ObjectivesMany medical schools in Taiwan have adopted a dignified “silent mentor” initiation ceremony to strengthen student’s medical humanity and increase their learning attitudes. This ceremony consists of introductions of the body donor’s conduct and deeds, wreath-laying, and a tea party. However, few empirical studies have examined the influences of the ceremony and dissection on medical humanity. This study explored if the initiation ceremony and the course can help students care more about others, develop more positive attitudes toward death, improve learning effectiveness in the course, and decrease negative emotions the first time they see a cadaver.MethodsThe Attitudes Towards Death and Love and Care subscales of the life attitude inventory, Learning Effectiveness of Gross Anatomy Laboratory Scale (LEGALS), and Emotional Reactions Towards Cadavers Scale were adopted to examine differences before (T1) and after (T2) medical students attended an initiation ceremony at a university in northern Taiwan. Whether these effects lasted to the end of the semester (T3) was also tested.ResultsAfter the ceremony, students’ attitudes towards death increased, negative emotions towards cadavers decreased, but love and care and the LEGALS did not significantly change. Data from T3 showed a similar pattern, but high-level emotions (e.g., being respected, cherished, and grateful) and the LEGALS were significantly higher than those at T1.DiscussionThe initiation ceremony, which showed a body donor’s deeds and attitudes toward life and death when they were alive, could help medical students gain more mature attitudes towards death and decreased negative emotions. Learning between T2 and T3 might have caused significant changes in high-level emotions and the LEGALS at T3. Arranging reflective writing with guided discussion by a teacher before and after the ceremony is highly recommended.

Excessive exposure to club drug (GHB) would cause cognitive dysfunction in which impaired hippocampal Ca2+-mediated neuroplasticity may correlate with this deficiency. However, the potential changes of in vivo Ca2+ together with molecular machinery engaged in GHB-induced cognitive dysfunction has never been reported. This study aims to determine these changes in bio-energetic level through ionic imaging, spectrometric, biochemical, morphological, as well as behavioral approaches. Adolescent rats subjected to GHB were processed for TOF-SIMS, immunohistochemistry, biochemical assay, together with Morris water maze to detect the ionic, molecular, neurochemical, and behavioral changes of GHB-induced cognitive dysfunction, respectively. Extent of oxidative stress and bio-energetics were assessed by levels of lipid peroxidation, Na+/K+ ATPase, cytochrome oxidase, and [14C]-2-deoxyglucose activity. Results indicated that in GHB intoxicated rats, decreased Ca2+ imaging and reduced NMDAR1, nNOS, and p-CREB reactivities were detected in hippocampus. Depressed Ca2+-mediated signaling corresponded well with intense oxidative stress, diminished Na+/K+ ATPase, reduced COX, and decreased 2-DG activity, which all contributes to the development of cognitive deficiency. As impaired Ca2+-mediated signaling and oxidative stress significantly contribute to GHB-induced cognitive dysfunction, delivering agent(s) that improves hippocampal bio-energetics may thus serve as a promising strategy to counteract the club drug-induced cognitive dysfunction emerging in our society nowadays.

The reuniens (Re) and rhomboid (Rh) nuclei (ReRh) of the midline thalamus interconnects the hippocampus (HPC) and the medial prefrontal cortex (mPFC). Several studies have suggested that the ReRh participates in various cognitive tasks. However, little is known about the contribution of the ReRh in Pavlovian trace fear conditioning, a procedure with a temporal gap between the conditioned stimulus (CS) and the unconditioned stimulus (US), and therefore making it harder for the animals to acquire. Because the HPC and mPFC are involved in trace, but not delay, fear conditioning and given the role of the ReRh in mediating this neurocircuitry, we hypothesized that ReRh inactivation leads to a learning deficit only in trace conditioning. In a series of experiments, we first examined the c-Fos expression in male Long-Evans rats and established that the ReRh was recruited in the encoding, but not the retrieval phase, of fear memory. Next, we performed behavioral pharmacology experiments and found that ReRh inactivation impaired only the acquisition, but not the consolidation or retrieval, of trace fear. However, although the ReRh was recruited during the encoding of delay fear demonstrated by c-Fos results, ReRh inactivation in any phases did not interfere with delay conditioning. Finally, we found that trace fear acquired under ReRh inactivation reprised when the ReRh was brought offline during retrieval. Together, our data revealed the essential role of the ReRh in a learning task with temporally discontinuous stimuli.

The present study examined the role of neurons in different pain-related functions of the anterior cingulate cortex (ACC) and primary sensorimotor cortex (SmI) by assessing their abilities to code different levels of noxious heat and activity changes evoked by classical fear conditioning involving electric shocks. Multiple single-unit activity was recorded with microwires implanted in the SmI and ACC of each rat. In the first set of experiments, the middle segment of the tail in each rat was irradiated with laser-heat pulses of various intensities. Neuronal responses in both the SmI and ACC increased with the intensity of the laser heat, although there was a significantly higher percentage of intensity-related units in the SmI. Furthermore, the stimulus-response curve of SmI ensemble activity had a steeper slope than that of the ACC. In the second set of experiments, rats were trained and tested on a conditioned fear-potentiated startle task in which a light was paired with an electric shock and, later, the startle response was elicited by a burst of noise in the presence or absence of light. A higher percentage of ACC units changed their neuronal responses to the conditioned stimulus after the light-shock pairing and the average activity change was also significantly stronger. Our results suggest that SmI neurons are better at coding laser-heat intensity than ACC neurons, whereas more ACC neurons are involved in conditioned fear associated with an electric shock than SmI neurons. These data provide evidence for differential contributions of the SmI and ACC to sensory and affective dimensions of pain.

No abstract