The Effectiveness of an Augmented Reality Head-Mounted Display in Learning Skull Anatomy at a Community College.

Despite an increase in the use of technology in undergraduate anatomy education, and the rising popularity of online anatomy courses at community colleges in the United States, there have been no reports on the efficacy of augmented reality on anatomy education in this population. The purpose of this study was to test the hypothesis that augmented reality is an effective and engaging tool for learning anatomy in community college students. Participants recruited from Cuyahoga Community College (Cleveland, OH) studied skull anatomy using either traditional tools (i.e., textbook and plastic skull model) or an augmented reality head-mounted display with an interactive virtual skull application. Comparison of knowledge before and following the study period revealed that augmented reality was an effective tool for learning skull anatomy: pre-quiz = 32.7% (± 25.2); mean (± SD), post-quiz = 61.8% (± 19.5); n = 15; t(28) = 3.53; P = 0.001. The traditional tools were equally effective: pre-quiz = 44.9 % (± 18.6), post-quiz = 67.9 % (± 17.3); n = 17; t(32) = 3.73; P = 0.0007. Students rated the augmented reality device as 9.6 (± 1.0); mean (± SD) when asked if it fit the statement "fun to use" on a semantic differential scale from 1 (poor) to 10 (excellent). In conclusion, this study found that augmented reality is an effective and engaging tool for the instruction of skull anatomy at a community college.

Genotypic differences in intruder-evoked immediate early gene activation in male, but not female, vasopressin 1b receptor knockout mice.

BACKGROUND: The neuropeptide arginine vasopressin (Avp) modulates social behaviors via its two centrally expressed receptors, the Avp 1a receptor and the Avp 1b receptor (Avpr1b). Recent work suggests that, at least in mice, Avp signaling through Avpr1b within the CA2 region of the hippocampus is critical for normal aggressive behaviors and social recognition memory. However, this brain area is just one part of a larger neural circuit that is likely to be impacted in Avpr1b knockout (-/-) mice. To identify other brain areas that are affected by altered Avpr1b signaling, genotypic differences in immediate early gene activation, i.e. c-FOS and early growth response factor 1 (EGR-1), were quantified using immunocytochemistry following a single exposure to an intruder. RESULTS: In females, no genotypic differences in intruder-evoked c-FOS or EGR-1 immunoreactivity were observed in any of the brain areas measured. In males, while there were no intruder-evoked genotypic differences in c-FOS immunoreactivity, genotypic differences were observed in EGR-1 immunoreactivity within the ventral bed nucleus of the stria terminalis and the anterior hypothalamus; with Avpr1b -/- males having less EGR-1 immunoreactivity in these regions than controls. CONCLUSIONS: These data are the first to identify specific brain areas that may be a part of a neural circuit that includes Avpr1b-expressing cells in the CA2 region of the hippocampus. It is thought that this circuit, when working properly, plays a role in how an animal evaluates its social context.

Fibroblast growth factor 8 regulates postnatal development of paraventricular nucleus neuroendocrine cells.

BACKGROUND: Fibroblast growth factors (FGFs) are crucial signaling molecules that direct the development of the vertebrate brain. FGF8 gene signaling in particular, may be important for the development of the hypothalamus-pituitary-adrenal (HPA)-axis. Indeed, newborn Fgf8 hypomorphic mice harbor a major reduction in the number of vasopressin (VP) neurons in the paraventricular nucleus (PVN), the central output component of the HPA-axis. Additionally, recent studies indicated that adult heterozygous ((+/neo)) Fgf8 hypomorphic mice exhibit more anxiety-like behaviors than wildtype (WT) mice. These studies led us to investigate whether Fgf8 hypomorphy abrogated VP and/or corticotropin-releasing hormone (CRH) neuronal development in the postnatal day (PN) 21 and adult mouse PVN. Furthermore, we studied whether Fgf8 hypomorphy disrupted HPA responsiveness in these mice. METHODS: Using immunohistochemistry, we examined the development of VP and CRH neurons located in the PVN of PN 21 and adult Fgf8 (+/neo) mice. Moreover, we used a restraint stress (RS) paradigm and measured corticosterone levels with enzyme immunoassays in order to assess HPA axis activation. RESULTS: The number of VP neurons in the PVN did not differ between WT and Fgf8 (+/neo) mice on PN 21 and in adulthood. In contrast, CRH immunoreactivity was much higher in Fgf8 (+/neo) mice than in WT mice on PN 21, this difference was no longer shown in adult mice. RS caused a higher increase in corticosterone levels in adult Fgf8 (+/neo) mice than in WT mice after 15 min, but no difference was seen after 45 min. CONCLUSIONS: First, Fgf8 hypomorphy did not eliminate VP and CRH neurons in the mouse PVN, but rather disrupted the postnatal timing of neuropeptide expression onset in PVN neurons. Second, Fgf8 hypomorphy may, in part, be an explanation for affective disorders involving hyperactivity of the HPA axis, such as anxiety.

