M. Gurelik, Mehmet Bolat, M. Öztürk, S. Polat, H. M. Göksel
Several different mechanisms contribute to the pathogenesis of cerebral vasospasm after subarachnoid haemorrhage. Whatever these mechanisms are, the vessel contraction is ultimately induced by an increase of free intracellular Ca2+ in the arterial wall. In this study, we investigated the effect on cerebral blood flow of a new dihydropyridine derivative Ca-channel blocker Niguldipine, in a rabbit experimental cerebral vasospasm model. The cerebral blood flow was significantly decreased in the saline treatment group when compared with control group. Niguldipine pretreatment caused a significant increase in cerebral blood flow. This effect should be investigated further.
{"title":"The effects of niguldipine pretreatment on cerebral vasospasm after subarachnoid haemorrhage in rabbits","authors":"M. Gurelik, Mehmet Bolat, M. Öztürk, S. Polat, H. M. Göksel","doi":"10.1002/NRC.10105","DOIUrl":"https://doi.org/10.1002/NRC.10105","url":null,"abstract":"Several different mechanisms contribute to the pathogenesis of cerebral vasospasm after subarachnoid haemorrhage. Whatever these mechanisms are, the vessel contraction is ultimately induced by an increase of free intracellular Ca2+ in the arterial wall. In this study, we investigated the effect on cerebral blood flow of a new dihydropyridine derivative Ca-channel blocker Niguldipine, in a rabbit experimental cerebral vasospasm model. The cerebral blood flow was significantly decreased in the saline treatment group when compared with control group. Niguldipine pretreatment caused a significant increase in cerebral blood flow. This effect should be investigated further.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"436 1","pages":"47-55"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79611624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jae-kwang Lee, E. Park, Hae‐Young Koh, Chang-Joong Lee
This study examined the role of the GABAergic system in generating epileptiform discharges in rat cortical slices in Mg2+-free aCSF by comparing two age groups using a whole cell patch recording. The discharges consisted of recurring slow bursts in the neonatal slices, whereas fast initial depolarization with after-discharges on the top of the gradual repolarization was mainly observed in the young slices. APV, an NMDA receptor antagonist, suppressed the slow bursts in the neonatal slices, and blocked late afterdischarges, leaving the fast depolarization discharges unaltered in the young slices. Interestingly, BMI, a GABAA receptor antagonist, reduced the frequency and amplitude of the discharges in the neonatal slices, while increasing in the young slices. The reversal potential of the slow bursts was shifted with a chloride ion gradient change across the membrane in the neonatal slices, but not in the young slices. These results demonstrated that the GABAA receptor activation during the neonatal period causes depolarization leading to epileptiform discharges under Mg2+-free conditions.
{"title":"GABA receptor‐mediated epileptiform discharges in the rat cortical slices in magnesium‐free aCSF","authors":"Jae-kwang Lee, E. Park, Hae‐Young Koh, Chang-Joong Lee","doi":"10.1002/NRC.10102","DOIUrl":"https://doi.org/10.1002/NRC.10102","url":null,"abstract":"This study examined the role of the GABAergic system in generating epileptiform discharges in rat cortical slices in Mg2+-free aCSF by comparing two age groups using a whole cell patch recording. The discharges consisted of recurring slow bursts in the neonatal slices, whereas fast initial depolarization with after-discharges on the top of the gradual repolarization was mainly observed in the young slices. APV, an NMDA receptor antagonist, suppressed the slow bursts in the neonatal slices, and blocked late afterdischarges, leaving the fast depolarization discharges unaltered in the young slices. Interestingly, BMI, a GABAA receptor antagonist, reduced the frequency and amplitude of the discharges in the neonatal slices, while increasing in the young slices. The reversal potential of the slow bursts was shifted with a chloride ion gradient change across the membrane in the neonatal slices, but not in the young slices. These results demonstrated that the GABAA receptor activation during the neonatal period causes depolarization leading to epileptiform discharges under Mg2+-free conditions.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"42 1","pages":"20-27"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77357477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Electrophysiological properties of basal forebrain (nucleus basalis area) neurons projecting directly to the frontal cortex were studied in urethane-anesthetized young and old male rats. Extracellular recordings demonstrated a total of 75 neurons (35 young and 40 old cells) which were antidromically activated by electrical stimulation of the frontal cortex. Post-antidromic orthodromic excitatory responses were seen, and the number of neurons showing such an orthodromic excitation was significantly smaller in aged rats. No significant differences were observed between young and aged rats in the threshold, latency or the conduction velocity of antidromic activation, or in the spontaneous firing rate of driven cells. The absolute refractory period was significantly longer and the degree of successful antidromic propagation into the somatodendritic complex was significantly lower in aged rats. The data provide evidence that there are marked changes with age in the physiological properties of basal forebrain neurons projecting to the frontal cortex.
