A school cook in Nebraska was canned after he mixed kangaroo meat into chili made for students.

U.S. Ed Secretary DeVos has approved plans for 46 states, plus the District of Columbia and Puerto Rico. Still waiting: California, Florida, Oklahoma, and Utah.

Nebraska's education department released an interactive instructional materials map last week, showing what curricula districts have adopted for English-language arts, math, and K-8 science.

This Quality Counts 2019 Highlights Report captures all the data you need to assess your state's performance on key educational outcomes.

This Quality Counts 2020 Highlights Report captures all the data you need to assess your state's performance on key educational outcomes.

A handful of districts and other groups are reshaping the after-school space to provide a wide range of social and linguistic supports for newcomer students.

The Montreal Canadiens are not the only team in the midst of a rebuild and it's not easy for anybody, especially not for Craig Conroy who's at the helm of the Calgary Flames and will be down a first-round pick at the next draft.

The latest update of the College Football Playoff rankings was officially released Tuesday night on ESPN, with the Alabama Crimson Tide seeing some movement as a result of their dominant 42-13 road win over the LSU Tigers on Saturday. In the rankings

No. 1 Oregon will travel to Madison this weekend to take on the Wisconsin Badgers at Camp Randall Stadium.

Texas A&M's Week 11 bye week was (hopefully) successful in terms of fixing the issues that plagued the Aggies, especially the defensive issues that led to 25 missed tackles in the 44-20 loss to South Carolina, which dropped the Aggies to No. 14 in the first Col

LSU landed 22nd in the latest College Football Rankings. Here’s a playoff picture for the Tigers. LSU fell seven spots, matching the tumble the Tigers took in the media polls. The fall was expected after Alabama boat raced LSU 42-13 in the Tiger Stadium. For LSU, the ranking…

Where did Georgia land in the latest CFP bracket and rankings? Here’s the College Football Playoff picture for the Bulldogs and path to championship.

Miami landed 9th in the latest CFP bracket. Here’s the College Football Playoff picture for the Hurricanes and path to the championship.

Penn State football landed Xth in the second CFP rankings. Here’s the College Football Playoff picture for the Nittany Lions.

The College Football Playoff selection committee released its second top-25 rankings of the season ahead of the first 12-team playoff, and unsurprisingly, the Oregon Ducks are still the No. 1 team. Of course, there are still many game

The second College Football Playoff top 25 rankings and a 12-team bracket projection were released on Tuesday. Tennessee (8-1, 5-1 SEC) is ranked No. 7 after defeating Mississippi State, 33-14, in Week 11. The Vols are also ranked No. 4 in the US LBM…

Georgia and Miami misery translates into joy for the Texas Longhorns. Thanks to losses by the 'Canes and Bulldogs on Saturday, the Horns move up two spots in the college football playoff ranki

Here's a look at the College Football Playoff bracket and playoff picture after the latest committee rankings were released.

Notre Dame football has one remaining game against a CFP-ranked team: Nov. 23 at Yankee Stadium against No. 24 Army (9-0).

The second release of College Football Playoff rankings changes the projected bracket. Here's what it looks like if the season ended today.

Georgia football tumbled nine spots in the College Football Playoff rankings Tuesday and fell out of the 12-team bracket. What committee chair said

We're now eleven weeks into the college football season and that means we have an idea of where Ohio State when it comes to the landscape of the 2024 season. The Buckeyes beat Penn State on the road two weeks ago to boost its resumé and remain right

The Big Ten captured four of the top five spots led by Oregon and Ohio State.

A handful of districts and other groups are reshaping the after-school space to provide a wide range of social and linguistic supports for newcomer students.

Alexis Markowski scored 22 points, Natalie Potts had a double-double and No. 21 Nebraska cruised to an 84-58 win over Southern on Tuesday night. Potts had 17 points and 12 rebounds, eight on the offensive end, for the Cornhuskers (3-0). Alberte Rimdal added 12 points.

