Neuroscience letters
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Neuroscience letters · Sep 2013
CB1 cannabinoid receptor agonist prevents NGF-induced sensitization of TRPV1 in sensory neurons.
The transient receptor potential vanilloid type 1 channel (TRPV1) and nerve growth factor (NGF) are important mediators of inflammatory pain. NGF released during inflammation sensitizes TRPV1 in afferent nerve endings of peripheral nociceptors, increasing pain sensation. Cannabinoids, by activating CB1 G protein-coupled receptors, produce analgesia in a variety of pain models, though the exact mechanisms are not known. ⋯ Neither this rate, nor the magnitude of the sensitization (198 ± 63% of baseline) were different from that seen in cells not treated with NGF (3 of 25 cells sensitized (12.0%), 253 ± 70% of baseline). Pretreatment with the CB1 antagonist AM-251 (100 nM) prevented the effect of ACEA on NGF-induced sensitization. These results support the hypothesis that cannabinoids, acting through CB1 receptors, may produce analgesia in part by preventing NGF-induced sensitization of TRPV1 in afferent nociceptor nerve endings.
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Neuroscience letters · Aug 2013
Alterations of mean diffusivity in brain white matter and deep gray matter in Parkinson's disease.
Although Parkinson's disease is a neurodegenerative disease primarily involving basal ganglia and midbrain, the deficit of white matter is also involved during the disease progression. As the diffusion tensor imaging method is sensitive to the microstructural changes, we investigated the microstructural alterations in white matter and deep gray matter in patients with Parkinson's disease. Brain images of 64 patients and sex- and age-matched 64 healthy controls were obtained from a 3T MRI scanner. ⋯ There were white matter deficits in the corticofugal tract, cingulum, uncinate fasciculus, crus of fornix or stria terminalis, corpus callosum, external capsule, superior longitudinal fasciculus, posterior thalamic radiation including optic radiation, and the tracts adjacent to the precuneus and supramarginal gyrus, as indicated by higher mean diffusivity in Parkinson's disease patients than in controls. There were also deficits in the left putamen, pallidum, thalamus, and caudate as indicated by higher mean diffusivity in Parkinson's disease patients than in controls. Using diffusion tensor imaging and multi-methods of image analysis, we successfully characterized and visualized brain white matter and deep gray matter areas with microstructural deficits in Parkinson's disease patients.
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Neuroscience letters · Aug 2013
The inhibition of cocaine-induced locomotor activity by CART 55-102 is lost after repeated cocaine administration.
CART peptide is known for having an inhibitory effect on cocaine- and dopamine-mediated actions after acute administration of cocaine and dopamine. In this regard, it is postulated to be a homeostatic, regulatory factor on dopaminergic activity in the nucleus accumbens (NAc). ⋯ The loss of CART peptide's inhibitory effect did not return for up to 9 weeks after stopping the repeated cocaine administration. It may not be surprising that homeostatic regulatory mechanisms in the NAc are lost after repeated cocaine administration, and that this may be a mechanism in the development of addiction.
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Neuroscience letters · Aug 2013
Involvement of the dorsal hippocampal dopamine D2 receptors in histamine-induced anxiogenic-like effects in mice.
Anxiety-related behaviors increase histamine and dopamine release in the brain. On the other hand, central histamine counteracts reward and reinforcement processes mediated by the mesolimbic dopamine system. We investigated the effects of the histaminergic system and dopamine D2 receptors agents and their interactions on anxiety-related behaviors using the elevated plus-maze (EPM). ⋯ Histamine can decrease dopaminergic tone in the dorsal hippocampus through decreasing the endogenous dopamine release, whereas quinpirole does the same via the postsynaptic DA receptors' activation. Sulpiride however renders the same effect through autoreceptors' blockade and potentiated dopamine transmission. Thus, quinpirole and sulpiride seem to compensate the effects of the intra-CA1 injection of exogenous histamine, and tend to exert anxiolytic effects in the presence of histamine.
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Neuroscience letters · Aug 2013
Randomized Controlled TrialThe dopamine agonist apomorphine enhances conditioned pain modulation in healthy humans.
Although cumulative evidence suggests that dopamine plays a role in pain processing, the mechanisms by which dopaminergic transmission affects pain remain elusive. Conditioned pain modulation (CPM) is a psychophysical paradigm based on endogenous descending inhibitory pain modulation. The current study was aimed to test the effects of apomorphine, a non-specific dopamine agonist, on the magnitude of CPM in healthy subjects. ⋯ RM-ANOVA revealed a significant interaction between 'session' and 'time' factors (F=5.316, p=0.023, η=0.054), and significant effect for the 'session' (F=5.719, p=0.019, η=0.006), but not for the 'time' (F=0.586, p=0.446, η=0.057). These results suggest that dopaminergic pathways both participate in and enhance pain modulation, represented by CPM. The role of dopamine in pain processing should be further studied.