Examining antecedents of caregivers' access to early childhood developmental screening: implications for campaigns promoting use of services in Appalachian Ohio.

Although developmental delays are common in the United States, only about one third of developmental delays are identified before a child enters school. As challenging as use of developmental screening is on a national basis, the Appalachian region faces extreme lack of screening, diagnosis, and treatment for developmental delay. Local health care providers attribute this lack to poor parent understanding and have called for communication interventions to educate caregivers. This investigation sought to understand the antecedents of Appalachian caregivers' intentions to access developmental screening and services for their children as formative research for a communication-based intervention. The investigation was grounded by the health belief model. Surveys completed by 366 caregivers were used to model antecedents to behavioral intention. Perceived severity, perceived benefits, and self-efficacy were found to be the strongest predictors of intention to access developmental screening. Implications for a communication-based intervention are provided.

Cotreatment with the kappa opioid agonist U69593 enhances locomotor sensitization to the D2/D3 dopamine agonist quinpirole and alters dopamine D2 receptor and prodynorphin mRNA expression in rats.

RATIONALE: The repeated coadministration of the kappa opioid receptor agonist U69593 with the D2/D3 dopamine (DA) agonist quinpirole (QNP) potentiates locomotor sensitization induced by QNP. Behavioral evidence has implicated both pre- and postsynaptic changes as being involved in this augmentation. OBJECTIVES: The objectives of this study were to obtain supporting molecular evidence of pre- and/or postsynaptic alterations in the DA system with U69593/QNP cotreatment and to examine the relationship of such changes to locomotor sensitization. MATERIALS AND METHODS: Gene expression of D1 and D2 receptors (D1R and D2R), the DA transporter, as well as the endogenous opioid prodynorphin (DYN), in the basal ganglia was examined by in situ hybridization in rats after one or ten drug injections. RESULTS: After one injection, changes that were specific to U69593/QNP cotreatment were decreased D1R and D2R messenger RNA (mRNA) in the nucleus accumbens (Acb) shell and increased DYN mRNA in the dorsal striatum (STR). After ten injections, U69593/QNP-specific changes were decreased D2R mRNA in substantia nigra (SN) and increased DYN mRNA in STR and Acb core. Only in U69593/QNP rats was the sensitized locomotor performance on injection ten positively correlated with DYN mRNA levels in Acb and STR. CONCLUSIONS: Distinct alterations of D2R and DYN mRNA levels in SN and Acb/STR, respectively, strengthen the evidence implicating pre- and postsynaptic changes in augmented locomotor sensitization to U69593/QNP cotreatment. It is suggested that repeated U69593/QNP cotreatment may augment locomotor sensitization to QNP by activating D1R-expressing DYN neurons and attenuating presynaptic D2R function.

Kappa-opioid agonist U69593 potentiates locomotor sensitization to the D2/D3 agonist quinpirole: pre- and postsynaptic mechanisms.

To assess whether the development and expression of behavioral sensitization to the dopamine D2/D3 agonist quinpirole (QNP) is influenced by coadministration of the kappa opioid receptor agonist U69593, rats received every 3-4 days for a total of 10 treatments an injection of U69593 (0.3 mg/kg) together with an injection of either a postsynaptic (0.5 mg/kg) or a presynaptic dose of QNP (0.05 mg/kg); locomotor activity was measured after each treatment. Control rats were injected as appropriate with QNP, U69593, and vehicle/saline. Following chronic treatment, dose-response profiles to QNP were obtained to assess the expression of sensitization; the effect of U69593 on locomotor activity in animals already sensitized to QNP was also assessed. Results showed that cotreatment of U69593 with a postsynaptic dose of QNP doubled the speed and magnitude of sensitization to QNP, while U69593 cotreatment with a presynaptic dose of QNP switched the effects of QNP from locomotor depression to locomotor sensitization. However, U69593 cotreatment with a presynaptic dose of QNP changed a different set of measures of sensitization than did cotreatment with a postsynaptic dose of the dopamine agonist. Together, findings suggest that sensitization to QNP is not a unitary phenomenon but has components that are relatively independent, mediated by distinct pre- and postsynaptic mechanisms and modulated by kappa receptor activity.

Immunological and physiological effects of chronic exposure of Peromyscus leucopus to Aroclor 1254 at a concentration similar to that found at contaminated sites.

Polychlorinated biphenyls (PCBs) are environmental contaminants known to cause adverse health effects to biological systems. Limited data are available on their effects on the immune system of wildlife species. Previously, we found that 4 and 6-week-old white-footed mice (Peromyscus leucopus) born from dams injected with a single dose (300 mg/kg) of Aroclor 1254, had altered immunological, hematological, and biochemical responses. Here, we examined the effect of transplacental, lactational and postnatal exposure to Aroclor 1254, at a concentration similar to that found at contaminated sites, on various physiological parameters of 22-week-old white-footed mice. Liver weight and liver somatic index of PCB treated animals were significantly higher, the combined weights of the adrenal glands were significantly lower and EROD and BROD enzyme activity was significantly higher compared to control values. The number of thymocytes of the treated mice was significantly lower than that of the controls; however, thymocytes of treated mice had a higher proliferative response to the mitogen Con A. These alterations were correlated with the PCBs body burdens. Some toxic effects of chronic exposure to PCBs, at levels comparable to exposure found in contaminated sites in the USA, are still evident in adult P. leucopus.

Effects of the serotonergic agonist mCPP on male rats in the quinpirole sensitization model of obsessive-compulsive disorder (OCD).

RATIONALE: The serotonergic agonist, meta-chlorophenylpiperazine (mCPP), produces inconsistent effects on obsessive-compulsive disorder (OCD) symptoms, perhaps because clinical studies have not utilized a homogenous OCD subgroup of patients. OBJECTIVES: This study aimed to evaluate mCPP effects on functional components of compulsive checking, using the quinpirole sensitization rat model of OCD. METHODS: In study 1, the effects of mCPP were evaluated in quinpirole rats with compulsive checking. Two experimental groups were co-injected with quinpirole (0.125 mg/kg) and mCPP (0.625 or 1.25 mg/kg), while one control group was co-injected with quinpirole (0.125 mg/kg) and saline and the other control group received co-injections of saline. In study 2, mCPP (0, 0.3125, 0.625, and 1.25 mg/kg) was administered repeatedly to naïve rats and induction of compulsive checking evaluated. RESULTS: mCPP significantly attenuated quinpirole-induced compulsive checking behavior by reducing vigor of checking (indexed by frequency of checking and length of check) and increasing rest after a bout of checking (indexed by time to the next checking bout), but it did not affect focus on the task of checking (indexed by recurrence time of checking and number of stops before returning to check). In naïve rats, mCPP did not induce compulsive behavior, but the highest dose reduced vigor of checking performance compared to saline controls. CONCLUSIONS: mCPP did not exacerbate or induce compulsive checking behavior. Instead, it ameliorated compulsive checking by reducing vigor of checking and increasing post-checking satiety, without affecting focus on checking. Ameliorative effects of mCPP may involve 5HT2A/2C receptors in substantia nigra pars reticulata that inhibit expression of motor vigor.