Low Vapor Pressure Solvents for Single-Molecule Junction Measurements.

Nonpolar solvents commonly used in scanning tunneling microscope-based break junction measurements exhibit hazards and relatively low boiling points (bp) that limit the scope of solution experiments at elevated temperatures. Here we show that low toxicity, ultrahigh bp solvents such as bis(2-ethylhexyl) adipate (bp = 417 °C) and squalane (457 °C) can be used to probe molecular junctions at ≥100 °C. With these, we extend solvent- and temperature-dependent conductance trends for junction components such as 4,4'-bipyridine and thiomethyl-terminated oligophenylenes and reveal the gold snapback distance is larger at 100 °C due to increased surface atom mobility. We further show the rate of surface transmetalation and homocoupling reactions using phenylboronic acids increases at 100 °C, while junctions comprising anticipated boroxine condensation products form only at room temperature in an anhydrous glovebox atmosphere. Overall, this work demonstrates the utility of low vapor pressure solvents for the comprehensive characterization of junction properties and chemical reactivity at the single-molecule limit.

What Role Does Striatal Dopamine Play in Goal-directed Action?

Evidence suggests that dopamine activity provides a US-related prediction error for Pavlovian conditioning and the reinforcement signal supporting the acquisition of habits. However, its role in goal-directed action is less clear. There are currently few studies that have assessed dopamine release as animals acquire and perform self-paced instrumental actions. Here we briefly review the literature documenting the psychological, behavioral and neural bases of goal-directed actions in rats and mice, before turning to describe recent studies investigating the role of dopamine in instrumental learning and performance. Plasticity in dorsomedial striatum, a central node in the network supporting goal-directed action, clearly requires dopamine release, the timing of which, relative to cortical and thalamic inputs, determines the degree and form of that plasticity. Beyond this, bilateral release appears to reflect reward prediction errors as animals experience the consequences of an action. Such signals feedforward to update the value of the specific action associated with that outcome during subsequent performance, with dopamine release at the time of action reflecting the updated predicted action value. More recently, evidence has also emerged for a hemispherically lateralised signal associated with the action; dopamine release is greater in the hemisphere contralateral to the spatial target of the action. This effect emerges over the course of acquisition and appears to reflect the strength of the action-outcome association. Thus, during goal-directed action, dopamine release signals the action, the outcome and their association to shape the learning and performance processes necessary to support this form of behavioral control.

Stimulus-outcome associations are required for the expression of specific Pavlovian-instrumental transfer.

A series of experiments employed a specific Pavlovian-instrumental transfer (PIT) task in rats to determine the capacity of various treatments to undermine two outcome-specific stimulus-outcome (S-O) associations. Experiment 1 tested a random treatment, which involved uncorrelated presentations of the two stimuli and their predicted outcomes. This treatment disrupted the capacity of the outcome-specific S-O associations to drive specific PIT. Experiment 2 used a negative-contingency treatment during which the predicted outcomes were exclusively delivered in the absence of their associated stimulus. This treatment spared specific PIT, suggesting that it left the outcome-specific S-O associations relatively intact. The same outcome was obtained in Experiment 3, which implemented a zero-contingency treatment consisting of delivering the predicted outcomes in the presence and absence of their associated stimulus. Experiment 4 tested a mixed treatment, which distributed the predicted outcomes at an equal rate during each stimulus. This treatment disrupted the capacity of the outcome-specific S-O associations to drive specific PIT. We suggest that the mixed treatment disrupted specific PIT by generating new and competing outcome-specific S-O associations. By contrast, we propose that the random treatment disrupted specific PIT by undermining the original outcome-specific S-O associations, indicating that these associations must be retrieved to express specific PIT. We discuss how these findings inform our theoretical understanding of the mechanisms underlying this phenomenon. (PsycInfo Database Record (c) 2024 APA, all rights reserved).