{"title":"Age-related changes in properties of cortically projecting basal forebrain neurons","authors":"J. Tanaka, J. Nishimura, F. Kimura","doi":"10.1002/NRC.10096","DOIUrl":"https://doi.org/10.1002/NRC.10096","url":null,"abstract":"Electrophysiological properties of basal forebrain (nucleus basalis area) neurons projecting directly to the frontal cortex were studied in urethane-anesthetized young and old male rats. Extracellular recordings demonstrated a total of 75 neurons (35 young and 40 old cells) which were antidromically activated by electrical stimulation of the frontal cortex. Post-antidromic orthodromic excitatory responses were seen, and the number of neurons showing such an orthodromic excitation was significantly smaller in aged rats. No significant differences were observed between young and aged rats in the threshold, latency or the conduction velocity of antidromic activation, or in the spontaneous firing rate of driven cells. The absolute refractory period was significantly longer and the degree of successful antidromic propagation into the somatodendritic complex was significantly lower in aged rats. The data provide evidence that there are marked changes with age in the physiological properties of basal forebrain neurons projecting to the frontal cortex.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"31 1","pages":"200-209"},"PeriodicalIF":0.0,"publicationDate":"2003-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80665206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
N. Unal, I. Akdoğan, E. Adiguzel, B. Özdemi̇r, A. Tufan
Experimental epileptic models have been developed to assess the pathophysiology of epileptic seizures. We have previously shown that epileptic seizures cause significant neuronal loss in hippocampus (p 0.05). This study suggests that the loss of hippocampal neurons in penicillin-induced epilepsy seizure is not directly correlated with a volume change in the hippocampus. Furthermore, our results indicate that it is important to assess both the neuron number and the volume of the affected area using stereological methods in an epilepsy model to objectively analyze the effects of the seizure.
{"title":"Effect of penicillin‐induced epilepsy seizure on the volume of hippocampus stratum pyramidalis in rat","authors":"N. Unal, I. Akdoğan, E. Adiguzel, B. Özdemi̇r, A. Tufan","doi":"10.1002/NRC.10097","DOIUrl":"https://doi.org/10.1002/NRC.10097","url":null,"abstract":"Experimental epileptic models have been developed to assess the pathophysiology of epileptic seizures. We have previously shown that epileptic seizures cause significant neuronal loss in hippocampus (p 0.05). This study suggests that the loss of hippocampal neurons in penicillin-induced epilepsy seizure is not directly correlated with a volume change in the hippocampus. Furthermore, our results indicate that it is important to assess both the neuron number and the volume of the affected area using stereological methods in an epilepsy model to objectively analyze the effects of the seizure.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"17 1","pages":"210-217"},"PeriodicalIF":0.0,"publicationDate":"2003-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89000881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
K. Saganová, J. Mars̆ala, T. Ondrejčák, I. Vanický, J. Gálik
We examined the early microglial response to spinal cord ischemia induced by occlusion of the descending aorta for 15 min, or more limited aortic occlusion (8, 10, 12 min( linked with blood volume reduction. The recovery of motor function and activation of microglia labeled by Griffonia simplicifolia B4-isolectin (GSA I-B4-HRP) were assessed up to 7 days post-ischemia. Activation of resident microglia characterized by both increased lectin binding and altered morphology was observed >48 hrs post-ischemia. Massive infiltration of the microglia/macrophages related to the severity of ischemic insult appeared at day 3. Our data suggest that (1) ischemia of different degrees gives rise to a generalized microglial response at the early post-ischemic phase; (2) graded activation of microglia/macrophases as a response to ischemic neuronal injury occurs within 48–72 hrs of post-ischemic reperfusion; (3) lectin labeling of microglia can serve for continuous study of the evolution of pathological changes associated with transient spinal cord ischemia.
