Effects of prolonged weak anodal direct current on electrocorticogram in awake rabbit.

The effects of prolonged weak anodal direct current (DC) on the electrocorticogram (ECoG) were investigated in awake rabbits. When the current (20-40 microA) was applied to the motor region of the cerebral cortex, seizure activity in the ECoG appeared from the frontal cortex. Repeated application of the DC decreased the threshold current for producing the seizure activity. Diazepam significantly elevated the threshold of the seizure activity. In contrast to the marked changes in the ECoG, no behavioral changes were observed during or after the application of weak anodal DC. The changes in the ECoG are discussed in relation to the intensity and duration of the DC.</p

Development of a method for environmentally friendly chemical peptide synthesis in water using water-dispersible amino acid nanoparticles

Due to the vast importance of peptides in biological processes, there is an escalating need for synthetic peptides to be used in a wide variety of applications. However, the consumption of organic solvent is extremely large in chemical peptide syntheses because of the multiple condensation steps in organic solvents. That is, the current synthesis method is not environmentally friendly. From the viewpoint of green sustainable chemistry, we focused on developing an organic solvent-free synthetic method using water, an environmentally friendly solvent. Here we described in-water synthesis technology using water-dispersible protected amino acids

The cyclic AMP-generating system of cobalt-induced epileptic cerebral cortex

A cobalt chloride solution was injected into the unilateral sensorimotor cortex of rats to induce epileptic activity. The cyclic AMP contents of slices incubated with or without adenosine and 2-chloroadenosine were determined in four cortical areas after electroencephalography and behavioral examination in cobalt-injected rats. Electrographic spike activity appeared immediately after injection of cobalt. In the majority of cobalt-injected rats, the spike activity was dominant in the primary epileptic region of the cortex. The spike frequency reached a maximum level two to three weeks after the injection and declined thereafter. The electrographic activity was followed by abnormal behavior. Adenosine and 2-chloroadenosine elevated the cyclic AMP levels in the cortical slices 6-to 10-fold and 10-to 16-fold, respectively. The elicitation of cyclic AMP accumulation was strongly inhibited by the adenosine antagonist 8-phenyltheophylline. The cyclic AMP accumulation elicited by adenosine or 2-chloroadenosine was increased in the primary cortical area of cobalt-induced epilepsy, but in the other cortical areas there was no deviation in cyclic AMP accumulation. The increase in cyclic AMP accumulation was observed regardless of the presence or absence of the adenosine uptake inhibitor dipyridamole, phosphodiesterase inhibitor Ro 20-1724, and adenosine deaminase. The increased accumulation of cyclic AMP in the primary epileptic cortex was detected as early as 8 days after the injection. The cyclic AMP accumulation slightly increased thereafter. It reached a plateau 17 to 19 days after the injection and then turned to the control levels, in harmony with the electrographic and behavioral profiles. These findings suggest that alterations in adenosine-sensitive generation of cyclic AMP in the primary epileptic region of the cortex are part of the neurochemical process of cobalt-induced epilepsy

A Neuropathologic Study of Disseminated Necrotizing Leukoencephalopathy Following Intrathecal Methotrexate Therapy

Neuropathologic findings of a case of disseminated necrotizing leukoencephalopathy following intrathecal methotrexate therapy are described. A five-year-old boy with acute lymphocytic leukemia was seen over a twenty-two month course and was administered methotrexate intrathecally for meningeal leukemia. After the seventh intrathecal administration he developed akinetic mutism and decorticated rigidity which persisted until the patient\u27s death seventeen months later. Neuropathologically, there were widespread necrotic lesions with scattered lipid-laden macrophages and extensive astrocytic gliosis mainly in the white matter of the cerebrum and cerebellum in addition to meningeal and perivascular infiltration by leukemia cells. Nerve cell loss was considerable in the thalamus, cerebellar cortex, dentate nucleus, pontine nucleus and inferior olivary nucleus. The disseminated necrotizing leukoencephalopathy in this case was thought to be caused mainly by the direct toxic effect of intrathecally administered methotrexate and not by irradiation or leukemia cell infiltration