Laurate Biosensors Image Brain Neurotransmitters In Vivo: Can an Antihypertensive Medication Alter Psychostimulant Behavior?

Broderick, Patricia A.; Ho, Helen Shen Ting; Wat, Karyn; Murthy, Vivek

doi:10.3390/s8074033

Cited by 15 publications

(10 citation statements)

References 69 publications

(66 reference statements)

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“…Contrary to the effects of cocaine, caffeine did not cause such changes and blocked the effects of cocaine when taken together. This pattern of neuroprotection via caffeine was similar to responses in previous studies of DA release, 13 conditioned place preference, 28 locomotor activity, 18,29 and acoustic startle response, 14 suggesting that DA, adenosine, and estrogen strongly interact with each other, causing increased sensitivity to cocaine that was reversed when the adenosine system was antagonized.…”

Section: Fig 1 (A-h)supporting

confidence: 83%

“…Doses were chosen based on peak effects from the literature [15][16][17] and previous NMI experiments done in this laboratory to correlate behavior with biochemistry. 12,13,18 Vaginal smears using exfoliate cytology Samples were collected before and after injections within a 30 min period. Females were swabbed with a saline-soaked cotton tip and dotted on a microscope slide.…”

Section: Drugs and Dosesmentioning

confidence: 99%

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Cocaine Shifts the Estrus Cycle Out of Phase and Caffeine Restores It

Broderick

Malave

2014

Journal of Caffeine Research

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Background: Sex differences in cocaine abuse are well established. Females have a higher sensitivity and thus higher vulnerability to cocaine abuse compared to males. There are many studies showing that sensitivity to cocaine reward varies during the estrus cycle. Methods: Vaginal smears were examined through a DIFF staining kit and viewed through a microscope to determine the estrus cycle stage. Smears were taken immediately before and after cocaine and/or caffeine injections. Furthermore, we suggest a new tool to analyze the estrus cycle by using electrical resistance of the vaginal mucosa. Results: In the present study, we discovered that cocaine directly induced changes in the estrus cycle. Interestingly, caffeine did not affect the estrus cycle and nor did the combination of cocaine and caffeine. We observed that caffeine blocked the cocaine-induced estrus cycle changes using conventional exfoliate cytology. Therefore, caffeine may have neuroprotective properties on the changes induced by cocaine. Conclusion: These phase changes in the estrus cycle may be the underlying cause of sex differences in cocaine addiction that can be blocked by caffeine. Thus, we propose a valuable insight into sex differences in cocaine abuse and reveal a possible treatment with antagonizing the adenosine system.

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Section: Fig 1 (A-h)supporting

confidence: 83%

Section: Drugs and Dosesmentioning

confidence: 99%

Cocaine Shifts the Estrus Cycle Out of Phase and Caffeine Restores It

Broderick

Malave

2014

Journal of Caffeine Research

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“…However, the BRODERICK PROBE biosensor is the first direct NMI that detects DA release on line and in real time. 18,20,24 DA release occurs in a dose-dependent manner. Cocaine enhanced the amount of DA in the synapse allowing for more activation on postsynaptic cells.…”

Section: Discussionmentioning

confidence: 98%

“…16,17,19,[21][22][23][24] Procedure and biosensor specifications are previously discussed. 18,25 In this article, results from NMI laurate biosensors are presented. Lauric acid has a hydrophobic head, hydrophilic tail, andactsasa surfactanttoreducesurface tension.The surfactant, lauric acid, also acts to assist the migration of molecules to form an oriented, adsorbed film on the interfacial surface of the indicator sensor.…”

Section: Neuromolecular Imagingmentioning

confidence: 98%

“…16,17 This biotechnological advance is based on conventional electrochemistry. 18 We focused on imaging DA directly in ventrolateral NAcc. The ventrolateral NAcc was selected because DA axons, which project from the ventral tegmental area, terminate on neurons in silver intensification procedures and also indicate high concentrations of DA in ventrolateral NAcc.…”

Section: Introductionmentioning

confidence: 99%

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Caffeine's Attenuation of Cocaine-Induced Dopamine Release by Inhibition of Adenosine

Malave

Broderick

2014

Journal of Caffeine Research

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It is well known that the reinforcing properties of cocaine addiction are caused by the sharp increase of dopamine (DA) in the reward areas of the brain. However, other mechanisms have been speculated to contribute to the increase. Adenosine is one system that is associated with the sleep-wake cycle and is most important in regulating neuronal activity. Thus, more and more evidence is pointing to its involvement in regulating DA release. The current study set out to examine the role of adenosine in cocaine-induced DA release. Increasing doses of cocaine, caffeine, and their combination, as well as, 8-cyclopentyltheophylline (CPT), an adenosine A1 antagonist (alone and in combination with cocaine) were used to denote a response curve. A novel biosensor, the BRODERICK PROBE was implanted in the nucleus accumbens to image the drug-induced surge of DA release , in the freely moving animal in real time. Combinations of cocaine and caffeine were observed to block the increased release of DA moderately after administration of the low dose (2.5 mg/kg cocaine and 12.5 mg/kg caffeine) and dramatically after administration of the high dose (10 mg/kg cocaine and 50 mg/kg caffeine), suggesting neuroprotection. Similarly, CPT and cocaine showed a decreased DA surge when administered in combination. Thus, the low and high dose of a nonselective adenosine antagonist, caffeine, and a moderate dose of a selective adenosine antagonist, CPT, protected against the cocaine-induced DA release. These results show a significant interaction between adenosine and DA release and suggest therapeutic options for cocaine addiction and disorders associated with DA dysfunction.

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