Correction: GABAergic regulation of striatal spiny projection neurons depends upon their activity state.

[This corrects the article DOI: 10.1371/journal.pbio.

Long-term frequent fire and cattle grazing alter dry forest understory vegetation.

Understanding fire and large herbivore interactions in interior western forests is critical, owing to the extensive and widespread co-occurrence of these two disturbance types and multiple present and future implications for forest resilience, conservation and restoration. However, manipulative studies focused on interactions and outcomes associated with these two disturbances are rare in forested rangelands. We investigated understory vegetation response to 5-year spring and fall prescribed fire and domestic cattle grazing exclusion in ponderosa pine stands and reported long-term responses, almost two decades after the first entry fires.

GABAergic regulation of striatal spiny projection neurons depends upon their activity state.

Synaptic transmission mediated by GABAA receptors (GABAARs) in adult, principal striatal spiny projection neurons (SPNs) can suppress ongoing spiking, but its effect on synaptic integration at subthreshold membrane potentials is less well characterized, particularly those near the resting down-state. To fill this gap, a combination of molecular, optogenetic, optical, and electrophysiological approaches were used to study SPNs in mouse ex vivo brain slices, and computational tools were used to model somatodendritic synaptic integration. In perforated patch recordings, activation of GABAARs, either by uncaging of GABA or by optogenetic stimulation of GABAergic synapses, evoked currents with a reversal potential near -60 mV in both juvenile and adult SPNs.

State-dependent GABAergic regulation of striatal spiny projection neuron excitability.

Synaptic transmission mediated by GABA receptors (GABA Rs) in adult, principal striatal spiny projection neurons (SPNs) can suppress ongoing spiking, but its effect on synaptic integration at sub-threshold membrane potentials is less well characterized, particularly those near the resting down-state. To fill this gap, a combination of molecular, optogenetic, optical and electrophysiological approaches were used to study SPNs in mouse brain slices, and computational tools were used to model somatodendritic synaptic integration. Activation of GABA Rs, either by uncaging of GABA or by optogenetic stimulation of GABAergic synapses, evoked currents with a reversal potential near -60 mV in perforated patch recordings from both juvenile and adult SPNs.

Cholinergic deficits selectively boost cortical intratelencephalic control of striatum in male Huntington's disease model mice.

Huntington's disease (HD) is a progressive, neurodegenerative disease caused by a CAG triplet expansion in huntingtin. Although corticostriatal dysfunction has long been implicated in HD, the determinants and pathway specificity of this pathophysiology are not fully understood. Here, using a male zQ175 knock-in mouse model of HD we carry out optogenetic interrogation of intratelencephalic and pyramidal tract synapses with principal striatal spiny projection neurons (SPNs).

Effects of ownership patterns on cross-boundary wildfires.

Understanding ownership effects on large wildfires is a precursor to the development of risk governance strategies that better protect people and property and restore fire-adapted ecosystems. We analyzed wildfire events in the Pacific Northwest from 1984 to 2018 to explore how area burned responded to ownership, asking whether particular ownerships burned disproportionately more or less, and whether these patterns varied by forest and grass/shrub vegetation types. While many individual fires showed indifference to property lines, taken as a whole, we found patterns of disproportionate burning for both forest and grass/shrub fires.

Mutant huntingtin enhances activation of dendritic Kv4 K channels in striatal spiny projection neurons.

Huntington's disease (HD) is initially characterized by an inability to suppress unwanted movements, a deficit attributable to impaired synaptic activation of striatal indirect pathway spiny projection neurons (iSPNs). To better understand the mechanisms underlying this deficit, striatal neurons in ex vivo brain slices from mouse genetic models of HD were studied using electrophysiological, optical and biochemical approaches. Distal dendrites of iSPNs from symptomatic HD mice were hypoexcitable, a change that was attributable to increased association of dendritic Kv4 potassium channels with auxiliary KChIP subunits.

Assessing Transboundary Wildfire Exposure in the Southwestern United States.

We assessed transboundary wildfire exposure among federal, state, and private lands and 447 communities in the state of Arizona, southwestern United States. The study quantified the relative magnitude of transboundary (incoming, outgoing) versus nontransboundary (i.e.

Wildfire spread, hazard and exposure metric raster grids for central Catalonia.

