Nov. 12—THE ASSOCIATED PRESS TOP 25 The top 25 teams in The Associated Press' women's college basketball poll, with first-place votes in parentheses, and total points based on 25 points for a first-place vote through one point for a 25th-place vote and previous ranking. Rk., Team ReC. Pts Prv 1. South Carolina (31) 2-0 775 1 2. Connecticut 2-0 733 2 3. Southern Cal 2-0 703 3 4. Texas 1-0 665 4 ...

LSU women's basketball bucked a bit of a slow start to blowout Charleston Southern Tuesday morning.

On Wednesday at Moody Center, a Lamar team that went 24-7 last season should provide a tougher test for the Longhorns than in their season opener.

It was Louisville women's basketball vs UT Martin at the Kathleen and Tom Elam Center. See score updates and highlights from the road clash.

Notre Dame sophomore guard Hannah Hidalgo is on the Women’s Basketball Coaches Association (WBCA) Wade Watch List. She's among 15 players being watched as a potential winner of the oldest, most prestigious player of the year award. She was a Region I finalist for…

Chance Gray scored 14 of her career-high 31 points in the third quarter and she tied a program-best with nine 3-pointers to help No. 12 Ohio State beat Charlotte 94-53 on Tuesday night. Gray finished 9 of 14 from 3-point range to top her previous best of six makes. Gray scored 11 points in the first half after making all three of her 3-pointers to help Ohio State build a 43-17 lead.

Lady Vols basketball relied on its best 3-point shooting night of the season to close out a win over Middle Tennessee State on Tuesday

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.

JuJu Watkins had 21 points, nine assists and six steals to help No. 3 Southern California trounce Cal State Northridge 124-39 on Tuesday night. The Trojans (3-0) had six players in double figures, including Kiki Iriafen with 15 points and Kayleigh Heckel with 14 points off the bench. All 13 Trojans who played scored.

Holly Oakley
Oct 4, 2006; 26:10129-10140
Neurobiology of Disease

Sharon G. Kujawa
Nov 11, 2009; 29:14077-14085
BehavioralSystemsCognitive

Elena Neumann
Oct 9, 2024; 44:e0591242024-e0591242024
Systems/Circuits

Robbert Havekes
Dec 12, 2012; 32:18137-18149
BehavioralSystemsCognitive

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

Lindsay P. Cameron
Nov 8, 2023; 43:7472-7482
Symposium and Mini-Symposium

Sukhbinder Kumar
Jun 30, 2021; 41:5762-5770
Neurobiology of Disease

Corey M. Ziemba
Oct 16, 2024; 44:e0349242024-e0349242024
Systems/Circuits

Evdokia Menelaou
Aug 8, 2012; 32:10925-10939
BehavioralSystemsCognitive

Hannah Grotzinger
May 29, 2024; 44:e1856232024-e1856232024
BehavioralSystemsCognitive

Mitchell G. Spring
Oct 9, 2024; 44:e0602242024-e0602242024
BehavioralSystemsCognitive

