the preliminary efficacy of a parent-led exposure therapy protocol (PLET) designed for young children with anxiety disorders. Twenty-two youth aged 4–7 years and their parents participated in this pilot randomized control trial. Families of youth with significant anxiety concerns were randomized to either PLET (n?=?12), a 10 session/5-week family-based exposure therapy program designed to target anxiety in young children, or treatment as usual (TAU; n?=?10). Children in the PLET condition demonstrated a greater reduction in anxiety symptoms compared to TAU (d?=?3.18), with 90.91% of PLET participants (active condition) being classified as treatment responders at post-treatment as opposed to 0 in the TAU condition. Gains were maintained at 1 month-follow-up. Although pilot in nature, these data suggest in a preliminary fashion that a parent led exposure therapy protocol that is adapted appropriately for developmental age and incorporates an active coaching component for parents may be efficacious for the treatment of young children with anxiety disorders. This clinical trial was registered through clinicaltrials.gov under the following identifier: NCT02051192.     

Place learning in the Morris water task: making the memory stick

Although the Morris water task has been used in hundreds of studies of place learning, there have been no systematic studies of retention of the place memory. We report that retention, as measured by selective search behavior on a probe trial, is excellent when the retention interval is short (5-10 min). However, performance rapidly deteriorates, so that by approximately 4 h the search is no longer selective. Additional experiments revealed that selective search at longer retention intervals was improved by inserting gaps between blocks of training trials, but this effect was a non-monotonic function of the interval separating trial blocks. Our experiments also revealed that the location of the first block of trials (Room A or Room B) was irrelevant to long-term retention. A memory modulation theoretical framework may provide a useful way to understand these findings.     

Stress-induced progesterone secretion and progesterone receptor immunoreactivity in the paraventricular nucleus are modulated by pubertal development in male rats

Male rats show a differential adrenocortical response to stress before and after pubertal development, such that prepubertal animals have a more prolonged stress-induced corticosterone response compared to adults. Whether pubertal maturation affects other adrenocortical responses to stress is currently unknown. To address this question, we assessed stress-induced progesterone secretion in both intact and gonadectomized prepubertal (28 days of age) and adult (77 days of age) male rats either before or after exposure to a 30 min session of restraint stress. We found that prepubertal males show a greater and more prolonged stress-induced progesterone response compared to adults. We also found a similar effect in castrated prepubertal and adult males, indicating the differential stress-induced progesterone response is not gonadal in origin. We also examined progesterone receptor (PR) levels by immunohistochemistry in the paraventricular nucleus (PVN) of the hypothalamus, a key regulatory nucleus of the hypothalamic-pituitary-adrenal (HPA) axis, and found lower PR protein expression in the PVN of prepubertal compared to adult males. These data indicate that in addition to corticosterone, stress-induced adrenocortical progesterone levels are differentially affected by pubertal maturation. Furthermore, these data raise the possibility of different progesterone sensitivity of the PVN before and after puberty. The significance of this differential response is presently unknown. However, given the pleiotropic effects of progesterone on male physiology and behaviour, it is likely that the disparate post-stress exposure to progesterone affects the prepubertal and adult male differently.     

The mind and the immune system

Stress-induced brain-mediated immunoregulation is effected by two pathways: autonomic outflow and (neuro)endocrine outflow. Particular attention is given to the interaction-effects of chronic an acute stress. Recent data have established that cells of the immune system produce neuro-peptides and hormones. In concert with cytokines released by these immune cells the brain can be informed on the nature of ongoing immune activity. The significance of conditioning of immune responses is discussed.     

Neonatal hyperthyroidism in the rat: thyroxine accelerates the development of unconditioned but not learned responses to tastes

The effects of neonatal hyperthyroidism induced by thyroxine injection on the development of unconditioned and learned behaviors mediated by the gustatory system of the rat were investigated. The development of unconditioned ingestive responses evoked by 10% sucrose and 0.1% HCl taste solutions was advanced several days by thyroxine treatment. However, the emergence of taste aversion learning involving 10% sucrose and LiCl injection was not advanced and may have been slightly delayed. Thus, the ontogenesis of unconditioned and learned behaviors mediated by the gustatory system was not influenced uniformly by neonatal thyroxine treatment.     

Logical relations and comprehension in conversation

This study examines how logical relations (e.g., causality and identity) in spoken discourse affect comprehension. Research on cohesion, which shows that specific unit template structures link discourse and text together, is used to build a model of language comprehension that places template structures at the base of a context comparison operation. Subjects were engaged in ordinary conversation with a confederate trained to produce specific types of logical utterances unobtrusively. The comprehension model predicted that systematically different latencies, topical response, and remedial response of subjects would follow the test items produced by the confederate. The data support the predictions. It is shown that comprehension occurs via one processing path if there is a direct tie between the target item and the immediately prior item in discourse, and a separate processing path if the tie is between the target item and the earlier context. Subject response in conversation is shown to display useful evidence on the nature of comprehension achieved. The findings specify and extend the recent research on the integration of new information into a textual structure.     

