This study tested a predictive and mediation model of teacher commitment. Teacher efficacy and sense of identification with school were hypothesized to mediate the relations of an individual antecedent (teaching experience) and two organizational antecedents (perceived organizational politics and reflective dialogue) to teacher commitment. Multigroup structural equation modeling was used to test and validate the mediation model across two independent samples of teachers. Perceived organizational politics was found to be negatively related to teacher commitment, whereas reflective dialogue and teaching experience were positively related. Teacher efficacy and identification with school were found to completely mediate the relations between the three antecedents and teacher commitment.

No abstract

Our findings highlighted that white matter abnormalities were present by the time of remission of first-episode mania. The widespread occurrence of these white matter abnormalities both in first-episode mania and chronic bipolar disorder suggested that disruption of white matter cortical-subcortical networks as well as projection, associative, and commissural tracts is a hallmark of the illness.

These findings are consistent with known ARVCF gene effects on neurodevelopment in terms of cellular arrangement, migration, and intracellular signaling involving the striatum and may involve interactions with other brain networks such as prefrontal cortex, and they underscore the importance of imaging-genetic studies to elucidate the genetic influences underlying intermediate phenotypes in complex neurobehavioral disorders.

The hypocretins (Hcrts, also known as orexins) are two peptides, both synthesized by a small group of neurons, most of which are in the lateral hypothalamic and perifornical regions of the hypothalamus. The hypothalamic Hcrt system directly and strongly innervates and potently excites noradrenergic, dopaminergic, serotonergic, histaminergic, and cholinergic neurons. Hcrt also has a major role in modulating the release of glutamate and other amino acid transmitters. Behavioral investigations have revealed that Hcrt neurons are maximally active in active waking. In rats, hypocretin neuronal activity is maximal during exploration and minimal during quiet waking and sleep. Degeneration of Hcrt neurons or genetic mutations that prevent the normal synthesis of Hcrt or of its receptors causes human and animal narcolepsy. Administration of Hcrt can reverse symptoms of narcolepsy in animals, may be effective in treating human narcolepsy, and may affect a broad range of motivated behaviors.The lateral hypothalamus (LH) has been implicated in wakefulness. One possibility is that it induces wakefulness by driving the basal forebrain (BF) wake-active neurons (Gerashchenko and Shiromani 2004). The activity of the BF wake-active neurons is hypothesized to release the sleep-inducing factor adenosine (AD), which begins to accumulate as wakefulness progresses. The AD is then hypothesized to inhibit the wake-active neurons (Strecker et al. 2000) and their silence allows the VLPO and median preoptic GABAergic sleep-active neurons to fire and sleep ensues. Here we measure AD levels in the BF and test the LH-BF circuit in Sprague-Dawley rats with lesions of the LH induced by hypocretin-2-saporin. 64 days after lesions the rats were implanted with sleep-recording electrodes and a guide cannula into the basal forebrain. Two weeks later, the rats were kept awake (gentle handling) for six hours (ZT 3-9) and microdialysis samples (5 mL) were collected hourly for 9 h (24 h after probe stabilization). AD levels were assessed using HPLC (see Murillo-Rodriguez et al. 2004 for details).Hypocretin-saporin ablated 95% of the hypocretin neurons with a resultant decline in CSF levels (-75% vs. control). AD levels increased with 6 h waking in saline control rats (n = 9), consistent with previous studies in cats (Strecker et al. 2000) and rats (Murillo-Rodriguez et al. 2004). However, in rats with LH lesions (n = 5) such an increase with waking did not occur. The homeostatic response to sleep loss was measured by conducting a rodent version of an MSLT where the rats were kept awake for 20 min and then allowed 20 min to sleep. This protocol was started at ZT2 and continued until lights were turned off. The lesioned rats were found to have more sleep during the 20 min sleep periods indicating a higher sleep drive in these rats.Previously, we (Gerashchenko et al. 2001) found that rats with LH lesions had increased sleep during the night, and here we found that they have increased sleep drive as measured by an MSLT. The increased sleep drive in thes...

No abstract