Neuroscience
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Supraoptic neurosecretory neurons express a prominent N-methyl-D-aspartate receptor system. Recent in vitro evidence reveals that N-methyl-D-aspartate receptor activation dramatically alters the spontaneous discharge patterns of supraoptic neurons. In this study we evaluate whether N-methyl-D-aspartate receptors in vivo contribute to the development of characteristic phasic discharge patterns displayed by vasopressin-secreting neurons. ⋯ Ketamine had no detectable effect on threshold or shape of antidromic action potentials. By comparison, the activity in 9/10 continuously active neurons (putative oxytocin-secreting) was unaffected by administration of identical doses of ketamine. These data suggest that N-methyl-D-aspartate receptors play an important role in regulating the onset and maintenance of spontaneous phasic activity patterns displayed by rat supraoptic vasopressin neurons in vivo.
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A recent study has described synchronous burst discharges of dentate hilar neurons and area CA3 pyramidal cells in the presence of the convulsants 4-aminopyridine and picrotoxin in guinea-pig hippocampal slices [Müller W. and Misgeld U. (1991) J. Neurophysiol. 65, 141-147]. To examine the synchronous activity of dentate cells and area CA3 pyramidal cells further, epileptiform burst discharges were examined in morphologically and/or electrophysiologically identified non-granule cells in the hilus and granule cell layer of the rat dentate gyrus and compared to simultaneously-recorded pyramidal cells of area CA3a, b, and c. ⋯ These findings suggest that, in the absence of GABAA receptor-mediated inhibition, excitatory pathways from area CA3 to the dentate gyrus are strong and widespread. These pathways, and possibly other mechanisms, can lead to tightly synchronized action potential discharge of pyramidal cells and dentate non-granule cells. The results also suggest that disinhibition alone is insufficient to cause synchronous bursts in the dentate gyrus, in contrast to area CA3.
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Comparative Study
Heterogeneity of evoked dopamine overflow within the striatal and striatoamygdaloid regions.
The heterogeneity of evoked dopamine overflow in vivo was examined and compared in striatal and striatoamygdaloid regions of the rat. The characteristics of appearance and disappearance rates and the maximum concentration elicited were determined from overflow curves measured by fast-scan cyclic voltammetry. Overall, the characteristics of evoked dopamine overflow were quite variable in the striatum compared to the relative uniformity of overflow in the basolateral amygdaloid nucleus. ⋯ In contrast, differences in evoked dopamine overflow within the striatoamygdaloid region were sharply defined dorsoventrally and appeared to be region-specific. Dopamine terminal fields in the striatum are not clearly demarcated into the caudate-putamen and nucleus accumbens, but may exist as a continuum. The uptake of dopamine appears to be the distinguishing characteristic for the regulation of extracellular dopamine levels in the striatum and the basolateral amygdaloid nucleus.
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In order to develop a rodent model displaying a progressive degeneration of the dopamine neurons of the substantia nigra, we bilaterally injected the tracer substance FluoroGold into the terminal field of the nigrostriatal projection, i.e. the striatum. One week later, rats received unilateral injections of 20 micrograms 6-hydroxydopamine into one of the two striatal tracer deposits. Groups of animals were killed one, two, four, eight and 16 weeks later. ⋯ We conclude that injection of 6-hydroxydopamine into the terminal field of nigral dopaminergic neurons causes a progressive degeneration of these cells, starting between one and two weeks after lesion and continuing over eight to 16 weeks. This degeneration is preceded, and accompanied by, cellular atrophy and a partial loss of marker enzyme expression, thus yielding an animal model which mimics the degenerative processes in Parkinson's disease more closely than the animal models available so far. The present model may be helpful in investigating the in vivo effects of putative neuroprotective agents and neurotrophic factors.