Evaluation of free-floating bike-share on a university campus using a multi-method approach.

Bike-sharing, especially free-floating bike-share, has tremendous potential for increasing active transport on a college campus. Increased bike use improves public health, reduces pollution, and solves traffic congestion problems. Like other innovations, free-floating bikeshare proceeds through various stages while disseminated and before being widely adopted and accepted. A multi-method study using quantitative bike usage data, a cross-sectional survey, and focus group discussions was used to evaluate the Spring 2018 launch of a free-floating bike-share program at a large public university. Three months after implementation, there were 19,504 registered users, 24,371 different riders, 165,854 rides, and 85,778 miles traveled. The average trip length was 0.52 miles and lasted 8.3 min. Survey data from 2845 students, faculty, and staff revealed that 33.6% had used the bikes. Bike users were more likely to be students, freshmen, living on campus, be a current biker, and have confidence in their biking ability. Focus groups revealed that safety was a concern, knowledge about how the program worked was low among non-users and faculty and staff, cost was a barrier, and that adherence to bike-share rules needed to be improved. A large segment of the university population quickly adopted free-floating bike-share. However, continued work needs to be done to enhance safety, provide clear guidelines on bike-share rules (e.g., bike parking), and increase knowledge of the program with a specific focus on use by faculty and staff to ensure continued success and ultimately improve health.

The role of connexin-36 gap junctions in alcohol intoxication and consumption.

Ventral tegmental area (VTA) GABA neurons appear to be critical substrates underlying the acute and chronic effects of ethanol on dopamine (DA) neurotransmission in the mesocorticolimbic system implicated in alcohol reward. The aim of this study was to examine the role of midbrain connexin-36 (Cx36) gap junctions (GJs) in ethanol intoxication and consumption. Using behavioral, molecular, and electrophysiological methods, we compared the effects of ethanol in mature Cx36 knockout (KO) mice and age-matched wild-type (WT) controls. Compared to WT mice, Cx36 KO mice exhibited significantly more ethanol-induced motor impairment in the open field test, but less disruption in motor coordination in the rotarod paradigm. Cx36 KO mice, and WT mice treated with the Cx36 antagonist mefloquine (MFQ), consumed significantly less ethanol than their WT controls in the drink-in-the-dark procedure. The firing rate of VTA GABA neurons in WT mice was inhibited by ethanol with an IC50 of 0.25 g/kg, while VTA GABA neurons in KO mice were significantly less sensitive to ethanol. Dopamine neuron GABA-mediated sIPSC frequency was reduced by ethanol (30 mM) in WT mice, but not affected in KO mice. Cx36 KO mice evinced a significant up-regulation in DAT and D2 receptors in the VTA, as assessed by quantitative RT-PCR. These findings demonstrate the behavioral relevance of Cx36 GJ-mediated electrical coupling between GABA neurons in mature animals, and suggest that loss of coupling between VTA GABA neurons results in disinhibition of DA neurons, a hyper-DAergic state and lowered hedonic valence for ethanol consumption.

Acute and chronic ethanol modulate dopamine D2-subtype receptor responses in ventral tegmental area GABA neurons.

BACKGROUND: Ventral tegmental area (VTA) gamma-aminobutyric acid (GABA) neurons appear to be critical substrates underlying the acute and chronic effects of ethanol on dopamine (DA) neurotransmission in the mesocorticolimbic system implicated in drug reward. VTA GABA neuron firing rate is reduced by acute ethanol and enhanced by DA via D2 receptor activation. The objective of this study was to evaluate the role of D2 receptors in acute ethanol inhibition of VTA GABA neuron activity, as well as the adaptation of D2 receptors by chronic ethanol consumption. METHODS: Using electrophysiological methods, we evaluated the effects of intraperitoneal ethanol on DA activation of VTA GABA neurons, the effects of DA antagonists on ethanol inhibition of their firing rate, as well as adaptations in firing rate following chronic ethanol consumption. Using single cell quantitative RT-polymerase chain reaction (PCR), we evaluated the expression of VTA GABA neuron D2 receptors in rats consuming ethanol versus pair-fed controls. RESULTS: In acute ethanol studies, microelectrophoretic activation of VTA GABA neurons by DA was inhibited by acute intraperitoneal ethanol, and intravenous administration of the D2 antagonist eticlopride blocked ethanol suppression of VTA GABA neuron firing rate. In chronic ethanol studies, while there were no signs of withdrawal at 24 hours, or significant adaptation in firing rate or response to acute ethanol, there was a significant down-regulation in the expression of D2 receptors in ethanol-consuming rats versus pair-fed controls. CONCLUSIONS: Inhibition of DA activation of VTA GABA neuron firing rate by ethanol, as well as eticlopride block of ethanol inhibition of VTA GABA neuron firing rate, suggests an interaction between ethanol and DA neurotransmission via D2 receptors, perhaps via enhanced DA release in the VTA subsequent to ethanol inhibition of GABA neurons. Down-regulation of VTA GABA neuron D2 receptors by chronic ethanol might result from persistent DA release onto GABA neurons.