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Query: UMLS:C0040822 (
tremor
)
18,428
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Kainic acid
(KA), an excitatory neurotoxin, was used as a tool to study the metabolism of hippocampal opioid peptides and their functional role in the expression of wet-dog shakes (WDS). A single intracerebral injection of KA (1 microgram/rat) caused recurrent motor seizures lasting 3-6 h. During the convulsive period, native Met5-enkephalin-like (ME-LI) and dynorphin A(1-8)-like (DYN-LI) immunoreactivities in hippocampus decreased by 31 and 63%, respectively. By 24 h after dosing, the hippocampal opioid peptides had returned to control levels, and by 48 h ME-LI had increased 270% and DYN-LI 150%. Immunocytochemical analysis revealed that ME-LI and Leu5-enkephalin-like (LE-LI) immunostaining in the mossy fibers of dentate granule cells and the perforant-temporoammonic pathway had decreased visibly by 6 h and had increased markedly by 48 h following KA. A visible decrease in DYN-LI in mossy fiber axons within 6 h was followed by a substantial increase at 48 h. To determine whether the increases in hippocampal ME-LI reflected changes in ME biosynthesis, levels of mRNA coding for preproenkephalin (mRNAenk) and cryptic ME-LI cleaved by enzyme digestion from preproenkephalin were measured. Following the convulsive period (6 h), mRNAenk was 400% of control, and by 24 h, cryptic ME-LI was 300% of control. Increases in native and cryptic ME-LI and in mRNAenk were also noted in entorhinal cortex, but not in hypothalamus or uninjected striatum. Our data suggest that KA-induced seizures cause an increase in ME release, followed by a compensatory increase in ME biosynthesis in the hippocampus and entorhinal cortex. Several lines of evidence from this study have suggested that hippocampal enkephalins are intimately related to KA-elicited WDS. The
shaking
behavior was attenuated by pretreatment with naloxone or antisera against [Met5]-enkephalin. We also observed that KA-induced WDS can be mimicked by intrahippocampal injection of enkephalin-related peptides. Furthermore, this study demonstrated that intact dentate granule cells are essential for KA- and enkephalin-induced WDS, since a colchicine injection into the ventral hippocampus, which selectively destroys granule cells, abolished this behavior.
...
PMID:Kainic acid as a tool to study the regulation and function of opioid peptides in the hippocampus. 289 Feb 24
The effects of excitatory amino acids, kainic acid and quisqualic acid, on the tremorine- and harmaline-induced
tremor
were quantitatively examined in mice using the power spectral analyzing method. The severity of the
tremor
was determined quantitatively in terms of the cumulative sum of the mean square value of the data.
Kainic acid
enhanced the
tremor
induced by tremorine but depressed the
tremor
induced by harmaline. Quisqualic acid depressed the
tremor
induced by both tremorine and harmaline in a dose-dependent manner.
Kainic acid
shifted the frequency of each component of the
tremor
induced by tremorine to the high frequency side, but quisqualic acid did not affect the frequency of
tremor
of the
tremor
induced by tremorine. The frequency of
tremor
of the
tremor
induced by harmaline was shifted by both excitatory amino acids to the low frequency side, and another component of
tremor
in the power spectral densities developed, of which the mean square values were very small. The present results suggest that, at least in part, the glutamatergic system can take a role on the modification of drug-induced
tremor
.
...
PMID:Modification of drug-induced tremor by systemic administration of kainic acid and quisqualic acid in mice. 355 May 15
Kainic acid
(KA) was injected systemically, intracerebroventricularly (i.c.v.) and focally in the amygdala and other deep brain structures in the rat. EEG and behavioral changes were studied in relation to the neuropathology which developed subsequently. Following intra-amygdaloid KA injection, diazepam blocked the epileptic events induced by the toxin, and abolished the neuronal loss usually seen in the lateral septum, claustrum, and contralateral cortex and hippocampus. The lesions in medial thalamic structures and ipsilateral hippocampus were also reduced by diazepam. Prior transection of the perforant path ipsilateral to the KA injection also decreased the severity of the electrographic and motor effects of the toxin and similarly reduced the extent of distant ("remote") pathological brain damage. Neither diazepam nor perforant path transection reduced the damage at the site of KA injection.
Kainic acid
(0.4-2 microgram) injected into the bed nucleus of the stria terminalis (BST) or the medial septum produced seizures with a longer latency and little brain damage outside the injection site. In contrast, intrastriatal KA injections were followed by ipsilateral hippocampal lesions. i.c.v. Injection of KA (0.4-1.6 microgram) produced a complex syndrome which included bilateral exophthalmos, mydriasis, foaming,
tremor
of the vibrissae, and paw and body
tremor
. The pattern of brain damage resembled that seen following intra-amygdaloid administration of the toxin. In addition, however, there was a bilateral necrosis of the pyriform and prepyriform cortices up to the rhinal fissure. Systemic administration of diazepam (i.p.) reduced the extent of the damage and in particular completely prevented the cortical damage. Systemic administration of KA (9-15 mg/kg i.p.) readily produced motor and EEG seizures similar to those seen after intra-amygdaloid injection of the toxin. The pattern of brain damage was however more symmetrical than that which followed focal i.c.v. injection of the toxin and included necrosis of the pyriform cortex. It is concluded that spread of seizure activity from the injection site plays a crucial role in the induction of "remote" brain damage after focal intracerebral injections.
...
PMID:The role of epileptic activity in hippocampal and "remote" cerebral lesions induced by kainic acid. 737 61