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At least 1,225 records · Page 68Linked to original sources
PubMed2004

[Establishment of temporal epilepsy models and its permanent epilepsy sensitivity].

OBJECTIVE: To explore a better method to establish an animal model of temporal epilepsy in rat and study the pathological basis of permanent epilepsy sensitivity. METHODS: Kainic acid (KA) with the dosage calculated according to the body weight was injected into 30 Wistar rats' hippocampuses by stereotactic operation. Videotape recording was used to record the seizures for 8 weeks. Two rats were randomly selected to undergo craniotomy and electroencephalography and then were killed to have their brains to be taken out to undergo slicing, staining, and histological examination 6 hours, 1 days, 3 days, 5 days, 7 days, 2 weeks, 3 weeks, 4 weeks, 5 weeks, 6 weeks, 7 weeks, and 8 weeks respectively after operation. RESULTS: Thirty minutes after the rats awoke from anesthesia, wet-dog shakes, lips and head self-movements, convulsion of forelimbs and hind limbs occurred successively. The seizures were paroxysmal with increased intervals during which, however, the rats still showed sluggish. Twenty-four hours after the rats' behavior recovered to normal. Then the seizure occurred 1 approximately 3 times every week. Epileptic waves were recorded in the hippocampus, striate body, cerebral cortex, and olfactory bulb from 5 hours to 2 months after the establishment of model. CONCLUSION: The seizure pattern and pathological basis of temporal epilepsy in the rat model established by stereotactic management were almost the same as those in human beings. Stereotactic method significantly decreased the needed dosage of KA and the cost in comparison with systematic injection. Loss of hippocampus neurons and hyperplasia of gliocytes are the basis of the permanent epilepsy sensitivity in the animal model.

Animals↗
PubMed2006

Splice variant of mouse Stam2 mRNA in nervous and muscle tissue contains additional exon with stop codon within region coding for VHS domain.

AIM: To analyze the alternatively spliced variant of Stam2 mRNA and determine its distribution in mouse tissues. METHODS: We identified a novel alternatively spliced exon by cloning and sequencing of Stam2 cDNA obtained from tissue samples of 3-5 months old male C57Bl/6NCrl mice. The sequence of the alternatively spliced exon was analyzed by bioinformatic tools. The tissue distribution of different Stam2 mRNA variants was determined by reverse transcription-polymerase chain reaction, and the consequences of the alternative splicing at the protein level were analyzed by western blot with the polyclonal anti-STAM2 antibody. RESULTS: The novel alternatively spliced exon 1A of mouse Stam2 gene was inserted within Stam2 coding region and it contained a stop codon. The exon did not bear similarities to any other cDNA or protein sequence in the mouse, rat, or human databases. Both mRNA variants, with and without exon 1A, were present in the cortex, hippocampus, olfactory bulb, medulla oblongata, spinal cord, cerebellum, and the skeletal and heart muscle, while the other analyzed organs contained only the variant without the additional exon. The mRNA with the included exon did not give rise to a protein form detectable by western blotting with the polyclonal anti-STAM2 antibody. CONCLUSION: The alternatively spliced exon 1A was included in mRNA splice variant present in the nervous and muscle tissues. The alternative splicing event did not have major impact on STAM2 production and functionality. It seems that exon 1A is an evolutionary new exon created by exonization of an intronic sequence.

Adaptor Proteins, Signal Transducing↗
PubMed1991

Quantitative autoradiography of the binding sites for [125I] iodoglyburide, a novel high-affinity ligand for ATP-sensitive potassium channels in rat brain.