We provide 40 m resolution wildfire spread, hazard and exposure metric raster grids for the 0.13 million ha fire-prone Bages County in central Catalonia (northeastern Spain) corresponding to node influence grid (NIG), crown fraction burned (CFB) and fire transmission to residential houses (TR). Fire spread and behavior data (NIG, CFB and fire perimeters) were generated with fire simulation modeling considering wildfire season extreme fire weather conditions (97 percentile).

Optimizing prescribed fire allocation for managing fire risk in central Catalonia.

We used spatial optimization to allocate and prioritize prescribed fire treatments in the fire-prone Bages County, central Catalonia (northeastern Spain). The goal of this study was to identify suitable strategic locations on forest lands for fuel treatments in order to: 1) disrupt major fire movements, 2) reduce ember emissions, and 3) reduce the likelihood of large fires burning into residential communities. We first modeled fire spread, hazard and exposure metrics under historical extreme fire weather conditions, including node influence grid for surface fire pathways, crown fraction burned and fire transmission to residential structures.

Network analysis of wildfire transmission and implications for risk governance.

We characterized wildfire transmission and exposure within a matrix of large land tenures (federal, state, and private) surrounding 56 communities within a 3.3 million ha fire prone region of central Oregon US. Wildfire simulation and network analysis were used to quantify the exchange of fire among land tenures and communities and analyze the relative contributions of human versus natural ignitions to wildfire exposure.

Wildfire exposure and fuel management on western US national forests.

Substantial investments in fuel management activities on national forests in the western US are part of a national strategy to reduce human and ecological losses from catastrophic wildfire and create fire resilient landscapes. Prioritizing these investments within and among national forests remains a challenge, partly because a comprehensive assessment that establishes the current wildfire risk and exposure does not exist, making it difficult to identify national priorities and target specific areas for fuel management. To gain a broader understanding of wildfire exposure in the national forest system, we analyzed an array of simulated and empirical data on wildfire activity and fuel treatment investments on the 82 western US national forests.

Impaired TrkB receptor signaling underlies corticostriatal dysfunction in Huntington's disease.

Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder. The debilitating choreic movements that plague HD patients have been attributed to striatal degeneration induced by the loss of cortically supplied brain-derived neurotrophic factor (BDNF). Here, we show that in mouse models of early symptomatic HD, BDNF delivery to the striatum and its activation of tyrosine-related kinase B (TrkB) receptors were normal.

Regulation of dendritic calcium release in striatal spiny projection neurons.

The induction of corticostriatal long-term depression (LTD) in striatal spiny projection neurons (SPNs) requires coactivation of group I metabotropic glutamate receptors (mGluRs) and L-type Ca(2+) channels. This combination leads to the postsynaptic production of endocannabinoids that act presynaptically to reduce glutamate release. Although the necessity of coactivation is agreed upon, why it is necessary in physiologically meaningful settings is not.

Variation in foliar nitrogen and albedo in response to nitrogen fertilization and elevated CO2.

Foliar nitrogen has been shown to be positively correlated with midsummer canopy albedo and canopy near infrared (NIR) reflectance over a broad range of plant functional types (e.g., forests, grasslands, and agricultural lands).

Synaptically driven state transitions in distal dendrites of striatal spiny neurons.

Striatal spiny neurons (SPNs) associate a diverse array of cortically processed information to regulate action selection. But how this is done by SPNs is poorly understood. A key step in this process is the transition of SPNs from a hyperpolarized 'down state' to a sustained, depolarized 'up state'.

The role of dopamine in modulating the structure and function of striatal circuits.

Dopamine (DA) is a key regulator of action selection and associative learning. The striatum has long been thought to be a major locus of DA action in this process. Although all striatal cell types express G protein-coupled receptors for DA, the effects of DA on principal medium spiny neurons (MSNs) understandably have received the most attention.

Kalirin regulates cortical spine morphogenesis and disease-related behavioral phenotypes.

Dendritic spine morphogenesis contributes to brain function, cognition, and behavior, and is altered in psychiatric disorders. Kalirin is a brain-specific guanine-nucleotide exchange factor (GEF) for Rac-like GTPases and is a key regulator of spine morphogenesis. Here, we show that KALRN-knockout mice have specific reductions in cortical, but not hippocampal, Rac1 signaling and spine density, and exhibit reduced cortical glutamatergic transmission.