This review is directed at understanding how neuronal death occurs in two distinct insults, global ischemia and focal ischemia. These are the two principal rodent models for human disease. Cell dea...

Ischemic Cell Death in Brain Neurons

Dendritic spines, the tiny protrusions that stud the surface of many neurons, are the location of over 90% of all excitatory synapses that occur in the CNS. Their small size has, in large part, made them refractory to conventional experimental approaches. Yet their widespread occurrence and likely involvement in learning and memory has motivated extensive efforts to obtain quantitative descriptions of spines in both steady state and dynamic onditions. Since the seminal mathematical analyses of D’Arcy Thompson (1992), the power of quantitatively establishing key parameters of structure has become recognized as a foundation of successful biological inquiry. For dendritic spines, highly precise determinations of structure and its variation are again proving to be essential for establishing a valid concept of function. The recent conjunction of high quality information about the structure, function, and theoretical implications of dendritic spines has, in fact, produced a flurry of

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Dendritic spines: cellular specializations imparting both stability and flexibility to synaptic function.

Basal lamina grafts for reconnecting severed nerves are prepared from muscle by removing cellular material therefrom while preserving the tubular structure of the basal lamina. When connected to nerve stumps the basal lamina surfaces promote axon regeneration therethrough, eventually reestablishing nerve function through the regenerated graft.

Peripheral nerve regeneration

Neurodegeneration in Excitotoxicity, Global Cerebral Ischemia, and Target Deprivation: A Perspective on the Contributions of Apoptosis and Necrosis

Mismatches between neurotransmitter and receptor localizations in brain: observations and implications.

This report provides findings of an investigation of the influence of traumatic subarachnoid hemorrhage on the development of delayed cerebral ischemia caused by vasospasm. The authors prospectively studied 130 patients with closed-head trauma, who exhibited subarachnoid blood on admission computerized tomography (CT) scans. Ten (7.7%) of these patients developed delayed ischemic symptoms between Days 4 and 16 after the head injury. They consisted of three (3.0%) of 101 patients with small amounts of subarachnoid blood and seven (24.1%) of 29 patients with massive quantities of subarachnoid blood on admission CT scans. In each of the 10 patients, severe vasospasm was demonstrated by angiography performed soon after development of ischemic symptoms. There was a close correlation between the main site of the subarachnoid blood and the location of severe vasospasm. In seven of the patients, follow-up CT scans showed development of focal ischemic areas in the cerebral territories corresponding to the vasospastic arteries. These results demonstrate that traumatic subarachnoid hemorrhage, especially if massive, is a predictable indicator of delayed ischemic symptoms.

Traumatic subarachnoid hemorrhage as a predictable indicator of delayed ischemic symptoms

FPF1070 is an aqueous protein-free solution, which consists of 85% free amino acids and 15% small peptides. Our previous study showed a potent neurotrophic factor-like activity in cultured embryonic cells of dorsal root ganglia. The present study investigated whether FPF1070 regenerated the cholinergic cells in the medial septal nucleus after axonal transections by cutting the fimbria-fornix. Fimbrial transection reduced the number of septal cholinergic cells by 30 +/- 3.6%, compared with the number on contralateral sides at 4 weeks. Intraperitoneal injections of FPF1070 caused 49.9 +/- 6.3% of the cholinergic neurons to survive. Furthermore, the cell sizes of the cholinergic neurons were significantly different: 16.4 +/- 4.2 microns, 14.3 +/- 3.8 microns in FPF1070 treatment and vehicle treatment, respectively. These results indicated that FPF1070 prevents the degeneration and atrophy of impaired cholinergic neurons by systemic administration.

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Neurotrophic factor-like effect of FPF1070 on septal cholinergic neurons after transections of fimbria-fornix in the rat brain.

The present study is a chronological morphological examination on the effects of collagen gel matrix on regeneration of severed sciatic nerves. The nerves (5 mm length) were resected, and both the distal and proximal stumps were inserted into a silicone tube with 5 mm gap in between. In the test side, the gap in the tube was then injected with liquid collagen which gels in the tissue when reconstructed with a certain buffer solution. The gap space in the tube of the control side was left empty. In a chronological examination of the tissue in the tube, considerably more rapid growth of sprouting axons toward the distal stump in the test side was revealed in comparison with the control side. The cells, including both fibroblasts and larger Schwann cells, were less in number. More orderly directions were observed in the collagen matrix than in the control tube. The result indicates that regeneration of the peripheral nerves in the silicone tube can be improved, by using appropriate exogenous fine materials, collagen matrix.

A morphological study on the effects of collagen gel matrix on regeneration of severed rat sciatic nerve in silicone tubes.

Ultrastructural damage leading to delayed neuronal death was investigated in the mid-CA1 region of the hippocampus from the stratum (str.) moleculare to oriens after transient bilateral forebrain ischemia in Mongolian gerbils. After ischemia for 5 min without recirculation, mild swelling of the peripheral part of the apical and basal dendrites was already apparent in the str. moleculare and str. oriens. Mitochondria in the dendrites were also swollen in the same area. During recirculation for 12 h to 3 days, swelling of the dendritic cytoplasm persisted with formation of microvacuoles, but swelling of mitochondria receded. Microvacuolation and loss of microtubules were also observed in the proximal part of the dendrites during this period, and swelling and disruption of internal cristae were observed in mitochondria after recirculation for 3 days. The dendrites became severely degenerated after recirculation for 4 days. In the pyramidal cell bodies, no abnormality was observed at the end of ischemia for 5 min, but disaggregation of polyribosomes and swelling of the endoplasmic reticulum were observed 12 h after recirculation. Proliferation of the endoplasmic reticulum in parallel arrays occurred after recirculation for 1 day and persisted. Severe degeneration of the pyramidal cell bodies was obvious after recirculation for 4 days. The findings observed in the present investigation suggested that the neuronal structure most vulnerable to ischemia was the peripheral part of the dendrites and postischemic neuronal damage occurred early in this part of the dendrites.

Fumiharu Akai

Papers

Traumatic subarachnoid hemorrhage as a predictable indicator of delayed ischemic symptoms

Neurotrophic factor-like effect of FPF1070 on septal cholinergic neurons after transections of fimbria-fornix in the rat brain.

A morphological study on the effects of collagen gel matrix on regeneration of severed rat sciatic nerve in silicone tubes.

Ultrastructural investigation of the CA1 region of the hippocampus after transient cerebral ischemia in gerbils

Immunocytochemical localization of manganese superoxide dismutase (Mn-SOD) in the hippocampus of the rat.