Neurons in the nucleus accumbens septi in brain slices from adult male rats were studied with patch clamp recording in the whole-cell conformation. Cells filled with Lucifer Yellow were identified as medium spiny neurons. Electrical stimulation close to the recorded cell evoked excitatory and inhibitory synaptic currents. In the presence of picrotoxin or bicuculline, stimulation at a holding potential of -90 mV evoked an inward excitatory current that was blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM), identifying it as an excitatory postsynaptic current (EPSC) mediated by glutamate acting at AMPA/kainate receptors. Serotonin (5-hydroxytryptamine, 5-HT; 3-100 microM in the bath) decreased the EPSC in about 90% of the cells. The action of 5-HT was mimicked by N-(3-trifluoromethylphenyl)-piperazine HCl (TFMPP), but not by (+/-)-8-hydroxydipropylaminotetralin (8-OH-DPAT) or (+/-)-2,5-dimethoxy-4-iodoamphetamine HCl (DOI). The 5-HT effect was antagonized by pindolol or cyanopindolol, but not by spiperone, ketanserin or tropisetron. Taken together, these results indicate that 5-HT acts at 5-HT1B receptors. The effect of 5-HT was potentiated by cocaine (0.3-3 microM) or the selective serotonin reuptake inhibitor citalopram. Miniature synaptic currents recorded in the presence of tetrodotoxin were inhibited by CNQX, identifying them as spontaneous miniature EPSCs. 5-HT reduced the frequency of these miniature EPSCs without affecting their amplitude, which indicates a presynaptic site of action. This presynaptic inhibition by 5-HT might be involved in the behavioural effects of cocaine.

This is the first study to show that patients who subsequently had chronic hydrocephalus requiring CSF shunting were associated with higher CSF levels of ferritin in the acute stage of SAH. Higher CSF ferritin levels may not reflect the amount of blood in the subarachnoid space that was intracranially metabolized, but rather more intense subarachnoid inflammatory reactions which may cause chronic hydrocephalus after SAH.

This is the first study to show that higher levels of bilirubin and ferritin in the cerebrospinal fluid after SAH were associated with no vasospasm in clinical settings. These findings support the concept that the induction of HO-1 and ferritin may be an intrinsic regulatory mechanism that acts against cerebral vasospasm.

Background and Purpose-We report the first case of pituitary apoplexy caused by the rupture of an intracavernous carotid artery aneurysm embedded in a pituitary adenoma. Case Description-A 46-year-old man presented with clinical and CT findings typical of pituitary apoplexy. MRI showed an unusual flow-void protrusion into the intratumoral hematoma, which, however, was not diagnosed as a ruptured aneurysm until severe intraoperative bleeding occurred. Angiography after surgery revealed an intracavernous carotid artery aneurysm. Conclusions-The

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Neuropathic pain induced by sciatic nerve injury not only causes peripheral dysfunctions but also affects the cortical and subcortical regions of the brain. It is still unknown whether neuropathic pain could relate to behavioral and neurochemical alterations in the central nervous system. This paper deals with the effect of peripheral neuropathic pain on mechanical allodynia, neuropeptide levels, neuropeptide-degrading enzyme activities, and microglial cells in the brain regions of rats by applying chronic constriction injury, a partial sciatic nerve injury. We examined the possible protection effect on the allodynia and changes in levels of neuropeptides and microglial activation in chronic constriction injury of the rat brain by memantine. On 4 days after chronic constriction injury, the induction of mechanical allodynia was suppressed by memantine treatment. Reductions in the substance P in the hypothalamus and somatostatin in the periaqueductal gray of chronic constriction injury rat brain were reversed by memantine. This suggests the role of these neuropeptides in pain information processing in the brain. Immunohistochemical experiments revealed that the expression of CD11b, a marker protein of microglia, was increased in the hypothalamus and periaqueductal gray in the chronic constriction injury rat brain as compared with the controls, and memantine treatment could suppress the activation of microglia, suggesting the involvement of microglia in pain mechanism. The present behavioral, biochemical, and immunohistochemical studies demonstrated that peripheral neuropathic pain affects the neuropeptide levels and microglial activation in the brain regions, and these events described above may play an important role in neuropathic pain pathogenesis.

Objective: To determine the incidence and clinical characteristics of spontaneous haemorrhage into metastatic brain tumours after radiosurgery. Methods: Intratumour haemorrhage rate, clinical features, and treatment were evaluated in 54 patients with 131 brain metastases of varying origin who were treated using linear accelerator radiosurgery. The marginal dose was maintained constant at 20 or 25 Gy, irrespective of tumour size. Results: Haemorrhage was identified in 7.4% of the metastases (five tumours in four patients) before radiosurgery and in 18.5% (10 tumours in 10 patients) after radiosurgery. In three cases, haemorrhage into the tumour after radiosurgery was symptomatic. Half the haemorrhages occurred within one month of radiosurgery. The changes in tumour size observed at the time of haemorrhage were an increase in one tumour, no change in five, and a decrease in four. Haemorrhage into a tumour after radiosurgery was more likely to occur in female patients, in tumours with a larger volume on pretreatment neuroimaging, and in tumours treated with a larger number of isocentres or a higher maximum dose. Haemorrhagic features in the patients or their tumours on presurgical assessment were not disposing factors to haemorrhage after radiosurgery. Conclusions: When larger brain metastases are aggressively treated by radiosurgery, better local control may be attained but there may also be a higher risk of haemorrhage soon after the treatment.

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