Effect of increments in norepinephrine concentrations on seizure intensity in the genetically epilepsy-prone rat.
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Acoustic Stimulation↗
Biomedical subjects
K H Ko
Publications and source records attributed to K H Ko.
Prevalence of the tarsal tunnel syndrome in rheumatoid arthritis.
Forty-eight patients with definite of classical rheumatoid arthritis (RA) were studied for the presence of tarsal tunnel syndrome (TTS). Nerve conduction velocities and distal latencies were determined in a constant temperature room and the findings compared with a group of 35 normal, age-matched subjects. After excluding four patients with peripheral neuropathy, a definite delay in the distal motor latency of the tibial nerve was documented in 11 subjects (25%). Two of the 11 had foot symptoms suggestive of TTS. These 11 patients with prolonged distal motor latencies did not otherwise differ from RA patients without TTS in terms of disease duration or severity, treatment, or the presence of foot deformity. Thus, compressive neuropathy of the branches of the posterior tibial nerve is a relatively frequent finding in patients with definite or classical RA.
Arthritis, Rheumatoid↗
The genetically epilepsy-prone rat (GEPR).
Two independently inbred strains of genetically epilepsy-prone rats (GEPRs) have been developed. GEPR-3s and GEPR-9s have moderate and severe degrees of seizure predisposition as well as expression, respectively. Seizure predisposition is a fundamental distinction between the normal and epileptic brain. Seizure predisposition in GEPRs and in humans with epilepsy includes spontaneous seizures and exaggerated seizure responsiveness and/or abnormally low thresholds to stimuli which also cause seizures in non-epileptic subjects. Activation of brainstem seizure circuitry by auditory input via the inferior colliculus causes electrographic and behavioral responses in GEPR-9s which replicates human generalized tonic/clonic seizures. Activation of brainstem seizure circuitry by input from forebrain seizure circuitry in GEPRs provides a newly discovered model of complex partial seizures with secondary generalization to tonic/clonic seizures. Thus, seizure predisposition in GEPRs offers a unique opportunity to study the human epilepsies that is not offered in studies of normal brain exposed to convulsant stimuli.
Animals↗
Inhaled ATP causes mucin release from goblet cells of intact rats.
Secretion of mucins from airway epithelial cells has been studied almost exclusively using in vitro cell culture systems. Our understanding of in vivo secretion is greatly limited due to the unavailability of both suitable model systems and adequate assays. It has been reported that ATP induces mucin release from the cultured primary tracheal surface epithelial cell, but there is no clear demonstration of the effect of ATP on mucin release in vivo, which is important to understand the mechanism of mucin release in vivo and also to devise means for regulation of mucin release. The objective of this experiment was to see if inhaled ATP could stimulate airway mucin release in intact rats using both enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry. The results were: (1) a new monoclonal antibody (mAbRT03) developed against purified rat mucins specifically recognized high-molecular-mass mucins; (2) ELISA results with conventional gel-filtration assay results are virtually superimposable; (3) inhalation of ATP in intact rats resulted in a dose-independent increase in the amount of mucins in the tracheal lavage fluid with a concomitant decrease in the number of mucin-positive cells in the trachea. We conclude that extracellular ATP can stimulate mucin release from the airway in vivo, and the present rat inhalation system combined with ELISA of the airway secretions should serve a useful model for studying the pharmacology of airway mucin secretion in vivo.
Adenosine Triphosphate↗
Noradrenergic abnormalities in the central nervous system of seizure-naive genetically epilepsy-prone rats.
Norepinephrine (NE) concentrations were measured in 15 discrete areas of the central nervous system of two types of genetically epilepsy-prone rats (GEPRs) and in nonepileptic controls. Both moderate-seizure (GEPR-3) and severe-seizure (GEPR-9) animals had extensive abnormalities in brain NE concentration. Deficits of equal magnitude in GEPR-3s and GEPR-9s were found in the spinal cord, midbrain minus the inferior colliculus, inferior colliculus, hypothalamus, amygdala, hippocampus, occipital + parietal cortex, frontal cortex, and olfactory septum. Because both types of GEPRs share these deficits and share seizure susceptibility, we hypothesize that these areas are candidates for regulation of seizure susceptibility in GEPRs. In addition, because GEPR-9s have more severe seizures than GEPR-3s and because GEPR-9s had greater NE deficits in several brain areas (cerebellum, pons-medulla, thalamus, and possibly the temporal cortex and olfactory bulbs), we hypothesize that these areas may be important in regulation of seizure severity in GEPRs. All animals used in these experiments had been protected from seizure-provoking stimuli and were naive to seizures. Because the abnormalities in NE concentration were present in seizure-predisposed animals that were protected from seizures, we conclude that these abnormalities are important components of the seizure-predisposition characteristic of GEPRs and do not result from seizure experience.
Acoustic Stimulation↗
Abnormal central serotonergic activities in spontaneously hypertensive rats (SHR).
We employed spontaneously hypertensive rats (SHR) to explore a possible role of central serotonergic activity in hypertension. The activities of serotonergic nervous system were assessed by measuring the serotonin turnover rates in rats treated with probenecid. Serotonin turnover rates in telencephalon and hypothalamus/thalamus of SHR were significantly lowered as compared to WKY rats whereas those in cerebellum of SHR were significantly elevated than those of WKY rats. There was no significant difference in serotonin turnover rates in midbrain and pons/medulla of SHR and WKY rats. These results suggest that the abnormal turnover rates of serotonin in brain may be one of the underlying neuronal factors for the manifestation of hypertension in SHR.
Animals↗