{"title":"Microglial response to early ischemia‐induced changes in the rat spinal cord","authors":"K. Saganová, J. Mars̆ala, T. Ondrejčák, I. Vanický, J. Gálik","doi":"10.1002/NRC.10094","DOIUrl":"https://doi.org/10.1002/NRC.10094","url":null,"abstract":"We examined the early microglial response to spinal cord ischemia induced by occlusion of the descending aorta for 15 min, or more limited aortic occlusion (8, 10, 12 min( linked with blood volume reduction. The recovery of motor function and activation of microglia labeled by Griffonia simplicifolia B4-isolectin (GSA I-B4-HRP) were assessed up to 7 days post-ischemia. Activation of resident microglia characterized by both increased lectin binding and altered morphology was observed >48 hrs post-ischemia. Massive infiltration of the microglia/macrophages related to the severity of ischemic insult appeared at day 3. Our data suggest that (1) ischemia of different degrees gives rise to a generalized microglial response at the early post-ischemic phase; (2) graded activation of microglia/macrophases as a response to ischemic neuronal injury occurs within 48–72 hrs of post-ischemic reperfusion; (3) lectin labeling of microglia can serve for continuous study of the evolution of pathological changes associated with transient spinal cord ischemia.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"38 1","pages":"179-188"},"PeriodicalIF":0.0,"publicationDate":"2003-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76908618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A. Songur, N. Akpolat, İ. Kuş, O. Ozen, I. Zararsız, M. Sarsılmaz
The aim of this study was to investigate the effects of formaldehyde (FA) gas inhalation during the early postnatal period on the heat shock proteins 70 kDa (Hsp70) synthesis and morphological changes in the hippocampus in developmental process of rats and to determine whether the changes was reversible or not. Neonatal rats were exposed to 0 (control), 6 and 12 ppm FA gas throughout 30 day period following the birth. After the exposure to FA, some animals from each concentration group were decapitated at the day 30. Despite cessation of FA exposure, other groups were left for decapitation until the days of 60th and 90th. The brain samples were stained with Hsp70 as immunohistochemically and H&E. In the samples, pyramidal cell layer in the hippocampus was examined. Hsp70(+) neurons were found in the hippocampus of rats that inhaled FA on the 30th day. Furthermore, a considerable increase on the count of pyknotic neurons in these groups. But, on the other hand, in the 60th and 90th days, Hsp70 immunostaining and the count of pyknotic cells were found to be diminishing in FA inhaled groups. In conclusion, inhalation of FA gas in cytotoxic concentrations during early postnatal period causes increase in Hsp70 synthesis and damages the rat's hippocampus. Diminishment or disappearance of these negative changes in the 60th and 90th days indicates a reversible change in rats.
{"title":"The effects of the inhaled formaldehyde during the early postnatal period in the hippocampus of rats: A morphological and immunohistochemical study","authors":"A. Songur, N. Akpolat, İ. Kuş, O. Ozen, I. Zararsız, M. Sarsılmaz","doi":"10.1002/NRC.10093","DOIUrl":"https://doi.org/10.1002/NRC.10093","url":null,"abstract":"The aim of this study was to investigate the effects of formaldehyde (FA) gas inhalation during the early postnatal period on the heat shock proteins 70 kDa (Hsp70) synthesis and morphological changes in the hippocampus in developmental process of rats and to determine whether the changes was reversible or not. \u0000 \u0000 \u0000 \u0000Neonatal rats were exposed to 0 (control), 6 and 12 ppm FA gas throughout 30 day period following the birth. After the exposure to FA, some animals from each concentration group were decapitated at the day 30. Despite cessation of FA exposure, other groups were left for decapitation until the days of 60th and 90th. The brain samples were stained with Hsp70 as immunohistochemically and H&E. In the samples, pyramidal cell layer in the hippocampus was examined. Hsp70(+) neurons were found in the hippocampus of rats that inhaled FA on the 30th day. Furthermore, a considerable increase on the count of pyknotic neurons in these groups. But, on the other hand, in the 60th and 90th days, Hsp70 immunostaining and the count of pyknotic cells were found to be diminishing in FA inhaled groups. \u0000 \u0000 \u0000 \u0000In conclusion, inhalation of FA gas in cytotoxic concentrations during early postnatal period causes increase in Hsp70 synthesis and damages the rat's hippocampus. Diminishment or disappearance of these negative changes in the 60th and 90th days indicates a reversible change in rats.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"6 1","pages":"168-178"},"PeriodicalIF":0.0,"publicationDate":"2003-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85364097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
L. Dokas, M. Haas, Scott M. Lilly, S. Ting, A. Dennis
The presynaptic protein B-50 (GAP-43) is a protein kinase CK2 (CK2) substrate phosphorylated in vitro in a polylysine-dependent manner. Polylysine was compared to other basic compounds to further define characteristics of this phosphorylation. Total histone stimulated CK2 to a similar extent, but at higher concentrations than did polylysine, while spermine was without effect. Histone H2A accounted for the stimulatory effect of the mixed histone. Correlation between CK2 activity and the length of polylysine was observed. Polylysine-dependent B-50 phosphorylation was observed with both recombinant human CK2 and purified rat brain CK2. Serine/threonine phosphorylation occurred on the fragment, B-501–132, and serine phosphorylation on B-50133–226. Phosphorylation of B-50 by CK2 was inhibited by actin and calmodulin. These results suggest that local interactions between CK2, basic proteins and/or actin at the neuronal membrane and calmodulin binding may determine the phosphorylated state of B-50 at CK2 sites.
