Children's fears have been the focus of a great deal of research over the past 10-15 years. Studies have centered on the developmental nature and frequency of children's fears, delineating the essential components of certain fears, as well as evaluating the efficacy of various treatment procedures. The present study examined the effects of three behavioral techniques on children's fear of the dark. Nine children who demonstrated a clinical fear of the dark were seen at a university clinic for two, one-half hour sessions each week over a seven week period, with follow-up assessment occurring one and two months after treatment. The three treatments employed were: symbolic modeling, self-instructional training and contact desensitization. A multiple baseline design across subjects was utilized, with dependent measures consisting of the motoric, cognitive, and physiological components of each child's fear and parent data were collected. Significant changes in dark tolerance between baseline and treatment were most consistently observed in those children receiving the symbolic modeling procedure. The next condition yielding the most consistent changes in duration between baseline and treatment was the contact desensitization treatment. No appreciable changes were found in the children in the self-instructional condition. The self-report and heart rate measures failed to demonstrate strong, reliable changes for any subject in the study except for one subject whose heart rate significantly increased after intervention. Examination of parent data yielded inconsistent results across conditions, thereby limiting any conclusions regarding generalization. The results were discussed in relation to the literature on fear reduction techniques. Limitations of the present study were discussed and topics for future research were delineated.

Corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) are major physiological stimulators of adrenocorticotropin (ACTH) secretion from the pituitary gland, while glucocorticoids act as inhibitors. In addition to acting alone, CRH, AVP and glucocorticoids interact with each other to regulate ACTH release in response to stress. Prolonged or repeated stimulus results in attenuated ACTH responsiveness, a process termed as desensitization. The aim of this study was to investigate the effects of interactions between CRH, AVP and steroids on desensitization of the ACTH response to AVP. Perifused ovine anterior pituitary cells were stimulated with three 5-min pulses of 100 nM AVP at 120, 200 and 280 min, and were continuously exposed to CRH (0.2 nM) from 80 min and/or cortisol (10-500 nM) from 0 min onwards. Desensitization was induced by a 15 min pre-treatment with 5 nM (0.5 nM for CRH alone) AVP immediately preceding the second AVP pulse. When CRH was absent, pre-treatment with 0.5 nM AVP did not influence the ACTH response to the second AVP pulse. In the presence of CRH, the response to the second AVP pulse was reduced to 66.7±2.2% of control (n=6, P<0.0001, t-test). On the other hand, following 5 nM AVP pre-treatment, continuous perifusion with cortisol (100 nM) results in a significantly smaller reduction in the response to the second AVP pulse compared with that seen in its absence (78.4±1.7% c.f. 66.7±1.9% of control; n=10, P<0.001, t-test). In contrast to this, following 5 nM AVP pre-treatment, continuous CRH and cortisol in combination results in a greater reduction in the response to the second AVP pulse compared with that obtained in the absence of these two hormones (46.5±1.7% c.f. 66.2±1.7 of control; n=8, P<0.0001, t-test). Taken together, these data suggest that desensitization of the ACTH response to AVP can be modulated by CRH and/or cortisol: CRH or CRH and cortisol in combination amplify this desensitization, whereas cortisol reduces it.

The problem with which this investigation was concerned was that of determining the effectiveness of massed group desensitization in the reduction of anxiety. Thirty test-anxious nursing students who scored in the upper quartile on the Test Anxiety Questionnaire (TAQ) served as the subjects. The subjects were assigned by the use of a randomized block procedure to one of the following three groups matched on the basis of their pre-test TAQ scores: (1) desensitization, (2) placebo, and (3) control.

Corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) are major physiological stimulators of adrenocorticotropin (ACTH) secretion from the pituitary gland, while glucocorticoids act as inhibitors. In addition to acting alone, CRH, AVP and glucocorticoids interact with each other to regulate ACTH release in response to stress. Prolonged or repeated stimulus results in attenuated ACTH responsiveness, a process termed as desensitization. The aim of this study was to investigate the effects of interactions between CRH, AVP and steroids on desensitization of the ACTH response to AVP. Perifused ovine anterior pituitary cells were stimulated with three 5-min pulses of 100 nM AVP at 120, 200 and 280 min, and were continuously exposed to CRH (0.2 nM) from 80 min and/or cortisol (10-500 nM) from 0 min onwards. Desensitization was induced by a 15 min pre-treatment with 5 nM (0.5 nM for CRH alone) AVP immediately preceding the second AVP pulse. When CRH was absent, pre-treatment with 0.5 nM AVP did not influence the ACTH response to the second AVP pulse. In the presence of CRH, the response to the second AVP pulse was reduced to 66.7±2.2% of control (n=6, P<0.0001, t-test). On the other hand, following 5 nM AVP pre-treatment, continuous perifusion with cortisol (100 nM) results in a significantly smaller reduction in the response to the second AVP pulse compared with that seen in its absence (78.4±1.7% c.f. 66.7±1.9% of control; n=10, P<0.001, t-test). In contrast to this, following 5 nM AVP pre-treatment, continuous CRH and cortisol in combination results in a greater reduction in the response to the second AVP pulse compared with that obtained in the absence of these two hormones (46.5±1.7% c.f. 66.2±1.7 of control; n=8, P<0.0001, t-test). Taken together, these data suggest that desensitization of the ACTH response to AVP can be modulated by CRH and/or cortisol: CRH or CRH and cortisol in combination amplify this desensitization, whereas cortisol reduces it.

No description available.

Developmental nicotine exposure (DNE) is associated with increased risk of cardiorespiratory, intellectual, and behavioral abnormalities in neonates, and is a risk factor for apnea of prematurity, altered arousal responses and Sudden Infant Death Syndrome. Alterations in nicotinic acetylcholine receptor signaling (nAChRs) after DNE lead to changes in excitatory neurotransmission in neural networks that control breathing, including a heightened excitatory response to AMPA microinjection into the hypoglossal motor nucleus. Here, we report on experiments designed to probe possible postsynaptic and presynaptic mechanisms that may underlie this plasticity. Pregnant dams were exposed to nicotine or saline via an osmotic mini-pump implanted on the 5th day of gestation. We used whole-cell patch clamp electrophysiology to record from hypoglossal motoneurons (XIIMNs) in thick medullary slices from neonatal rat pups (N = 26 control and 24 DNE cells). To enable the translation of our findings to breathing-related consequences of DNE, we only studied XIIMNs that were receiving rhythmic excitatory drive from the respiratory central pattern generator. Tetrodotoxin was used to isolate XIIMNs from presynaptic input, and their postsynaptic responses to bath application of L-glutamic acid (glutamate) and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) were studied under voltage clamp. DNE had no influence on inward current magnitude evoked by either glutamate or AMPA. However, in cells from DNE animals, bath application of AMPA was associated with a right shift in the amplitude distribution (P = 0.0004), but no change in the inter-event interval distribution of miniature excitatory postsynaptic currents (mEPSCs). DNE had no influence on mEPSC amplitude or frequency evoked by glutamate application, or under (unstimulated) baseline conditions. Thus, in the presence of AMPA, DNE is associated with a small but significant increase in quantal size, but no change in the probability of glutamate release.

Since fear of public speaking has been considered a good example of anxiety and an example that is correlated with behavioral and cognitive measures of anxiety levels, a study of Rogerian therapy, desensitization, and modeling techniques in reducing this anxiety seemed appropriate.

The present study was concerned with comparing the relative effectiveness of behavior rehearsal and systematic desensitization in the treatment of social anxiety.

No description available.

Treatise (D.M.A.) -- Florida State University, 2004. / Advisor: Douglas Fisher, Florida State University, School of Music. Title and description from treatise home page (viewed 9-29-04). Document formatted into pages; contains 73 pages. Includes biographical sketch. Includes bibliographical references.