Wen Grace Chen
Nov 9, 2022; 42:8498-8507
Symposium and Mini-Symposium

Christelle Anaclet
Dec 12, 2012; 32:17970-17976
BehavioralSystemsCognitive

Yasmin L. Hurd
Oct 16, 2019; 39:8250-8258
Symposium and Mini-Symposium

Krista L. Hyde
Mar 11, 2009; 29:3019-3025
Development Plasticity Repair

Elle M. Murata
Sep 18, 2024; 44:e0573242024-e0573242024
BehavioralSystemsCognitive

Emerging research in nonhuman animals implicates cerebellar projections to the ventral tegmental area (VTA) in appetitive behaviors, but these circuits have not been characterized in humans. Here, we mapped cerebello-VTA white matter connectivity in a cohort of men and women using probabilistic tractography on diffusion imaging data from the Human Connectome Project. We uncovered the topographical organization of these connections by separately tracking from parcels of cerebellar lobule VI, crus I/II, vermis, paravermis, and cerebrocerebellum. Results revealed that connections between the cerebellum and VTA predominantly originate in the right cerebellar hemisphere, interposed nucleus, and paravermal cortex and terminate mostly ipsilaterally. Paravermal crus I sends the most connections to the VTA compared with other lobules. We discovered a mediolateral gradient of connectivity, such that the medial cerebellum has the highest connectivity with the VTA. Individual differences in microstructure were associated with measures of negative affect and social functioning. By splitting the tracts into quarters, we found that the socioaffective effects were driven by the third quarter of the tract, corresponding to the point at which the fibers leave the deep nuclei. Taken together, we produced detailed maps of cerebello-VTA structural connectivity for the first time in humans and established their relevance for trait differences in socioaffective regulation.

Neuronal cytotoxic edema is implicated in neuronal injury and death, yet mitigating brain edema with osmotic and surgical interventions yields poor clinical outcomes. Importantly, neuronal swelling and its downstream consequences during early brain development remain poorly investigated, and new treatment approaches are needed. We explored Ca²⁺-dependent downstream effects after neuronal cytotoxic edema caused by diverse injuries in mice of both sexes using multiphoton Ca²⁺ imaging in vivo [Postnatal Day (P)12–17] and in acute brain slices (P8–12). After different excitotoxic insults, cytosolic GCaMP6s translocated into the nucleus after a few minutes in a subpopulation of neurons, persisting for hours. We used an automated morphology-detection algorithm to detect neuronal soma and quantified the nuclear translocation of GCaMP6s as the nuclear to cytosolic intensity (N/C ratio). Elevated neuronal N/C ratios occurred concurrently with persistent elevation in Ca²⁺ loads and could also occur independently from neuronal swelling. Electron microscopy revealed that the nuclear translocation was associated with the increased nuclear pore size. The nuclear accumulation of GCaMP6s in neurons led to neocortical circuit dysfunction, mitochondrial pathology, and increased cell death. Inhibiting calpains, a family of Ca²⁺-activated proteases, prevented elevated N/C ratios and neuronal swelling. In summary, in the developing brain, we identified a calpain-dependent alteration of nuclear transport in a subpopulation of neurons after disease-relevant insults leading to long-term circuit dysfunction and cell death. The nuclear translocation of GCaMP6 and other cytosolic proteins after acute excitotoxicity can be an early biomarker of brain injury in the developing brain.

Abnormal neuronal morphological features, such as dendrite branching, axonal branching, and spine density, are thought to contribute to the symptoms of depression and anxiety. However, the role and molecular mechanisms of aberrant neuronal morphology in the regulation of mood disorders remain poorly characterized. Here, we show that neuritin, an activity-dependent protein, regulates the axonal morphology of serotonin neurons. Male neuritin knock-out (KO) mice harbored impaired axonal branches of serotonin neurons in the medial prefrontal cortex and basolateral region of the amygdala (BLA), and male neuritin KO mice exhibited depressive and anxiety-like behaviors. We also observed that the expression of neuritin was decreased by unpredictable chronic stress in the male mouse brain and that decreased expression of neuritin was associated with reduced axonal branching of serotonin neurons in the brain and with depressive and anxiety behaviors in mice. Furthermore, the stress-mediated impairments in axonal branching and depressive behaviors were reversed by the overexpression of neuritin in the BLA. The ability of neuritin to increase axonal branching in serotonin neurons involves fibroblast growth factor (FGF) signaling, and neuritin contributes to FGF-2-mediated axonal branching regulation in vitro. Finally, the oral administration of an FGF inhibitor reduced the axonal branching of serotonin neurons in the brain and caused depressive and anxiety behaviors in male mice. Our results support the involvement of neuritin in models of stress-induced depression and suggest that neuronal morphological plasticity may play a role in controlling animal behavior.

