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Although high rates of injury occur in youth ice hockey, disagreements exist about the risks and benefits of permitting bodychecking. We sought to evaluate associations between experience with bodychecking and rates of injury and concussion among ice hockey players aged 15-17 years.We obtained data from a prospective cohort study of ice hockey players aged 15-17 years in Alberta who played in leagues that permitted bodychecking. We collected data over 3 seasons of play (2015/16-2017/18). We compared players based on experience with bodychecking (≤ 2 v. ≥ 3 yr), estimated using local and national bodychecking policy and region of play. We used validated methodology of ice hockey injury surveillance to identify all injuries related to ice hockey games and defined concussions according to the Consensus Statement on Concussion in Sport.We included 941 players who contributed to 1168 player-seasons, with 205 players participating in more than 1 season. Compared with players with 2 years or less of bodychecking experience, those with 3 or more years of experience had higher rates of all injury (adjusted incidence rate ratio [IRR] 2.55, 95% confidence interval [CI] 1.57-4.14), injury with more than 7 days of time loss (adjusted IRR 2.65, 95% CI 1.50-4.68) and concussion (adjusted IRR 2.69, 95% CI 1.34-5.42).Among ice hockey players aged 15-17 years who participated in leagues permitting bodychecking, more experience with bodychecking did not protect against injury. This provides further support for removing bodychecking from youth ice hockey.

The Award Committee for the Society for the History of Psychology is happy to announce the following Division 26 award winners for 2022

Increasing rates of sport-related concussion (SRC) in youth impose a significant burden on public health systems and the lives of young athletes. Accurate prediction for those likely to develop persistent post-concussion symptomology (PPCS) using a fluid biomarker, reflecting both acute injury and recovery processes, would provide the opportunity for early intervention. Cortisol, a stress hormone released through the hypothalamic-pituitary-adrenal (HPA) axis following injury, may provide a missing physiological link to clinical recovery. This cohort study investigated the change in saliva cortisol following SRC and the association between cortisol and symptom burden in pediatric ice hockey players. Further, the association between cortisol levels and medical clearance to return to play was explored. In total, cortisol samples from 233 players were included; 165 athletes (23.6% female) provided pre-injury saliva and 68 athletes (19.1% female) provided post-SRC saliva samples for cortisol analysis. Quantile (median) regressions were used to compare cortisol between pre-injury and post-SRC groups, and the association between total symptoms (/22) and symptom severity scores (/132) reported on the Sport Concussion Assessment Tool (SCAT)3/SCAT5 and post-SRC cortisol (adjusting for age, sex, history of concussion, and time from injury to sample collection). Results demonstrated significantly lower saliva cortisol in post-SRC athletes compared with the pre-injury group (β = -0.62, 95% confidence interval [CI; -1.08, -0.16]

ObjectivesTo compare rates of injury and concussion among U-15 (ages 13–14 years) ice hockey players playing in leagues allowing body checking, but who have a varying number of years of body checking experience.MethodsThis 5-year longitudinal cohort included U-15 ice hockey players playing in leagues where policy allowed body checking. Years of body checking experience were classified based on national/local body checking policy. All ice hockey game-related injuries were identified using a validated injury surveillance methodology. Players with a suspected concussion were referred to a study sport medicine physician. Multiple multilevel Poisson regression analysis was performed, adjusting for important covariates and a random effect at a team level (offset by game exposure hours), to estimate injury and concussion incidence rate ratios (IRRs).ResultsIn total, 1647 players participated, contributing 1842 player-seasons (195 players participating in two seasons). Relative to no body checking experience, no significant differences were found in the adjusted IRRs for game-related injury for players with 1 year (IRR=1.06; 95% CI: 0.77 to 1.45) or 2+ years (IRR=1.16; 95% CI: 0.74 to 1.84) body checking experience. Similarly, no differences were found in the rates of concussion for players with 1 year (IRR=0.92; 95% CI: 0.59 to 1.42) or 2+ years (IRR=0.69; 95% CI: 0.38 to 1.25) body checking experience.ConclusionsAmong ice hockey players aged 13–14 years participating in leagues permitting body checking, the adjusted rates of all injury and concussion were not significantly different between those that had body checking experience and those that did not. Based on these findings, no association was found between body checking experience and rates of injury or concussion specifically in adolescent ice hockey.

