Makoto Furuichi

Growth of totally thrombosed giant aneurysm within the posterior cranial fossa

SummaryWe report a case in which growth of a totally thrombosed giant aneurysm of the posterior cranial fossa was demonstrated by computed tomography (CT) scans repeated after 4 years. A magnetic resonance (MR) image demonstrated an onion-skin-like, laminated structure within a calcified wall. The laminated structure had developed around an old thrombosis, without any communication to the flowing blood. It showed intensities indicating recent clots, revealing that the giant aneurysm had grown by recurrent intramural hemorrhage rather than by intraluminal accumulation of thrombotic materials. This case illustrates that totally thrombosed giant aneurysms still have the potential of growth.

Post-ischemic potentiation of Schaffer collateral/CA1 pyramidal cell responses of the rat hippocampus in vivo: involvement of N-methyl-d-aspartate receptors

The present study examined the functional changes in the hippocampal CA1 pyramidal cell system in vivo occurring after 12-min forebrain ischemia in the rat. A population excitatory postsynaptic potential and orthodromic population spike of CA1 pyramidal cells to stimulation of the Schaffer collaterals were potentiated at 6-8 h post-ischemia. These changes were not associated with an increase in excitability of the CA1 pyramidal cells as evaluated from the antidromic population spike induced by alveus stimulation, suggesting the presence of an increased synaptic efficacy. The post-ischemic potentiation was prevented by pretreatment with the N-methyl D-aspartate (NMDA) receptor antagonist, MK801, in a dose-dependent manner. These findings suggest that 12-min forebrain ischemia in the rat activates NMDA receptors, which results in an increase in synaptic efficacy to the CA1 pyramidal cells at 6-8 h post-ischemia.

N-methyl-D-aspartate receptor-mediated, prolonged afterdischarges of CA1 pyramidal cells following transient cerebral ischemia in the rat hippocampus in vivo.

We previously reported the post-ischemic potentiation (PIP) of synaptic efficacy in hippocampal Schaffer collateral/CA1 responses of the rat beginning at 6-8 h following 12 min transient cerebral ischemia in vivo. The present study demonstrated that repetitive stimulation with a relatively low frequency (5 Hz, 6 s), which produced short-lasting afterdischarges (ADs; duration, 4.49 +/- 4.26 s; n = 7) in sham-controls, resulted in prolonged ADs (duration, 26.33 +/- 12.63 s; n = 6; P < 0.001) at the same period after ischemia. The PIP was not affected by 2-amino-5-phosphonovalerate (APV) administered via microdialysis at 7 h post-ischemia. The prolonged ADs in response to repetitive stimulation were, however, reversed to short-lasting ADs (duration, 7.13 +/- 1.44 s; n = 4; P < 0.02) by the same procedure, leaving the response to single stimulation unaffected. These findings suggest that, during the reperfusion period, Ca2+ influx into the CA1 pyramidal cells can be greatly increased through N-methyl-D-aspartate (NMDA) receptor-coupled ion channels if appropriately timed multiple synaptic inputs bombard these cells. Such Ca2+ influx may contribute to delayed death of CA1 pyramidal cells after transient cerebral ischemia if synaptic activity is maintained at relatively high levels during the reperfusion period.

Impairment of hippocampal long-term potentiation following transient cerebral ischaemia in rat: Effects of bifemelane, a potent inhibitor of ischaemia-induced acetylcholine release

