Commodity discounting: Obstacles and solutions.

Addictive behaviors involve patterns of impulsive choices. Discount functions are a useful means of describing the behavioral contingencies involved in those impulsive choices. Although monetary discounting tasks have proven useful, most impulsive behaviors of interest involve nonmonetary consequences. OBJECTIVE: Developing effective commodity discounting tasks is critical for assessing how delay (and other variables) influences choice with respect to meaningful real-world commodities (e.g., high-calorie foods, alcohol, opioids, and other drugs). METHOD: Identifying the obstacles specific to nonmonetary commodity discounting and evaluating solutions to those obstacles. RESULTS: Those obstacles include (1) real versus hypothetical commodities, (2) framing, (3) commodity indivisibility, (4) diminishing marginal utility, and (5) variations in economic context. CONCLUSIONS: Solutions are presented and evaluated for each of these five obstacles, including the following: (1) assessing relevant experiences and explicitly stipulating transportation and storage issues, (2) systematic analyses across various wordings and holding wording constant across commodities, (3) using an adjusting delay procedure with only whole commodities, (4) assessing value for different commodity amounts (without delay) and adopting quantitative models of discounting that include marginal utility, and (5) controlling for motivating operations, accounting for individual histories, and using closed economies. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Quaternary Centers by Nickel-Catalyzed Cross-Coupling of Tertiary Carboxylic Acids and (Hetero)Aryl Zinc Reagents.

This work bridges a gap in the cross-coupling of aliphatic redox-active esters with aryl zinc reagents. Previously limited to primary, secondary, and specialized tertiary centers, a new protocol has been devised to enable the coupling of general tertiary systems using nickel catalysis. The scope of this operationally simple method is broad, and it can be used to simplify the synthesis of medicinally relevant motifs bearing quaternary centers.

Accessing alternative reaction pathways of the intermolecular condensation between homo-propargyl alcohols and terminal alkynes through divergent gold catalysis.

An intermolecular condensation of alkynols and terminal alkynes is reported. Using IPrAuNTf2, an efficient Au-catalyzed cyclization-alkynylation strategy furnishes (2-arylalkynyl) cyclic ethers in moderate to excellent yields (up to 94%). This strategy is extended to the synthesis of functionalized 2,3-dihydrooxepines via the sequential Au-catalyzed ring expansion of the cyclic ether substrates.

Gold-Catalyzed Vinyl Ether Hydroalkynylation: An Alternative Pathway for the Gold-Catalyzed Intermolecular Reaction of Alkenes and Alkynes.

In this report, the gold-catalyzed intermolecular reaction of vinyl ethers and terminal alkynes is investigated. Utilizing a triazole gold catalyst lessens gold decomposition in the presence of the vinyl ether and affords an alkynylation product instead of the [2 + 2] product. This protocol has been expanded to include glycal substrates, which undergo a one-pot alkynylation-Ferrier reaction to produce functionalized sugars in moderate to excellent yields with high diastereoselectivity.

Electroencephalography in children with and without sensory processing disorders during auditory perception.

OBJECTIVE: We sought to determine whether children with sensory processing disorder (SPD) differ from typically developing children on a neurophysiological measure, the P300 component of event-related potentials produced in response to brief auditory stimulation. METHOD: We used electroencephalographic measures (i.e., N200 and P300 components) to examine auditory processing in 20 children with SPD and 71 typically developing children, ages 5-10 yr. RESULTS: Children with SPD demonstrated significantly smaller P300 amplitudes and shorter N200 latencies than typically developing children. Brain activity correctly distinguished children with SPD from typically developing children with 77% accuracy. We also found a significant relationship between the neurophysiological measures and functional performance on sensory and motor tasks. CONCLUSION: This study presents empirical evidence that children with SPD display unique brain processing mechanisms compared with typical children and, therefore, provide further evidence for the neural deviations associated with SPD.

Target selection of proprioceptive and motor axon synapses on neonatal V1-derived Ia inhibitory interneurons and Renshaw cells.