{"title":"In vitro modulation of protein kinase CK2‐mediated phosphorylation of the neuronal growth‐associated protein B‐50 (GAP‐43)","authors":"L. Dokas, M. Haas, Scott M. Lilly, S. Ting, A. Dennis","doi":"10.1002/NRC.10095","DOIUrl":"https://doi.org/10.1002/NRC.10095","url":null,"abstract":"The presynaptic protein B-50 (GAP-43) is a protein kinase CK2 (CK2) substrate phosphorylated in vitro in a polylysine-dependent manner. Polylysine was compared to other basic compounds to further define characteristics of this phosphorylation. Total histone stimulated CK2 to a similar extent, but at higher concentrations than did polylysine, while spermine was without effect. Histone H2A accounted for the stimulatory effect of the mixed histone. Correlation between CK2 activity and the length of polylysine was observed. Polylysine-dependent B-50 phosphorylation was observed with both recombinant human CK2 and purified rat brain CK2. Serine/threonine phosphorylation occurred on the fragment, B-501–132, and serine phosphorylation on B-50133–226. Phosphorylation of B-50 by CK2 was inhibited by actin and calmodulin. These results suggest that local interactions between CK2, basic proteins and/or actin at the neuronal membrane and calmodulin binding may determine the phosphorylated state of B-50 at CK2 sites.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"26 1","pages":"189-199"},"PeriodicalIF":0.0,"publicationDate":"2003-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75929719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The hippocampus is one of the brain areas where neurogenesis persists during adulthood. To determine whether chronic ethanol administration affects production of the new cells in the dentate gyrus adult mice received ethanol via the inhalation route for 4 weeks and newly born cells were determined after administration of the proliferation marker bromodeoxyuridine (BrdU). An inhibition of the generation of the new cells at the end of ethanol intoxication was observed, whereas ethanol withdrawal induced a transient increase in the number of dividing cells in the dentate gyrus. The differentiation of the newly born cells into mature calbindin-positive neurons during ethanol intoxication or withdrawal was retarded. Although the functional significance of the observed changes is not known, we suggest that retardation of the differentiation of the new cells following ethanol administration might have an impact on the ethanol-induced impairment of hippocampal functions.