We have developed a high specific activity ligand for localization of ATP-sensitive potassium channels in the brain. When brain sections were incubated with [125I]iodoglyburide (N-[2-[[[(cyclohexylamino)carbonyl]amino]sulfonyl]ethyl]-5-125I-2- methoxybenzamide), the ligand bound to a single site with a KD of 495 pM and a maximum binding site density of 176 fmol/mg of tissue. Glyburide was the most potent inhibitor of specific [125I]iodoglyburide binding to rat forebrain sections whereas iodoglyburide and glipizide were slightly less potent. The binding was also sensitive to ATP which completely inhibited binding at concentrations of 10 mM. Autoradiographic localization of [125I]iodoglyburide binding indicated a broad distribution of the ATP-sensitive potassium channel in the brain. The highest levels of binding were seen in the globus pallidus and ventral pallidum followed by the septohippocampal nucleus, anterior pituitary, the CA2 and CA3 region of the hippocampus, ventral pallidum, the molecular layer of the cerebellum and substantia nigra zona reticulata. The hilus and dorsal subiculum of the hippocampus, molecular layer of the dentate gyrus, cerebral cortex, lateral olfactory tract nucleus, olfactory tubercle and the zona incerta contained relatively high levels of binding. A lower level of binding (approximately 3- to 4-fold) was found throughout the remainder of the brain. These results indicate that the ATP-sensitive potassium channel has a broad presence in the rat brain and that a few select brain regions are enriched in this subtype of neuronal potassium channels.

Affinity Labels↗
PubMed1991

Sub-chronic exposure of the adult rat to Aroclor 1254 yields regionally-specific changes in central dopaminergic function.

Laboratory rats were exposed to chow adulterated with either 500 or 1000 ppm Aroclor 1254 for 30 days. Analysis of biogenic amines and their metabolites in the dorsal frontal cortex, lateral olfactory tract, striatum, basal hypothalamus, hippocampus and brainstem revealed significant decreases in dopamine concentrations and metabolism in only the striatum and lateral olfactory tract. Concentrations of individual PCB congeners in the striatum, lateral olfactory tract and hippocampus were measured by gas chromatography with electron capture detection. Neither total concentration nor variations in concentrations of individual congeners between regions could explain this regional specificity. The susceptibility of the striatum and lateral olfactory tract to insult by PCBs may be due to their innervation by midbrain dopaminergic neurons which have been shown to be particularly sensitive to insult from environmental, infectious and pharmacologic agents.

Acetone↗
PubMed1985

Antibody against nerve growth factor-inducible large external (NILE) glycoprotein labels nerve fiber tracts in the developing rat nervous system.

The NILE (nerve growth factor-inducible large external) glycoprotein is a 230,000-dalton molecule found on the surface of PC12 cells. Immunologically cross-reactive glycoproteins in the molecular weight range of 215,000 to 230,000 have been found on many types of neurons in culture. Using immunohistochemical methods, we have shown that NILE-related glycoproteins are present in neuronal fiber tracts of the developing rat brain. Antibody against the NILE glycoprotein specifically labels processes that appear identical to those recognized by antibodies against the neurofilament triplet of proteins. These processes are clearly distinct from the radial glial fibers recognized by antibody against the intermediate filament protein vimentin. NILE glycoprotein is not distributed uniformly over the entire neuronal surface but is concentrated on neurites and is much less abundant on cell bodies. NILE-positive fiber tracts are first seen in the spinal cord and rhombencephalon on embryonic day 11 and over the next 2 days appear in the mesencephalon and diencephalon. Staining in the telencephalon is not seen until embryonic day 15. The appearance of NILE immunoreactivity in these various regions closely parallels the appearance of neurofilament polypeptides, suggesting that NILE-related glycoproteins are present during the early phases of fiber tract formation. This idea is supported by the finding that the NILE glycoprotein can be found postnatally in parts of the nervous-system such as the cerebellar cortex and olfactory bulb which undergo major histogenesis during the postnatal period. In the cerebellum the appearance of NILE immunoreactivity in the two major fiber zones, the molecular layer and the white matter, parallels the development of the fiber structure of these layers. These findings support tissue culture studies which suggest a role for the NILE glycoprotein in mediating nerve fiber fasciculation.

Animals↗
PubMed1984

Cholecystokinin receptors: biochemical demonstration and autoradiographical localization in rat brain and pancreas using [3H] cholecystokinin8 as radioligand.