Cheiron's Book Prize Committee is pleased to announce that the recipient of the 2022 Prize is Nadine Weidman, Lecturer on the History of Science at Harvard University, for her book Killer Instinct: The Popular Science of Human Nature in Twentieth-Century America. In other news from the Society for the History of Psychology, Marjorie Lorch has recently published an article on how the concept of a matched control group was initially developed in neuropsychological testing. Lorch, M. P. (2022). Defining 'normal': Methodological issues in Aphasia and intelligence research. Cortex, 153, 224-234. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Congenital stationary night blindness 2A (CSNB2A) is an X-linked retinal disorder, characterized by phenotypically variable signs and symptoms of impaired vision. CSNB2A is due to mutations in CACNA1F, which codes for the pore-forming α1F subunit of a L-type voltage-gated calcium channel, Cav1.4. Mouse models of CSNB2A, used for characterizing the effects of various Cacna1f mutations, have revealed greater severity of defects than in human CSNB2A. Specifically, Cacna1f-knockout mice show an apparent lack of visual function, gradual retinal degeneration, and disruption of photoreceptor synaptic terminals. Several reports have also noted cone-specific disruptions, including axonal abnormalities, dystrophy, and cell death. We have explored further the involvement of cones in our ‘G305X’ mouse model of CSNB2A, which has a premature truncation, loss-of-function mutation in Cacna1f. We show that the expression of genes for several phototransduction-related cone markers is down-regulated, while that of several cellular stress- and damage-related markers is up-regulated; and that cone photoreceptor structure and photopic visual function – measured by immunohistochemistry, optokinetic response and electroretinography – deteriorate progressively with age. We also find that dystrophic cone axons establish synapse-like contacts with rod bipolar cell dendrites, which they normally do not contact in wild-type retinas – ectopically, among rod cell bodies in the outer nuclear layer. These data support a role for Cav1.4 in cone synaptic development, cell viability, and synaptic transmission of cone-dependent visual signals. Although our novel finding of cone-to-rod-bipolar cell contacts in this mouse model of a retinal channelopathy may challenge current views of the role of Cav1.4 in photopic vision, it also suggests a potential new target for restorative therapy.

The most widespread models to study blindness, rats and mice, have retinas containing less than 3% cones. The diurnal rodent Arvicanthis niloticus retina has around 35% cones. Using ERG recordings, we studied retina function in this species. Several features differed from that reported in rats and mice: (a) fivefold larger photopic a-wave amplitudes; (b) photopic hill effect in Nile grass rats only; and (c) flicker amplitude plateau between 5 to 35Hz with fusion beyond 60Hz in Nile grass rats only. We conclude that A. niloticus might complement rats and mice for studying retinal function and pathologies involving cones.

The auditory cortex (AC) is the major origin of descending auditory projections and is one of the targets of the cholinergic basal forebrain, nucleus basalis (NB). In the big brown bat, cortical activation evokes frequency-specific plasticity in the inferior colliculus and the NB augments this collicular plasticity. To examine whether cortical descending function and NB contributions to collicular plasticity are different between the bat and mouse and to extend the findings in the bat, we induced plasticity in the central nucleus of the mouse inferior colliculus by a tone paired with electrical stimulation of the NB (hereafter referred to as tone-ES(NB)). We show here that tone-ES(NB) shifted collicular best frequencies (BFs) towards the frequency of the tone paired with ES(NB) when collicular BFs were different from tone frequency. The shift in collicular BF was linearly correlated to the difference between collicular BFs and tone frequencies. The changes in collicular BFs after tone-ES(NB) were similar to those found in the big brown bat. Compared with cortical plasticity evoked by tone-ES(NB), the pattern of collicular BF shifts was identical but the shifting range of collicular BFs was narrower. A GABA(A) agonist (muscimol) or a muscarinic acetylcholine receptor antagonist (atropine) applied to the AC completely abolished the collicular plasticity evoked by tone-ES(NB). Therefore, our findings strongly suggest that the AC plays a critical role in experience-dependent auditory plasticity through descending projections.

Macrophages function as phagocytes and antigen-presenting cells in the body. As has been demonstrated in mammals, administration of clodronate [dichloromethylene bisphosphonate (Cl2MBP)] encapsulated liposomes results in depletion of macrophages. Although this compound has been used in chickens, its effectiveness in depleting macrophages has yet to be fully determined. Here, we show that a single administration of clodronate liposomes to chickens results in a significant depletion of macrophages within the spleen and lungs of chickens up to 4 d post-treatment. This finding suggests that, in order to obtain depletion of macrophages in chickens for greater than 5 d, it is necessary to administer clodronate liposomes 4 d apart. The study also showed that 2 treatments of clodronate liposomes at 4-day intervals resulted in the depletion of macrophages for up to 10 d. The findings of the present study will encourage more precise studies to be done on the potential roles of macrophages in immune responses and in the pathogenesis of microbial infections in chickens.Les macrophages agissent comme phagocytes et cellules présentatrices d’antigènes dans l’organisme. Tel que démontré chez les mammifères, l’administration de liposomes encapsulés de clodronate [biphosphanate de dichlorométhylène (Cl

