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Biomedical subjects

Ken Ikeda

Publications and source records attributed to Ken Ikeda.

43 records · Page 3Linked to original sources
PubMed2002

Trophic effect of olmesartan, a novel AT1R antagonist, on spinal motor neurons in vitro and in vivo.

Olmesartan is a novel compound which has been shown to exhibit various neuropharmacological effects. For the purpose of clarifying the effect of Olmesartan on spinal motor neurons, we studied the following tests. We studied the effect in vitro of Olmesartan on neurite outgrowth and choline acetyltransferase (ChAT) activity in primary explant cultures of ventral spinal cord (VSCC) of fetal rats. Olmesartan-treated VSCC, compared with control VSCC, had a significant neurite outgrowth and increased activity of ChAT. The effect was dose-related in neurite outgrowth. However, there was no relationship between activity of ChAT andgiven doses of Olmesartan. We examined in vivo the effect of Olmesartan on axotomized spinal motor neuron death in the rat spinal cord. After post-natal unilateral section of sciatic nerve, there was approximately a 50% survival of motor neurons in the fourth lumbar segment. In comparison with vehicle, intraperitoneal injection of Olmesartan for consecutive 14 days reduced spinal motor neuron death. There was no relationship between number of surviving neurons and doses of Olmesartan. These in vitro and in vivo studies showed that Olmesartan has a neurotrophic effect on spinal motor neurons. Our data suggest a potential therapeutic use of Olmesartan in treating diseases that involve degeneration and death of motor neurons, such as motor neuropathy and amyotrophic lateral sclerosis.

Amyotrophic Lateral Sclerosis↗
PubMed2002

Neuroprotective actions of FK506 and cyclosporin A on motor neuron survival following neonatal axotomy.

We show that nonimmunosuppressive analogues of the immunosuppressive drugs FK506 and cyclosporin A (CsA) rescue axotomized neonatal motor neuron death. Unilateral sciatic nerve was transected in neonatal rats. Animals were then treated daily with different doses of FK506 and CsA for 14 days with intraperitoneal injection. Control rats received phosphate buffer saline (PBS) in the same fashion. After treatment, the number of spinal motor neurons was determined at L4 level. In comparison with vehicle, both FK506 (5.0 mg kg(-1)) and CsA (10.0 mg kg(-1)) rescued motor neuron death in a similar way. These results indicate therapeutic relevance in the treatment of damaged motor neuron disorders, such as motor neuropathy or amyotrophic lateral sclerosis.

Animals↗
PubMed2002

Protective effect of interleukin-3 and erythropoietin on motor neuron death after neonatal axotomy.

Several members of hematopoietic factors are known to have neuroprotective effects against axotomized motor neuron death. We carried out a study to determine whether interleukin-3 (IL-3) and erythropoietin (EPO) rescue spinal motor neuron death following axotomy. Unilateral sciatic nerve was transected in neonatal rats. Different doses of IL-3, EPO, or vehicle were administered daily for two weeks by intraperitoneal injection. After treatment, the number of spinal motor neurons was determined at the level of L4 segment In comparison with vehicle, both IL-3 (10 microg kg(-1)) and EPO (5.0 mg kg(-1)) significantly prevented the loss of motor neurons. Protective potentials is the same between them. These results suggest that IL-3 and EPO play a role for motor neuron survival in vivo and suggest the potential use of these hematopoietic factors in treating diseases that involve degeneration and death of motor neurons, such as motor neuropathy and amyotrophic lateral sclerosis.

Animals↗
PubMed2002

Unusual fatty infiltration of the soleus muscle in a patient with congenital nemaline myopathy: fat-suppression muscle MRI.

A 27-year-old man developed gait disturbance over a three-year period. Histochemical analysis suggested nemaline bodies, type I fiber atrophy and type II fiber hypertrophy. Conventional magnetic resonance imaging (MRI) showed a severe degree of homogenous hyperintensity in the soleus muscle. Fat-suppression MRI exhibited marked diffuse hypointensity in the soleus muscle. MRIs demonstrated unusual fatty proliferation of the soleus muscle. Fat-suppression MRI of skeletal muscles is beneficial in evaluating the accurate topography and degree of fatty infiltration. Radiological patterns of muscle damage are variable in patients with congenital nemaline myopathy, similar to the heterogeneous clinical aspects.

Adipose Tissue↗
PubMed2002

Acetazolamide-induced muscle weakness in hypokalemic periodic paralysis.

A 46-year-old man with hypokalemic periodic paralysis (HypoPP) and diabetes mellitus (DM) had worsened muscle weakness after acetazolamide (ACZ) treatment. During the paralytic episode, serum potassium levels were reduced, and serum chloride and insulin levels were increased. The data suggested proximal renal tubular acidosis due to ACZ. We determined arterial-venous concentrations of potassium, insulin and glucose across the forearm. Venous potassium levels were markedly reduced. ACZ is thought to potentiate potassium uptake into muscles. Hyperinsulinemia and DM could contribute to ACZ-induced exacerbation in our patient. We should pay more attention to ACZ-treated HypoPP patients with hyperinsulinemia and DM.

Acetazolamide↗
PubMed2002

Molecular and cellular mechanism of glutamate receptors in relation to amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder of the central nervous system (CNS) with an unknown etiology. This disorder is characterized clinically by muscular weakness and wasting, and pathologically by selective degeneration of the corticospinal tracts and motor neurons of the brain stem and spinal cord. Median survival following onset is 3 to 5 years. Riluzole, an antiglutamatergic agent has been shown to have modest beneficial effects on survival. Glutamate is the main excitatory neurotransmitter in the CNS and excessive activation of glutamate receptors is excitotoxic to neurons. Glutamate receptor-mediated excitotoxicity has been proposed to explain the pattern of selective neuronal cell death and clinical manifestation of ALS. Activation of glutamate receptors leading to elevation of intracellular calcium may play a major role. This review will focus on the current understanding of the molecular and cellular mechanisms of glutamate receptors in relation to ALS.

Amyotrophic Lateral Sclerosis↗