The diversity of premotor interneurons in the mammalian spinal cord is generated from a few phylogenetically conserved embryonic classes of interneurons (V0, V1, V2, V3). Their mechanisms of diversification remain unresolved, although these are clearly important to understand motor circuit assembly in the spinal cord. Some Ia inhibitory interneurons (IaINs) and all Renshaw cells (RCs) derive from embryonic V1 interneurons; however, in adult they display distinct functional properties and synaptic inputs, for example proprioceptive inputs preferentially target IaINs, while motor axons target RCs. Previously, we found that both inputs converge on RCs in neonates, raising the possibility that proprioceptive (VGLUT1-positive) and motor axon synapses (VAChT-positive) initially target several different V1 interneurons populations and then become selected or deselected postnatally. Alternatively, specific inputs might precisely connect only with predefined groups of V1 interneurons. To test these hypotheses we analyzed synaptic development on V1-derived IaINs and compared them to RCs of the same age and spinal cord levels. V1-interneurons were labeled using genetically encoded lineage markers in mice. The results show that although neonatal V1-derived IaINs and RCs are competent to receive proprioceptive synapses, these synapses preferentially target the proximal somato-dendritic regions of IaINs and postnatally proliferate on IaINs, but not on RCs. In contrast, cholinergic synapses on RCs are specifically derived from motor axons, while on IaINs they originate from Pitx2 V0c interneurons. Thus, motor, proprioceptive, and even some interneuron inputs are biased toward specific subtypes of V1-interneurons. Postnatal strengthening of these inputs is later superimposed on this initial preferential targeting.

Gamma motor neurons express distinct genetic markers at birth and require muscle spindle-derived GDNF for postnatal survival.

BACKGROUND: Gamma motor neurons (gamma-MNs) selectively innervate muscle spindle intrafusal fibers and regulate their sensitivity to stretch. They constitute a distinct subpopulation that differs in morphology, physiology and connectivity from alpha-MNs, which innervate extrafusal muscle fibers and exert force. The mechanisms that control the differentiation of functionally distinct fusimotor neurons are unknown. Progress on this question has been limited by the absence of molecular markers to specifically distinguish and manipulate gamma-MNs. Recently, it was reported that early embryonic gamma-MN precursors are dependent on GDNF. Using this knowledge we characterized genetic strategies to label developing gamma-MNs based on GDNF receptor expression, showed their strict dependence for survival on muscle spindle-derived GDNF and generated an animal model in which gamma-MNs are selectively lost. RESULTS: In mice heterozygous for both the Hb9::GFP transgene and a tau-lacZ-labeled (TLZ) allele of the GDNF receptor Gfralpha1, we demonstrated that small motor neurons with high Gfralpha1-TLZ expression and lacking Hb9::GFP display structural and synaptic features of gamma-MNs and are selectively lost in mutants lacking target muscle spindles. Loss of muscle spindles also results in the downregulation of Gfralpha1 expression in some large diameter MNs, suggesting that spindle-derived factors may also influence populations of alpha-MNs with beta-skeletofusimotor collaterals. These molecular markers can be used to identify gamma-MNs from birth to the adult and to distinguish gamma- from beta-motor axons in the periphery. We also found that postnatal gamma-MNs are also distinguished by low expression of the neuronal nuclear protein (NeuN). With these markers of gamma-MN identity, we show after conditional elimination of GDNF from muscle spindles that the survival of gamma-MNs is selectively dependent on spindle-derived GDNF during the first 2 weeks of postnatal development. CONCLUSION: Neonatal gamma-MNs display a unique molecular profile characterized by the differential expression of a series of markers - Gfralpha1, Hb9::GFP and NeuN - and the selective dependence on muscle spindle-derived GDNF. Deletion of GDNF expression from muscle spindles results in the selective elimination of gamma-MNs with preservation of the spindle and its sensory innervation. This provides a mouse model with which to explore the specific role of gamma-fusimotor activity in motor behaviors.