The present study examined the changes in the long-term potentiation (LTP) of the hippocampal Schaffer collateral/CA1 pyramidal cell system in vivo occurring after 12-min forebrain ischaemia in the rat. A population spike (PS) of CA1 pyramidal cells were recorded in 18 rats at 7 h post-ischaemia. While the threshold and amplitude of pretetanic PS were not depressed, the induction of LTP was significantly impaired following ischaemic insult (155 +/- 28% of baseline PS, mean +/- SD, n = 6, p < 0.001), as compared to sham-controls (337 +/- 84%, n = 5), without reduction of single pulse responses. Pretreatment with 4(o-benzylphenoxy)-N-methylbutylamine hydrochloride (Bifemelane; 50 mg kg-1 i.p.) slightly but significantly attenuated the impairment in LTP induction (196 +/- 23%, n = 6; p < 0.02). The findings in the present study indicate that CA1 pyramidal cells are dysfunctional in synaptic plasticity long before their death. Bifemelane has been demonstrated to inhibit acetylcholine release strongly during cerebral ischaemia but not interfere with normal cholinergic synaptic transmission. The effect of bifemelane suggests that Ach release during ischaemia is partially involved in the post-ischaemic impairment of LTP induction.

Pleomorphic xanthoastrocytoma: Ultrastructural study and origin of the tumor

An origin for the tumor cells of a pleomorphic xanthoastrocytoma (PXA) in a 50‐year‐old female is proposed on the basis of electron microscopic findings. The tumor was located in the superficial supratentorial region. Cytoplasmic positivity for GFAP in both the spindle cells and most of the bizarre giant cells was revealed by immunostaining, indicating an astocytic origin of the tumor. The presence of relatively few organelles, abundant filaments and microtubules, as demonstrated by electron microscopy, also indicated characteristics of astrocytes. Ultrastructural examinations revealed the existence of basal laminas in the extracellular space surrounding the surface of the tumor cells and the presence of localized cytoplasmic densities associated with the plasma membrane adjacent to the basal lamina resembling hemidesmosomes. This suggests a close relationship between the basal lamina and astrocytes, such as that between astrocytes and the investing basal in the glia limitans. The structures strongly indicated a cell origin for PXA that was not from non‐specific astrocytes with secondary proliferation of meningeal fibroblasts, but from astrocytes in the glia limitans with investing basal lamina.

Fine structure of epithelioid cells in cerebral tuberculoma

The ultrastructure of epithelioid cells from a tuberculous granuloma in the cerebrum of a 26‐year‐old male was studied. Light microscopic examinations of the border zone of the brain tuberculoma constantly revealed epithelioid cells. Fine structural examinations demonstrated two main types (type 1 and type 2) of epithelioid cells. Both types of epithelioid cells contained similar large pale nuclei. The cell membrane had many finger‐like processes interdigitating with those of the adjacent cells. The type 1 cells were distinguished by the presence of abundant organellae such as lamellar rough endoplasmic reticulum and mitochondria making a dark tone of cytoplasm. The type 2 cells showed a pale cytoplasm containing a few Golgi complexes and associated variably shaped vesicles. Another finding of note in the type 2 cells was the presence of subplasmalemmal linear densities (SLD). The morphology of the type 1 epithelioid cells was reminiscent of that of plasma cells displaying a biosynthetic function. Type 2 epithelioid cells with SLD, however, appeared to have a reduced biosynthetic function and to have contributed to a persistence of the granuloma structure. Neither type revealed identifiable phagocytosed material, and evidence of pinocytosis was practically absent. The presence of morphologic features of transitional cells, intermediate between type 1 and type 2 cells, suggests that these cells are related. It appears likely that type 1 is an early form of type 2. This is supported by the fact that type 2 corresponded roughly to the type ‘B’, which is thought to be a terminal‐stage cell. Furthermore, dying cells exhibited the structure of type 2 rather than type 1 cells.

Prolonged Stimulation-Induced Afterdischarges of Hippocampal CA1 Pyramidal Cells After Ischemia In Vivo

Transient cerebral ischemia causes selective death of hippocampal CA1 pyramidal cells after a period of 3–5 days [1]. We previously demonstrated that Schaffer collateral/CA1 responses of the rat are potentiated beginning at 6–8 h after transient cerebral ischemia in vivo [2]. The present study examined whether the utilization of N-methyl-d-aspartate (NMDA) receptorcoupled ion channels is increased or not during the period in which postischemic potentiation (PIP) of Schaffer collateral/CAl responses is observed.