Hippocampal and extrahippocampal systems compete for control of contextual fear: Role of ventral subiculum and amygdala

Two neural systems, a hippocampal system and an extrahippocampal system compete for control over contextual fear, and the hippocampal system normally dominates. Our experiments reveal that output provided by the ventral subiculum is critical for the hippocampal system to win this competition. Bilateral electrolytic lesions of the ventral subiculum after conditioning, but not before conditioning, impaired contextual fear conditioning. Reversibly inactivating this region by bilateral injections of muscimol produced the same results—no impairment when the injection occurred prior to conditioning but a significant impairment when this region was inactivated after conditioning. Thus, the extrahippocampal system can support contextual fear conditioning if the ventral subiculum is disabled before conditioning but not if it is disabled after conditioning. Our experiments also reveal that the basolateral region of the amygdala (BLA) is where the two systems compete for associative control of the fear system. To test this hypothesis we reasoned that the extrahippocampal system would also acquire associative control over the fear system, even if the hippocampal system were functional, if the basal level of plasticity potential in the BLA could be increased. We did this by injecting the D1 dopamine agonist, {"type":"entrez-protein","attrs":{"text":"SKF82958","term_id":"1156217255","term_text":"SKF82958"}}SKF82958, into the BLA just prior to conditioning. This treatment resulted in a significant increase in freezing when the ventral subiculum was disabled prior to the test. These results are discussed in relationship to the idea that D1 agonists increase plasticity potential by increasing the pool of available extrasynaptic GluR1 receptors in the population of neurons supporting acquired fear.It is generally believed that contextual fear conditioning depends on the hippocampus. However, it is now clear that an extrahippocampal system exists that can also support contextual fear conditioning. The last statement is based on the fact that damage to the hippocampus prior to conditioning has a minor impact on contextual fear (Maren et al. 1997; Frankland et al. 1998; Cho et al. 1999; Wiltgen et al. 2006). In fact, the conclusion that the hippocampus is normally involved in contextual fear conditioning is now based primarily on the finding that damage to the hippocampus after conditioning greatly impairs fear to the context in which conditioning occurs (Maren et al. 1997; Frankland et al. 1998; Anagnostaras et al. 1999; Bannerman et al. 1999; Richmond et al. 1999; Fanselow 2000; Rudy et al. 2004; Wiltgen et al. 2006). Maren et al. (1997) were the first to appreciate the implications of this set of findings. Specifically, they proposed that (1) in the normal animal there is competition between the hippocampal system and an extrahippocampal system for support of contextual fear conditioning, and (2) the hippocampal system normally dominates the extrahippocampal system—preventing it from acquiring the information needed to support fear to the context. This competition hypothesis provides a reasonable account of the lesion data. If the hippocampus is damaged prior to conditioning, then the extrahippocampal system will be able to acquire control over the fear system and generate a fear response at the time of testing. However, if the hippocampal system is functional during conditioning, it will (1) acquire control of the fear system, and (2) prevent the acquisition of control by the extrahippocampal system. Thus, if the hippocampal system is damaged after conditioning, the expression of contextual fear will be impaired, because the information that was acquired by the hippocampal system will not be available and the extrahippocampal system never acquired the relevant information.Maren et al.''s competition hypothesis is accepted by a number of other researchers (Wiltgen and Fanselow 2003; Rudy et al. 2004; Driscoll et al. 2005; Wiltgen et al. 2006). Nevertheless, very little is known about the mediators of this competition. The experiments in this study were aimed at filling some of the gaps in our knowledge of the neural basis of this competition. They are organized around two hypotheses:

• The ability of the hippocampal system to dominate the extrahippocampal system depends on information it provides through the ventral subiculum, a major output region of the hippocampus.
• The locus of the competition is the basolateral region of the amygdala (BLA), which is thought to be critical to the acquisition of conditioned fear and is where information from the hippocampal and extrahippocampal system can converge.

     

Damage to the hippocampal formation in rats selectively impairs the ability to learn cue relationships

We assessed the contribution of the hippocampal formation to performance in tasks that require rats to respond to a relationship between discriminative stimuli. The first experiment employed a nonmatching-to-sample procedure in a Y-maze. Three pairs of boxes were used which differed in brightness of the walls and in the odors that they contained. The rats were trained prior to receiving kainic acid and colchicine-induced damage to the hippocampal formation or electrolytic damage to the amygdala. After surgery all rats performed the nonmatching-to-sample task accurately if both brightness and odor cues were present in the sample and choice boxes or if the boxes contained either visual cues alone or odor cues alone. If the available cue modality was different in sample and choice boxes, then the amygdala-damaged, but not the hippocampal-damaged, rats performed accurately. In the second experiment control rats or rats with hippocampal formation damage were trained postoperatively in a conditional black/white discrimination task in a Y-maze. Only the control group successfully learned to select the white arm if the start box was illuminated and the black arm if the start box was dark. Subsequently, both groups learned a simple black/white discrimination. The same rats were tested in the hidden platform version of the Morris water task and only the control group learned to swim accurately to the goal. Both groups learned to swim accurately to a visible black platform. The results are consistent with the notion that the hippocampal formation is essential to learning that involves control exerted by a configural relationship among cues, independently of the spatial or conditional requirements of tasks.