Sources of stress in a pharmacy student population.

OBJECTIVE: To assess the sources of stress for pharmacy students and relationships to demographic factors and perceived stress. METHODS: Survey study of students at three pharmacy schools investigating student stress using the Perceived Stress Scale (PSS10), a two-tiered sources of stress questionnaire and demographic information. RESULTS: Student perceived stress levels were significantly higher than standard populations, but consistent with other pharmacy student populations. The strongest predictor of perceived stress was when students anticipated lower stress levels than actually experienced, followed by pressure to succeed. Additional variables were self-reported grade point average (GPA) and stress from relationships and experiential rotations. For first year (P1) students, having less than a bachelor's degree significantly influenced perceived stress. For the entire sample, male gender and health-related stress were significant. Academic performance (81%) and pressure to succeed (77%) were the most frequently reported general sources of stress. School B students were significantly less likely to report stress about postgraduate opportunities, career choices, and health issues. Students at school C were significantly less likely to report stress about academic issues. CONCLUSIONS: Pharmacy students' perceived stress is associated with their expectations, several general stressor categories, and demographic characteristics. Sources of stress appear to differ between pharmacy programs. Programs could examine their policies to see if there were more effective and timely means to address student stress. By better understanding the specific reasons for stress, we may be better able to mitigate its negative effects.

Ameliorating effects of preadolescent aniracetam treatment on prenatal ethanol-induced impairment in AMPA receptor activity.

Ethanol-induced damage in the developing hippocampus may result in cognitive deficits such as those observed in fetal alcohol spectrum disorder (FASD). Cognitive deficits in FASD are partially mediated by alterations in glutamatergic synaptic transmission. Recently, we reported that synaptic transmission mediated by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) is impaired following fetal ethanol exposure. This finding led us to develop a rational approach for the treatment of alcohol-related cognitive deficits using aniracetam, an allosteric AMPAR modulator. In the present study, 28 to 34-day-old rats exposed to ethanol in utero were treated with aniracetam, and subsequently exhibited persistent improvement in mEPSC amplitude, frequency, and decay time. Furthermore, these animals expressed positive changes in synaptic single channel properties, suggesting that aniracetam ameliorates prenatal ethanol-induced deficits through modifications at the single channel level. Specifically, single channel open probability, conductance, mean open and closed times, and the number and burst duration were positively affected. Our findings emphasize the utility of compounds which slow the rate of deactivation and desensitization of AMPARs such as aniracetam.

Aniracetam reversed learning and memory deficits following prenatal ethanol exposure by modulating functions of synaptic AMPA receptors.

Specific pharmacological treatments are currently not available to address problems resulting from fetal ethanol exposure, described as Fetal Alcohol Syndrome or Fetal Alcohol Spectrum Disorders (FASD). The present study evaluated the therapeutic effects of aniracetam against cognitive deficits in a well-characterized and sensitive FASD Sprague-Dawley rat model. Ethanol, administered orally at a moderate dose (4 g/kg/24 h; 38% v/v) during the entire course of pregnancy, caused severe cognitive deficits in offspring. Furthermore, both progeny genders were affected by a spectrum of behavioral abnormalities, such as a delay in the development of the righting reflex, poor novelty seeking behavior, and high anxiety levels in female rats. Cognitive disabilities, monitored in adult rats by a two-way active avoidance task, correlated well with a significant reduction of AMPA (alpha-amino-3 hydro-5 methyl-isoxazole propionic acid) receptor-mediated miniature excitatory postsynaptic responses (mEPSCs) in the hippocampus. Administration of aniracetam for 10 days (post-natal days (PND) 18-27), at a dose of 50 mg/kg reversed cognitive deficits in both rat genders, indicated by a significant increase in the number of avoidances and the number of 'good learners'. After the termination of the nootropic treatment, a significant increase in both amplitude and frequency of AMPA receptor-mediated mEPSCs in hippocampal CA-1 pyramidal cells was observed. Significant anxiolytic effects on PND 40 also preceded acquisition improvements in the avoidance task. This study provides evidence for the therapeutic potential of aniracetam in reversing cognitive deficits associated with FASD through positive post-natal modulation of AMPA receptors.

Postnatal aniracetam treatment improves prenatal ethanol induced attenuation of AMPA receptor-mediated synaptic transmission.

Aniracetam is a nootropic compound and an allosteric modulator of AMPA receptors (AMPARs) which mediate synaptic mechanisms of learning and memory. Here we analyzed impairments in AMPAR-mediated synaptic transmission caused by moderate prenatal ethanol exposure and investigated the effects of postnatal aniracetam treatment on these abnormalities. Pregnant Sprague-Dawley rats were gavaged with ethanol or isocaloric sucrose throughout pregnancy, and subsequently the offspring were treated with aniracetam on postnatal days (PND) 18 to 27. Hippocampal slices prepared from these pups on PND 28 to 34 were used for the whole-cell patch-clamp recordings of AMPAR-mediated spontaneous and miniature excitatory postsynaptic currents in CA1 pyramidal cells. Our results indicate that moderate ethanol exposure during pregnancy results in impaired hippocampal AMPAR-mediated neurotransmission, and critically timed aniracetam treatment can abrogate this deficiency. These results highlight the possibility that aniracetam treatment can restore synaptic transmission and ameliorate cognitive deficits associated with the fetal alcohol syndrome.

An assessment of the long-term developmental and behavioral teratogenicity of prenatal nicotine exposure.

Maternal tobacco use during pregnancy adversely affects prenatal and postnatal growth and increases the risk of developmental and behavioral deficits in children and adolescents. In the present study, the effects of prenatal nicotine exposure (infused at 6mg/kg/day) and maternal withdraw during neonatal development, was examined in Sprague-Dawley rats on an array of behavioral tasks during different stages of ontogenesis. Offspring of both genders were monitored for exploratory, locomotor, and novelty-seeking activity, anxiety, and learning and memory in an active-avoidance task. Nicotine-exposed animals showed growth retardation, hyperactivity, and poor adaptation in a new environment, increased level of anxiety during the early adolescent period, and robust cognitive deficits in early adulthood. In addition, the deficits were generally more severe in the female nicotine-exposed offspring. Cross-fostering also revealed that while maternal behavior and nicotine withdraw did not affect postnatal somatic growth retardation or cognitive ability of the offspring; measures of exploration and adaptation in a new environment were impacted during the post-weanling and early adolescence period. Nicotine-exposed offspring, and the saline-treated offspring cross-fostered to nicotine-exposed mothers, showed higher measures of anxiety in the elevated plus-maze and decreased novelty-seeking behavior on the hole-board apparatus. These studies demonstrated that prenatal nicotine exposure produced significant long-term developmental and behavioral teratogenic effects. The study design provides a model system for studying the mechanism(s) responsible for the decline in central nervous system function following prenatal nicotine exposure, as well as that of other neurological and behavioral teratogens during pregnancy.

Nicotinic receptor expression following nicotine exposure via maternal milk.

Studies have shown nicotine is excreted into maternal milk, so that suckling offspring would be a target of the drug during the pre-weaning period. Since nicotine exposure leads to an upregulation of neuronal nicotinic receptors, this study examines the hypothesis that nicotine delivered via maternal milk is capable of altering neuronal nicotinic receptor regulation in the drug-exposed rat pups. The present study showed that postnatal nicotine exposure via maternal milk was sufficient to induce an upregulation in brain nicotinic receptors similar to that seen in adults that smoke. Such exposure may result in altered neuronal development and synaptic activity and structure, potentially leading to long-term behavioral, learning, and memory deficits.