Rabbit model simulating transient hyperglycinemia following transurethral prostatectomy.

Glycine was intravenously injected in rabbits and resulted in a dose dependent hyperglycinemia. A dose of 10mmol/kg was sufficient to achieve plasma levels of 10 to 16mM comparable to serum levels in patients at the end of a transurethral prostatectomy. The experiments documented that hyperglycinemia is associated with a significant increase of this substance in tissues outside the plasma compartment.

Guanidino compound levels in brain regions of non-dialyzed uremic patients.

Guanidino compounds have been suggested to contribute to the complex neurological complications associated with uremia. Several of them have previously been reported to accumulate in physiological fluids of renal insufficient subjects. We report on guanidino compound levels in 28 brain regions in control and uremic brains.

Effect of amphetamine on long-term retention of verbal material.

A series of five experiments was conducted to investigate the temporal aspects of human memory consolidation of symbolic material through the administration of amphetamine. Subjects had to recall or recognise unrelated words from a previously presented list. The first experiments support the conjecture, based on animal studies, that amphetamine enhances long-term memory performance.

Ontogenetic differences in convulsive action and cerebral uptake of uremic guanidino compounds in juvenile mice.

Guanidinosuccinate (GSA) and methylguanidine (MG) are endogenous, convulsant guanidino compounds which have been shown to be greatly increased in uremic patients. In the present study, we have investigated the age-related differences in convulsive action and cerebral uptake of these compounds in juvenile mice of 7, 14 and 21 days old. An age-dependent decrease was apparent in the severity of the GSA- and MG-induced convulsions and toxicity.

Amphetamine enhances human-memory consolidation.

Although it is generally accepted that CNS stimulants have enhancing effects on long-term storage processes in laboratory animals, little is known about their influence on human learning. We report a series of experiments with free recall of lists of unrelated words, demonstrating a significant enhancement on long-term retention after amphetamine administration. A gradual increase of recall was observed up to 1 h after learning, remaining stable for at least 3 days, after oral administration before learning as well as intramuscular injection after learning.

N-methyl-D-aspartate receptors contribute to guanidinosuccinate-induced convulsions in mice.

Increased levels of the endogenous convulsant guanidinosuccinate (GSA) might contribute to the epileptic symptomatology presenting in patients with renal failure. Little is known, however, about the underlying epileptogenic mechanism of guanidinosuccinate-induced convulsions. In this paper, we present pharmacological evidence for a direct excitatory action of this compound.

The uremic guanidino compound guanidinosuccinic acid induces behavioral convulsions and concomitant epileptiform electrocorticographic discharges in mice.

As yet, the in vivo epileptogenic properties of guanidinosuccinic acid (GSA) remained highly conjectural, still requiring the demonstration of GSA-induced behavioral convulsions accompanied by epileptiform electrographic discharges. Therefore, Swiss mice were injected intraperitoneally (i.p.

Behavioral toxicity of guanidinosuccinic acid in adult and young mice.

Guanidinosuccinic acid (GSA), a guanidino compound found to be greatly increased in uremia, was administered by intraperitoneal (i.p.) injection to adult albino mice and to young mice 7, 14 and 21 days old.

Convulsive action and toxicity of uremic guanidino compounds: behavioral assessment and relation to brain concentration in adult mice.

Four guanidino compounds that are known to accumulate in uremia, namely creatinine, guanidine, guanidinosuccinic acid and methylguanidine, were administered intraperitoneally and intracerebroventricularly to adult albino mice and the compounds epileptogenic and toxic properties were behaviorally assessed. After intraperitoneal injection, brain concentration of the compounds as a function of injected dose was monitored additionally. Guanidino compound brain concentration was determined by cation exchange chromatography with fluorescence ninhydrin detection.

Chemical models of epilepsy with some reference to their applicability in the development of anticonvulsants.

This paper reviews chemical models of epilepsy and their relevance in the identification and characterization of anticonvulsants. For each convulsant we discuss possible modes of administration, clinical type(s) of seizures induced, proposed mechanism(s) of epileptogenesis and, where available, responsiveness of the induced seizures to anticonvulsants. The following compounds are reviewed: pentylenetetrazol, bicuculline, penicillin, picrotoxin, beta-carbolines, 3-mercaptopropionic acid, hydrazides, allylglycine; the glycine antagonist strychnine; gamma-hydroxybutyrate; excitatory amino acids (glutamate, aspartate, N-methyl-D-aspartate, quisqualate, kainate, quinolinic acid); monosubstituted guanidino compounds, metals (alumina, cobalt, zinc, iron); neuropeptides (opioid peptides, corticotropin releasing factor, somatostatin, vasopressin); cholinergic agents (acetylcholine, acetylcholinesterase inhibitors, pilocarpine); tetanus toxin; flurothyl; folates; homocysteine and colchicine.

Biochemical characterization of particles from rat striatum containing dopamine, cholecystokinin or both.

Cholecystokinin (CCK) containing particles were isolated from rat striatum. After differential and isopycnic sucrose density gradient centrifugation, CCK containing particles equilibrated around 1.2 M sucrose.

Clinical and pathophysiological aspects of neurological complications in renal failure.

A review of the neurological complications presenting in uremia and an account of their presumed pathophysiology is given. With the introduction of different dialytic procedures during the last twenty years, the incidence and severity of neurological complications have declined. Nevertheless, some disturbances related to the uremic syndrome fail to respond to dialytic therapy and these therapeutic measures may even be responsible for the appearance of some new abnormalities.

Storage and fast transport of noradrenaline, dopamine beta-hydroxylase and neuropeptide Y in dog sciatic nerve axons.

The axonal transport and subcellular distribution of noradrenaline (NA), dopamine beta-hydroxylase (DBH) and neuropeptide Y (NPY) were determined in dog sciatic nerve using an accumulation technique. The results were compared with those obtained by application of the same procedures and methods on the splenic nerve in the same animal species. Evidence was found for the coexistence of NA and NPY in large dense-cored vesicles in dog sciatic nerve axons.

Subcellular distribution and axonal transport of noradrenaline, dopamine-?-hydroxylase and neuropeptide Y in dog splenic nerve.

The accumulation of noradrenaline, dopamine-?-hydroxylase and neuropeptide Y was determined at different intervals (6, 12, 24 and 48 h) after ligation of the dog splenic nerve. The calculated anterograde transport velocities for dopamine-?-hydroxylase and neuropeptide Y were quite similar, 9.6 and 9.