Neuroscience
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High frequency stimulation (HFS) of the subthalamic nucleus (STN) has been performed to reverse motor dysfunction in severe parkinsonian patients. Recent studies suggested that neural circuitry in the basal ganglia might regulate micturition function as well. In 15 adult male cats under ketamine anesthesia, in which spontaneous isovolumetric micturition reflex had been generated, we performed electrical stimulation and extracellular single unit recording in the STN. ⋯ All neurons were tonically active throughout storage/micturition cycles with storage phase predominance, with almost constant firing activities during the storage phase. In conclusion, our results showed that HFS-STN inhibited the micturition reflex and there were micturition-related neuronal firings in the STN in cats, suggesting the STN may be involved in neural control of micturition. The results also provide an implication that clinical HFS-STN may alter urinary function in parkinsonian patients.
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Comparative Study
The eyes suppress a circadian rhythm of FOS expression in the suprachiasmatic nucleus in the absence of light.
Photic information transmitted from the eyes to the suprachiasmatic nucleus (SCN) is essential for entrainment of circadian behavioral and physiological rhythms in mammals. Under conditions of constant darkness, these rhythms are maintained by the circadian pacemaker cells of the SCN [Bioessays 22 (2000) 23]. ⋯ Indeed, it was shown recently that removal of the eyes abolishes an endogenous circadian rhythm within cells of the SCN [Nat Neurosci 6 (2003) 111], a finding that led to the suggestion that specific rhythms of the SCN are driven by input from the eyes. In contrast, we show here that removal of the eyes amplifies a normally dampened endogenous circadian rhythm within the SCN, indicating that the eyes can suppress the expression of specific rhythms within the SCN while promoting others.
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Comparative Study
Non-apoptotic neurite degeneration in apoptotic neuronal death: pivotal role of mitochondrial function in neurites.
The length and thinness of neurites render them greatly susceptible to a variety of insults. Accumulating evidence suggests that neurite degeneration is not a passive, but an active and causative, event in some neurodegenerative diseases. Nonetheless, the mechanisms underlying neurite degeneration remain largely unknown. ⋯ In contrast, neurites of mutant neurons were markedly resistant to vinblastine-induced degeneration, and both the MMP and the ATP content in the neurites were well maintained. Exposure of mutant neurons to carbonyl cyanide m-chlorophenyl-hydrazone, an uncoupler, caused extreme neurite degeneration following rapid MMP loss. Collectively, our findings suggest that: 1) neurite degeneration is regulated through a non-apoptotic process achieved by mitochondrial dysfunction in neurites; 2) the mitochondrial functional status is controlled separately in neurites and in the neuronal soma.
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Fatty acid amide hydrolase (FAAH) catalyses hydrolysis of the endocannabinoid arachidonoylethanolamide ("anandamide") in vitro and regulates anandamide levels in the brain. In the cerebellar cortex, hippocampus and neocortex of the rat brain, FAAH is located in the somata and dendrites of neurons that are postsynaptic to axon fibers expressing the CB(1) cannabinoid receptor [Proc R Soc Lond B 265 (1998) 2081]. This complementary pattern of FAAH and CB(1) expression provided the basis for a hypothesis that endocannabinoids may function as retrograde signaling molecules at synapses in the brain [Proc R Soc Lond B 265 (1998) 2081; Phil Trans R Soc Lond 356 (2001) 381] and subsequent experimental studies have confirmed this [Science 296 (2002) 678]. ⋯ Here FAAH may nevertheless influence endocannabinoid signaling but more remotely. Finally, there are regions of the brain where FAAH-immunoreactive neurons and/or oligodendrocytes occur in the absence of CB(1)-immunoreactive fibers and here FAAH may be involved in regulation of signaling mediated by other endocannabinoid receptors or by receptors for other fatty acid amide signaling molecules. In conclusion, by comparing the distribution of FAAH and CB(1) in the mouse brain, we have provided a neuroanatomical framework for comparative analysis of the role of FAAH in regulation of the spatiotemporal dynamics of retrograde endocannabinoid signaling in different regions of the brain.
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For peripheral iron to reach the brain, it must transverse the blood-brain barrier. In order for the brain to obtain iron, transferrin receptors are present in the vascular endothelial cell to facilitate movement of transferrin bound iron into the brain parenchyma. However, a number of significant voids exist in our knowledge about transport of iron into the brain. ⋯ Blocking pinocytosis had no effect on either transferrin or iron transcytosis. These results indicate that there is both transferrin-mediated and non-transferrin-mediated transcytosis of iron and that the process is influenced by the iron status of the cells. These data have considerable implications for common neurodegenerative diseases that are associated with excess brain iron accumulation and the numerous neurological complications associated with brain iron deficiency.