Lesions to the CA2 region of the hippocampus impair social memory in mice.

The function of the CA2 region of the hippocampus is poorly understood. Although the CA1 and CA3 regions have been extensively studied, for years the CA2 region has primarily been viewed as a linking area between the two. However, the CA2 region is known to have distinct neurochemical and structural features that are different from the other parts of the hippocampus and in recent years it has been suggested that the CA2 region may play a role in the formation and/or recall of olfactory-based memories needed for normal social behavior. Although this hypothesis has been supported by hippocampal lesion studies that have included the CA2 region, no studies have attempted to specifically lesion the CA2 region of the hippocampus in mice to determine the effects on social recognition memory and olfaction. To fill this knowledge gap, we sought to perform excitotoxic N-methyl-D-aspartate lesions of the CA2 region and determine the effects on social recognition memory. We predicted that lesions of the CA2 region would impair social recognition memory. We then went on to test olfaction in CA2-lesioned mice, as social memory requires a functional olfactory system. Consistent with our prediction, we found that CA2-lesioned animals had impaired social recognition. These findings are significant because they confirmed that the CA2 region of the hippocampus is a part of the neural circuitry that regulates social recognition memory, which may have implications for our understanding of the neural regulation of social behavior across species.

Ontogenesis of gonadotropin-releasing hormone neurons: a model for hypothalamic neuroendocrine cell development.

The vertebrate hypothalamo-pituitary-gonadal axis is the anatomical framework responsible for reproductive competence and species propagation. Essential to the coordinated actions of this three-tiered biological system is the fact that the regulatory inputs ultimately converge on the gonadotropin-releasing hormone (GnRH) neuronal system, which in rodents primarily resides in the preoptic/hypothalamic region. In this short review we will focus on: (1) the general embryonic temporal and spatial development of the rodent GnRH neuronal system, (2) the origin(s) of GnRH neurons, and (3) which transcription - and growth factors have been found to be critical for GnRH neuronal ontogenesis and cellular fate-specification. Moreover, we ask the question whether the molecular and cellular mechanisms involved in GnRH neuronal development may also play a role in the development of other hypophyseal secreting neuroendocrine cells in the hypothalamus.

The vasopressin 1b receptor and the neural regulation of social behavior.

To date, much of the work in rodents implicating vasopressin (Avp) in the regulation of social behavior has focused on its action via the Avp 1a receptor (Avpr1a). However, there is mounting evidence that the Avp 1b receptor (Avpr1b) also plays a significant role in Avp's modulation of social behavior. The Avpr1b is heavily expressed on the anterior pituitary cortiocotrophs where it acts as an important modulator of the endocrine stress response. In the brain, the Avpr1b is prominent in the CA2 region of the hippocampus, but can also be found in areas such as the paraventricular nucleus of the hypothalamus and the olfactory bulb. Studies that have employed genetic knockouts or pharmacological manipulation of the Avpr1b point to the importance of central Avpr1b in the modulation of social behavior. However, there continues to be a knowledge gap in our understanding of where in the brain this is occurring, as well as how and if the central actions of Avp acting via the Avpr1b interact with the stress axis. In this review we focus on the genetic and pharmacological studies that have implicated the Avpr1b in the neural regulation of social behaviors, including social forms of aggressive behavior, social memory, and social motivation. This article is part of a Special Issue entitled Oxytocin, Vasopressin, and Social Behavior.

Social dominance in male vasopressin 1b receptor knockout mice.

We have previously reported that mice with a targeted disruption of their vasopressin 1b receptor gene, Avpr1b, have mild impairments in social recognition and reduced aggression. The reductions in aggression are limited to social forms of aggression, i.e., maternal and inter-male aggression, while predatory aggression remains unaffected. To further clarify the role of the Avpr1b in the regulation of social behavior we first examined anxiety-like and depression-like behaviors in Avpr1b knockout (Avpr1b -/-) mice. We then went on to test the ability of Avpr1b -/- mice to form dominance hierarchies. No major differences were found between Avpr1b -/- and wildtype mice in anxiety-like behaviors, as measured using an elevated plus maze and an open field test, or depression-like behaviors, as measured using a forced swim test. In the social dominance study we found that Avpr1b -/- mice are able to form dominance hierarchies, though in early hierarchy formation dominant Avpr1b -/- mice display significantly more mounting behavior on Day 1 of testing compared to wildtype controls. Further, non-socially dominant Avpr1b -/- mice spend less time engaged in attack behavior than wildtype controls. These findings suggest that while Avpr1b -/- mice may be able to form dominance hierarchies they appear to employ alternate strategies.