Background: The retina has a unique three-dimensional architecture, the precise organization of which allows for complete sampling of the visual field. Along the radial or apicobasal axis, retinal neurons and their dendritic and axonal arbors are segregated into layers, while perpendicular to this axis, in the tangential plane, four of the six neuronal types form patterned cellular arrays, or mosaics. Currently, the molecular cues that control retinal cell positioning are not well-understood, especially those that operate in the tangential plane. Here we investigated the role of the PTEN phosphatase in establishing a functional retinal architecture. Methodology/Principal Findings: In the developing retina, PTEN was localized preferentially to ganglion, amacrine and horizontal cells, whose somata are distributed in mosaic patterns in the tangential plane. Generation of a retina-specific Pten knock-out resulted in retinal ganglion, amacrine and horizontal cell hypertrophy, and expansion of the inner plexiform layer. The spacing of Pten mutant mosaic populations was also aberrant, as were the arborization and fasciculation patterns of their processes, displaying cell type-specific defects in the radial and tangential dimensions. Irregular oscillatory potentials were also observed in Pten mutant electroretinograms, indicative of asynchronous amacrine cell firing. Furthermore, while Pten mutant RGC axons targeted appropriate brain regions, optokinetic spatial acuity was reduced in Pten mutant animals. Finally, while some features of the Pten mutant retina appeared similar to those reported in Dscam-mutant mice, PTEN expression and activity were normal in the absence of Dscam. Conclusions/Significance: We conclude that Pten regulates somal positioning and neurite arborization patterns of a subset of retinal cells that form mosaics, likely functioning independently of Dscam, at least during the embryonic period. Our findings thus reveal an unexpected level of cellular specificity for the multi-purpose phosphatase, and identify Pten as an integral component of a novel cell positioning pathway in the retina. © 2012 Cantrup et al.

Cellular Prion Protein (PrP(C)) is known to mediate a protective role in several neurological conditions such as ischemia and epilepsy. However, so far, little information is available concerning the role of PrP(C) in psychiatric disorders such as depression. Here, we have used PrP(C) null mice to examine a putative role of PrP(C) in depressive-like states. Prion protein null mice exhibited depressive-like behaviour when compared to wild-type mice in both the Forced Swimming Test (FST) and Tail Suspension Test (TST). The clinical antidepressant drug imipramine and the NMDA receptor antagonist MK-801 reversed the depressive-like behaviour observed for knockout mice in the TST. The present data thus indicate that PrP(C) exerts a critical role in modulating the depressive-like state in mice, reinforcing the notion that PrP(C) might be associated with alterations in mood disorder states, and suggests a possible role of PrP(C) as a potential drug target for treating depressive disorders.

Background: Mutations in CACNA1F, which encodes the Cav1.4 subunit of a voltage-gated L-type calcium channel, cause X-linked incomplete congenital stationary night blindness (CSNB2), a condition of defective retinal neurotransmission which results in night blindness, reduced visual acuity, and diminished ERG b-wave. We have characterized two putative murine CSNB2 models: an engineered null-mutant, with a stop codon (G305X); and a spontaneous mutant with an ETn insertion in intron 2 of Cacna1f (nob2).

Unlike laboratory rats and mice, muridae of the Arvicanthis family (A. ansorgei and A. niloticus) are adapted to functioning best in daylight. To date, they have been used as experimental models mainly in studies of circadian rhythms. However, recent work aimed at optimizing photoreceptor-directed gene delivery vectors (Khani et al. [2007] Invest Ophthalmol Vis Sci 48:3954-3961) suggests their potential usefulness for studying retinal pathologies and therapies. In the present study we analyzed the retinal anatomy and visual performance of the Nile grass rat (A. niloticus) using immunohistofluorescence and the optokinetic response (OKR). We found that approximately 35-40% of photoreceptors are cones; that many neural features of the inner retina are similar to those in other diurnal mammals; and that spatial acuity, measured by the OKR, is more than two times that of the usual laboratory rodents. These observations are consistent with the known diurnal habits of this animal, and further support its pertinence as a complementary model for studies of structure, function, and pathology in cone-rich mammalian retinae.