Does sodium oxybate inhibit brain dopamine release in humans? An exploratory neuroimaging study

Author(s):  
Stephen J Kish ◽  
Gerald O'Leary ◽  
Mortimer Mamelak ◽  
Tina McCluskey ◽  
Jerry J Warsh ◽  
...  
2006 ◽  
Vol 63 (7) ◽  
pp. 808 ◽  
Author(s):  
Arthur L. Brody ◽  
Mark A. Mandelkern ◽  
Richard E. Olmstead ◽  
David Scheibal ◽  
Emily Hahn ◽  
...  

Author(s):  
Dianna Samuelson Dibble ◽  
Kaitlin R. Van Alstyne ◽  
Sam Ridgway

We have long observed dolphins producing recognizable sounds—bursts of pulses with sweeping peak frequencies—at prey capture. We call this the victory squeal. When dolphins hunt fish, there are three sequential sounds: sonar clicks, terminal buzz, and the victory squeal. When dolphins find a fish with sonar clicks, but reject the fish during the terminal buzz phase, they omit or truncate the victory squeal. We also observe dolphins producing the victory squeal after a trainer’s bridge, which serves as secondary reinforcement that bridges the time gap between the dolphin’s performance and delivery of food reinforcement. It signals the dolphins that they responded correctly and that reward is forthcoming. Before training, the victory squeal came after fish capture, but with successive trials, there was a forward shift in the victory squeal to come about 200 ms after the bridge. The victory squeal immediately following the bridge suggests the dolphin expects reward. Although there are no direct studies of dopamine release in cetaceans, early brain stimulation studies demonstrated consistent timing that may link the victory squeal with brain dopamine release. In the current study, we asked if dolphins might produce the victory squeal after task completion, but without the trainer’s bridge. Dolphins carried cameras, recording video and sound, while performing tasks in the open ocean, away from trainers, during swimmer/mine marking and retrieving. In each task, we observed the victory squeal immediately upon completion of task components. We suggest that the victory squeal signals that these experienced dolphins recognized their success.


2011 ◽  
Vol 60 (2-3) ◽  
pp. 295-302 ◽  
Author(s):  
Jia-Qian Ren ◽  
Yan Jiang ◽  
Zhihui Wang ◽  
Deirdre McCarthy ◽  
Anjali M. Rajadhyaksha ◽  
...  

1995 ◽  
Vol 269 (2) ◽  
pp. H487-H490 ◽  
Author(s):  
M. T. Lin ◽  
T. Y. Kao ◽  
C. C. Chio ◽  
Y. T. Jin

To explore the importance of brain dopamine in the heatstroke-induced striatal ischemia and neuronal injury, we compared the temporal profile of the heatstroke-induced striatal extracellular dopamine release, striatal blood flow, and striatal neuronal loss in rats with or without striatal dopamine depletion produced by 6-hydroxydopamine. In vivo voltammetry was used in rats to measure changes in extracellular concentrations of dopamine in the corpus striatum. Striatal neuronal damage was rated on a scale from zero to three (0, no damage; 3, maximum cell loss). The autoradiographic diffusible tracer technique was used for the measurement of striatal blood flow. After the onset of heatstroke, the heatstroke rats without brain dopamine depletion displayed hyperthermia, decreased mean arterial pressure, increased intracranial pressure, decreased cerebral perfusion pressure, decreased striatal blood flow, increased striatal dopamine release, and increased score of striatal neuronal damage as compared with those of normothermic controls. However, when the striatal dopamine system was destroyed by 6-hydroxydopamine, the heatstroke-induced arterial hypotension, intracranial hypertension, ischemic damage to the striatum, and elevated striatal dopamine release were reduced. In addition, the survival time of the heatstroke rats was prolonged after depleting striatal dopamine. Thus it appears that dopamine depletion protects striatal neurons from heatstroke-induced ischemia and cell death.


2010 ◽  
Vol 43 (14) ◽  
pp. 5
Author(s):  
ELIZABETH MECHCATIE
Keyword(s):  

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