Human sleep exhibits multiple, recurrent temporal regularities, ranging from circadian rhythms to sleep stage cycles and neuronal oscillations during nonrapid eye movement sleep. Moreover, recent evidence revealed a functional role of aperiodic activity, which reliably discriminates different sleep stages. Aperiodic activity is commonly defined as the spectral slope of the 1/frequency (1/f) decay function of the electrophysiological power spectrum. However, several lines of inquiry now indicate that the aperiodic component of the power spectrum might be better characterized by a superposition of several decay processes with associated timescales. Here, we determined multiple timescales, which jointly shape aperiodic activity using human intracranial electroencephalography. Across three independent studies (47 participants, 23 female), our results reveal that aperiodic activity reliably dissociated sleep stage-dependent dynamics in a regionally specific manner. A principled approach to parametrize aperiodic activity delineated several, spatially and state-specific timescales. Lastly, we employed pharmacological modulation by means of propofol anesthesia to disentangle state-invariant timescales that may reflect physical properties of the underlying neural population from state-specific timescales that likely constitute functional interactions. Collectively, these results establish the presence of multiple intrinsic timescales that define the electrophysiological power spectrum during distinct brain states.

We used virus-mediated anterograde and retrograde tracing, optogenetic modulation, immunostaining, in situ hybridization, and patch-clamp recordings in acute brain slices to study the release mechanism and μ-opioid modulation of the dual glutamatergic/GABAergic inputs from the ventral tegmental area and supramammillary nucleus to the granule cells of the dorsal hippocampus of male and female mice. In keeping with previous reports showing that the two transmitters are released by separate active zones within the same terminals, we found that the short-term plasticity and pharmacological modulation of the glutamatergic and GABAergic currents are indistinguishable. We further found that glutamate and GABA release at these synapses are both virtually completely mediated by N- and P/Q-type calcium channels. We then investigated μ-opioid modulation of these synapses and found that activation of μ-opioid receptors (MORs) strongly inhibits the glutamate and GABA release, mostly through inhibition of presynaptic N-type channels. However, the modulation by MORs of these dual synapses is complex, as it likely includes also a disinhibition due to downmodulation of local GABAergic interneurons which make direct axo-axonic contacts with the dual glutamatergic/GABAergic terminals. We discuss how this opioid modulation may enhance LTP at the perforant path inputs, potentially contributing to reinforce memories of drug-associated contexts.

The superior colliculus receives a direct projection from retinal ganglion cells. In primates, it remains unknown if the same ganglion cells also supply the lateral geniculate nucleus. To address this issue, a double-label experiment was performed in two male macaques. The animals fixated a target while injection sites were scouted in the superior colliculus by recording and stimulating with a tetrode. Once suitable sites were identified, cholera toxin subunit B-Alexa Fluor 488 was injected via an adjacent micropipette. In a subsequent acute experiment, cholera toxin subunit B-Alexa Fluor 555 was injected into the lateral geniculate nucleus at matching retinotopic locations. After a brief survival period, ganglion cells were examined in retinal flatmounts. The percentage of double-labeled cells varied locally, depending on the relative efficiency of retrograde transport by each tracer and the precision of retinotopic overlap of injection sites in each target nucleus. In counting boxes with extensive overlap, 76–98% of ganglion cells projecting to the superior colliculus were double labeled. Cells projecting to the superior colliculus constituted 4.0–6.7% of the labeled ganglion cell population. In one particularly large zone, there were 5,746 cells labeled only by CTB-AF555, 561cells double labeled by CTB-AF555 and CTB-AF488, but no cell labeled only by CTB-AF488. These data indicate that retinal input to the macaque superior colliculus arises from a collateral axonal branch supplied by ~5% of the ganglion cells that project to the lateral geniculate nucleus. Surprisingly, there exist no ganglion cells that project exclusively to the SC.

Hyperbilirubinemia (HB) is a key risk factor for hearing loss in neonates, particularly premature infants. Here, we report that bilirubin (BIL)-dependent cell death in the auditory brainstem of neonatal mice of both sexes is significantly attenuated by ZD7288, a blocker for hyperpolarization-activated cyclic nucleotide-gated (HCN) channel-mediated current (I_h), or by genetic deletion of HCN1. GABAergic inhibitory interneurons predominantly express HCN1, on which BIL selectively acts to increase their intrinsic excitability and mortality by enhancing HCN1 activity and Ca²⁺-dependent membrane targeting. Chronic BIL elevation in neonatal mice in vivo increases the fraction of spontaneously active interneurons and their firing frequency, I_h, and death, compromising audition at the young adult stage in HCN1^+/+, but not in HCN1^–/– genotype. We conclude that HB preferentially targets HCN1 to injure inhibitory interneurons, fueling a feedforward loop in which lessening inhibition cascades hyperexcitability, Ca²⁺ overload, neuronal death, and auditory impairments. These findings rationalize HCN1 as a potential target for managing HB encephalopathy.

The artists known as OSGEMEOS showcase the largest exhibition of their work in the United States at the Hirshhorn Museum and Sculpture Garden

Soils are essential to life [...]