William W. Seeley
Dec 11, 2019; 39:9878-9882
Progressions

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

Kyle E. Mathewson
Mar 4, 2009; 29:2725-2732
BehavioralSystemsCognitive

Pietro Mazzoni
Apr 5, 2006; 26:3642-3645
BRIEF COMMUNICATION

AP Georgopoulos
Nov 1, 1982; 2:1527-1537
Articles

Jordan A. Taylor
Feb 19, 2014; 34:3023-3032
BehavioralSystemsCognitive

Shiaoching Gong
Sep 12, 2007; 27:9817-9823
Toolbox

Yulia Lerner
Feb 23, 2011; 31:2906-2915
BehavioralSystemsCognitive

Martijn P. van den Heuvel
Nov 2, 2011; 31:15775-15786
BehavioralSystemsCognitive

Holly Oakley
Oct 4, 2006; 26:10129-10140
Neurobiology of Disease

α-Neurexins are essential and highly expressed presynaptic cell-adhesion molecules that are frequently linked to neuropsychiatric and neurodevelopmental disorders. Despite their importance, how the elaborate extracellular sequences of α-neurexins contribute to synapse function is poorly understood. We recently characterized the presynaptic gain-of-function phenotype caused by a missense mutation in an evolutionarily conserved extracellular sequence of neurexin-3α (A687T) that we identified in a patient diagnosed with profound intellectual disability and epilepsy. The striking A687T gain-of-function mutation on neurexin-3α prompted us to systematically test using mutants whether the presynaptic gain-of-function phenotype is a consequence of the addition of side-chain bulk (i.e., A687V) or polar/hydrophilic properties (i.e., A687S). We used multidisciplinary approaches in mixed-sex primary hippocampal cultures to assess the impact of the neurexin-3α^A687 residue on synapse morphology, function and ligand binding. Unexpectedly, neither A687V nor A687S recapitulated the neurexin-3α A687T phenotype. Instead, distinct from A687T, molecular replacement with A687S significantly enhanced postsynaptic properties exclusively at excitatory synapses and selectively increased binding to neuroligin-1 and neuroligin-3 without changing binding to neuroligin-2 or LRRTM2. Importantly, we provide the first experimental evidence supporting the notion that the position A687 of neurexin-3α and the N-terminal sequences of neuroligins may contribute to the stability of α-neurexin–neuroligin-1 trans-synaptic interactions and that these interactions may specifically regulate the postsynaptic strength of excitatory synapses.

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.

Serotonin modulates diverse phenotypes and functions including depressive, aggressive, impulsive, and feeding behaviors, all of which have reward-related components. To date, research has focused on understanding these effects by measuring and manipulating dorsal raphe serotonin neurons and using single-receptor approaches. These studies have led to a better understanding of the heterogeneity of serotonin actions on behavior; however, they leave open many questions about the timing and location of serotonin's actions modulating the neural circuits that drive these behaviors. Recent advances in genetically encoded fluorescent biosensors, including the GPCR activation-based sensor for serotonin (GRAB-5-HT), enable the measurement of serotonin release in mice on a timescale compatible with a single rewarding event without corelease confounds. Given substantial evidence from slice electrophysiology experiments showing that serotonin influences neural activity of the striatal circuitry, and the known role of the dorsal medial striatal (DMS) in reward-directed behavior, we focused on understanding the parameters and timing that govern serotonin release in the DMS in the context of reward consumption, external reward value, internal state, and cued reward. Overall, we found that serotonin release is associated with each of these and encodes reward anticipation, value, approach, and consumption in the DMS.

GABAergic neurons and GABA_A receptors (GABA_ARs) are critical elements of almost all neuronal circuits. Most GABA_ARs of the CNS are heteropentameric ion channels composed of two α, two β, and one subunits. These receptors serve as important drug targets for benzodiazepine (BDZ) site agonists, which potentiate the action of GABA at GABA_ARs. Most GABA_AR classifications rely on the heterogeneity of the α subunit (α1–α6) included in the receptor complex. Heterogeneity of the subunits (1–3), which mediate synaptic clustering of GABA_ARs and contribute, together with α subunits, to the benzodiazepine (BDZ) binding site, has gained less attention, mainly because 2 subunits greatly outnumber the other subunits in most brain regions. Here, we have investigated a potential role of non-2 GABA_ARs in neural circuits of the spinal dorsal horn, a key site of nociceptive processing. Female and male mice were studied. We demonstrate that besides 2 subunits, 1 subunits are significantly expressed in the spinal dorsal horn, especially in its superficial layers. Unlike global 2 subunit deletion, which is lethal, spinal cord-specific loss of 2 subunits was well tolerated. GABA_AR clustering in the superficial dorsal horn remained largely unaffected and antihyperalgesic actions of HZ-166, a nonsedative BDZ site agonist, were partially retained. Our results thus suggest that the superficial dorsal horn harbors functionally relevant amounts of 1 subunits that support the synaptic clustering of GABA_ARs in this site. They further suggest that 1 containing GABA_ARs contribute to the spinal control of nociceptive information flow.

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.