Brain research
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We investigated the effect of methylprednisolone on pathophysiological alterations in experimental pneumococcal meningitis. Untreated rats injected with pneumococcal cell wall components after hydrolization with M1 muramidase (PCW-M) developed an increase of regional cerebral blood flow (rCBF; 165.0 +/- 12.8%, baseline 100%, mean +/- S. E. ⋯ However, methylprednisolone did not inhibit the increase of rCBF (163.5 +/- 13.7% and 160.9 +/- 6.8%, resp.), whereas dexamethasone significantly attenuated microvascular changes. Hypercapnia-induced reactivity of cerebral vessels tested 8 h after i.c. injection was preserved in all groups. In conclusion, we found that methylprednisolone significantly attenuated the increase of brain water content, ICP and CSF WBC count, but had no effect on microvascular changes during the early phase of experimental pneumococcal meningitis.
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Synaptic inhibition in rat spinal cord is mediated by the amino acids gamma-aminobutyric acid (GABA) and glycine. Most spinal cord neurons respond to both neurotransmitters, suggesting co-expression of GABAA- and strychnine-sensitive glycine-receptors in individual cells. While the distribution of glycine-receptors has been extensively characterized, much less is known about the cellular localization of GABAA-receptors in spinal cord neurons. ⋯ Double-immunofluorescence staining showed that most GABAA-receptor-positive cells in layers III-VIII and X also exhibited a prominent glycine-receptor immunoreactivity. Both types of receptors had very similar distribution patterns in the cell membrane and were frequently co-localized in sites apposed to GABAergic axon terminals. These results indicate that GABAA- and glycine-receptors may co-exist within single postsynaptic densities, suggesting a possible synergism in the action of GABA and glycine in spinal cord neurons.
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Comparative Study
Rostral-caudal differences in effects of nucleus accumbens amphetamine on VTA ICSS.
The effects of amphetamine along the rostrocaudal axis of the nucleus accumbens (NAcc) on ventral tegmental area (VTA) intracranial self-stimulation (ICSS) were studied. Eighteen rats were trained to lever press for ICSS in the VTA. Rate-frequency functions were determined by logarithmically decreasing the frequency of cathodal pulses in a stimulation train from a value that induced maximal responding to one that induced no responding (thresholds). ⋯ Further analyses revealed a significant positive correlation (r13 = 0.51, P < 0.05) between the site of injection along the rostrocaudal axis of the NAcc and the size of the amphetamine-produced potentiation of VTA stimulation reward. Others have reported topographical differences, including dopamine terminal density and D1 receptor density, in the NAcc. The present results indicate that these anatomical and neurochemical differences appear to be correlated with behavioural differences.
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The effects of chronic 'continuous' infusion and 'intermittent' modes of levodopa/carbidopa administration on apomorphine induced circling behaviour, DA uptake sites (labelled with [3H]mazindol) and D1 and D2 DA receptor binding (labelled with [3H]SCH 23390 and [3H]sulpiride, respectively) were investigated in rats with unilateral 6-OHDA lesions of the medial forebrain bundle. The circling behaviour in response to apomorphine was greatly enhanced following chronic 'intermittent' but not 'continuous' levodopa treatments. Following the 'intermittent' regime, the lower dose of apomorphine induced a period of intense circling with delayed onset and rapid offset, than in rats given either 'continuous' infusion of levodopa or saline. ⋯ This asymmetry in striatal [3H]sulpiride binding was reduced in both groups of rats receiving levodopa. [3H]sulpiride binding in the NAc and OT and [3H]SCH 23390 binding in the striatum, NAc, OT and SNr were unaffected by DA denervation or either regime of levodopa treatments. 'Continuous' infusion and not 'intermittent' injections of levodopa reduced [3H]mazindol binding in the striatal subregions and the frontal cortex on both the denervated and intact sides. The potentiation of the behavioural response to apomorphine by chronic 'intermittent' levodopa treatment does not correspond with the levodopa induced alterations in striatal or extrastriatal DA receptors. In the same group of animals the narrowing of the duration of response to the lower dose of apomorphine may mimic the fluctuations in response to levodopa, seen clinically in long-term levodopa treated parkinsonian patients.
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Intracellular recordings from neurons in the dorsal root ganglion (DRG) and dorsal horn (DH), in an in vitro spinal cord-dorsal root ganglion preparation, were used to investigate the role of tetrodotoxin-resistant (TTX-R) afferent fibers in the sensory synaptic transmission in the superficial DH. Bath application of 25-50 mM potassium to the DRG depolarized the DRG neurons, blocked action potentials in the large neurons, evoked action potentials in slow conducting neurons, and synaptically excited dorsal horn neurons. Excitatory postsynaptic potentials (EPSP) which were evoked in DH neurons by electrical stimulation of large myelinated fibers, but not those evoked by stimulation of small unmyelinated fibers, were blocked by the potassium treatment of the primary afferents. ⋯ Furthermore, high potassium potentiated electrically evoked, TTX-resistant EPSPs in the majority of neurons. This effect was abolished in Na(+)-free solution. These findings indicate that high [K+]e applied to the DRG, dorsal root and peripheral process selectively activates a primary afferent input to the DH, which is sodium-dependent and tetrodotoxin resistant.