Since cholecystokinin8 (CCK8) seems to be the physiological ligand of CCK receptors in the brain, it would be the most suitable probe for the characterization of CCK receptors in radioligand binding studies. [3H]CCK8 was synthetized with a specific radioactivity sufficient for the detection of high affinity binding sites. [3H]CCK8 binds saturably and reversibly to distinct sites in rat brain and pancreas with nanomolar affinity. While the C-terminal tetrapeptide of CCK is the minimal structure required for nanomolar affinity in the brain, the entire octapeptide sequence is required for binding affinity in pancreas. Desulfated CCK8 and several gastrin-I peptides, which are likewise unsulfated, show virtually no affinity to the binding sites in pancreas but high affinity in cerebral cortex. The ligand specificity of the CCK peptides corresponds to their electrophysiological potency in the brain and their stimulation of secretion in pancreas, respectively. Autoradiographically, high densities of [3H]CCK8 binding sites were found in cerebral cortex and olfactory bulb, medium levels in nucleus accumbens, hippocampus, dentate gyrus, and striatum with virtually no labeling in cerebellum. This pattern is similar to the distribution of CCK-like immunoreactivity in the brain. In pancreas, equally high levels of [3H]CCK8 labeling were found in the exocrine and endocrine region. [3H]CCK8 binding sites differ from those identified previously with [125I]Bolton-Hunter-CCK33 by their sensitivity to guanyl nucleotides in the brain, their ion dependency in the brain, and pancreas, and their different autoradiographical localization in some parts of the brain. The distribution of CCK binding sites labeled with [3H]CCK8 appears to correlate better with the CCK immunoreactivity than those labeled with [125I]Bolton-Hunter-CCK33. Thus, [3H]CCK8 appears to be the radioligand of choice for the investigation of CCK receptors.

Animals↗
PubMed1995

GABA neurotransmission in the hypothalamus: developmental reversal from Ca2+ elevating to depressing.

GABA is the primary inhibitory transmitter of the adult hypothalamus, synthesized by many neurons and found in 50% of the presynaptic boutons. GABA causes a decrease in Ca2+ in mature hypothalamic neurons in vitro by depressing cellular activity through opening Cl- channels. Despite the early expression of GABAA receptors in the embryonic hypothalamus (E15), the cellular function of GABA in the developing hypothalamus has received little attention. In the present study the role of GABA in modulating intracellular Ca2+ in developing hypothalamic neurons was studied with fura-2 digital imaging. GABA (0.5-500 microM) applied to embryonic hypothalamic neurons elicited a dramatic and rapid increase in intracellular Ca2+ This Ca2+ rise could be completely blocked by the GABAA antagonist bicuculline (20 microM) and persisted in the presence of tetrodotoxin (1 microM). The Ca2+ elevation induced by GABA was greater than that of equimolar concentrations of the excitatory transmitter glutamate in early development. The number of E15 neurons that responded to GABA with a Ca2+ rise increased during the first few days of culture, reaching 78% after 4 d in vitro. The Ca2+ rise was 87% blocked by cadmium (100 microM) and 85% blocked by nimodipine (1 microM), indicating that the mechanism of Ca2+ increase was primarily via L-type voltage operated Ca2+ channels. Addition of bicuculline to synaptically coupled cultures caused a significant decrease in Ca2+ 4-10 d after culturing, indicating hypothalamic neurons were secreting GABA at an early age of development, and that sufficient GABA was released to elicit an increase in Ca2+. This effect was seen even after blocking all glutamatergic activity with glutamate receptor antagonists. In contrast, GABA elicited no Ca2+ rise in older neurons (> 18 d in vitro), and the action of bicuculline reversed and caused a large increase in Ca2+ in spontaneously active neurons. Similar findings were obtained in cultures enriched in GABAergic neurons from the suprachiasmatic nucleus. To determine if the Ca2+ stimulating role of GABA on developing neurons was restricted to the hypothalamus and a few other regions, or whether it might exist throughout the brain, we examined the Ca2+ responses in cultured olfactory bulb, cortex, medulla, striatum, thalamus, hippocampus, and colliculus. The majority (75%) of developing neurons from each region showed a Ca2+ rise in response to GABA. Together these data suggest that GABA elevates Ca2+ in developing, but not mature, neurons from the hypothalamus and all other brain regions examined.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