{"title":"Ethanol intoxication reduces, whereas ethanol withdrawal transiently enhances, production of the neural progenitor cells in the adult mouse dentate gyrus","authors":"K. Jaako, T. Zharkovsky, A. Kaasik, A. Zharkovsky","doi":"10.1002/NRC.10092","DOIUrl":"https://doi.org/10.1002/NRC.10092","url":null,"abstract":"The hippocampus is one of the brain areas where neurogenesis persists during adulthood. To determine whether chronic ethanol administration affects production of the new cells in the dentate gyrus adult mice received ethanol via the inhalation route for 4 weeks and newly born cells were determined after administration of the proliferation marker bromodeoxyuridine (BrdU). An inhibition of the generation of the new cells at the end of ethanol intoxication was observed, whereas ethanol withdrawal induced a transient increase in the number of dividing cells in the dentate gyrus. The differentiation of the newly born cells into mature calbindin-positive neurons during ethanol intoxication or withdrawal was retarded. Although the functional significance of the observed changes is not known, we suggest that retardation of the differentiation of the new cells following ethanol administration might have an impact on the ethanol-induced impairment of hippocampal functions.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"38 1","pages":"158-167"},"PeriodicalIF":0.0,"publicationDate":"2003-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90555313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
We have investigated the post-inhibitory rebound (PIR) properties of dopamine cells in the ventral tegmental area of the rat midbrain. Using microelectrodes to record intracellularly from rat cells in the midbrain slice, we found that 54% of all recorded DA cells exhibited rebound depolarization in the presence of TTX. We observed primarily two types of rebound responses distinguished by their maximum amplitude and inactivation time constant, which we have termed as the ‘slowly inactivating PIR’ and low-threshold spike (LTS). 35% of DA cells exhibited a ‘slowly inactivating PIR’ and 19% showed LTS. A subset of the latter exhibited repetitive LTS. The PIR was enhanced in high K+ medium and suppressed in low-calcium medium. Under voltage clamp conditions, inward rebound currents at the end of a hyperpolarizing voltage step were partially blocked by specific T-type channel blocker, Ni2+. Repetitive LTSs were reversibly changed to single LTS by blocking the potassium SK current.
{"title":"Post‐inhibitory rebound properties of dopaminergic cells of the ventral tegmental area","authors":"K. Paul, Steven W. Johnson","doi":"10.1002/NRC.10091","DOIUrl":"https://doi.org/10.1002/NRC.10091","url":null,"abstract":"We have investigated the post-inhibitory rebound (PIR) properties of dopamine cells in the ventral tegmental area of the rat midbrain. Using microelectrodes to record intracellularly from rat cells in the midbrain slice, we found that 54% of all recorded DA cells exhibited rebound depolarization in the presence of TTX. We observed primarily two types of rebound responses distinguished by their maximum amplitude and inactivation time constant, which we have termed as the ‘slowly inactivating PIR’ and low-threshold spike (LTS). 35% of DA cells exhibited a ‘slowly inactivating PIR’ and 19% showed LTS. A subset of the latter exhibited repetitive LTS. The PIR was enhanced in high K+ medium and suppressed in low-calcium medium. Under voltage clamp conditions, inward rebound currents at the end of a hyperpolarizing voltage step were partially blocked by specific T-type channel blocker, Ni2+. Repetitive LTSs were reversibly changed to single LTS by blocking the potassium SK current.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"22 1","pages":"147-157"},"PeriodicalIF":0.0,"publicationDate":"2003-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84686964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
B. Park, M. S. Kim, M. Lee, M. Choi, D. Choi, Nam-Yong Doh
Unilateral labyrinthectomy produces vestibular symptoms that abate over time in a process of behavioral recovery known as vestibular compensation. To investigate the role of glutamate receptors in vestibulo-autonomic symptoms, we measured spontaneous nystagmus and c-Fos expression in the medial vestibular nucleus (MVN) and the solitary tract nucleus (STN) in unilateral labyrinthectomized Sprague-Dawley rats treated with kynurenic acid, a broad spectrum glutamate receptor antagonist, 30 min before labyrinthectomy. Spontaneous nystagmus occurred after unilateral labyrinthectomy (UL), and nystagmus decreased gradually over time. Spatial expression of c-Fos in the MVN following UL corresponded to disappearance of spontaneous nystagmus. Expression of c-Fos in the STN decreased 24 h after UL. Pretreatment with kynurenic acid decreased c-Fos expression in both the MVN and STN and decreased spontaneous nystagmus. These results suggest that pretreatment with kynurenic acid facilitates recovery of autonomic symptoms as well as behavioral response following UL.
单侧迷路切除会产生前庭症状，随着时间的推移，前庭症状会随着行为的恢复而减弱，这一过程被称为前庭代偿。为了研究谷氨酸受体在前庭自主神经症状中的作用，我们在迷路切除前30分钟，用广谱谷氨酸受体拮抗剂犬尿酸治疗的Sprague-Dawley大鼠，测量了自发性眼震和前庭内侧核(MVN)和孤立束核(STN)中c-Fos的表达。单侧迷路切除术后发生自发性眼球震颤，眼球震颤随时间逐渐减轻。术后MVN中c-Fos的空间表达与自发性眼球震颤的消失相对应。l后24 h STN中c-Fos的表达降低。肌尿酸预处理可降低MVN和STN中c-Fos的表达，减少自发性眼球震颤。这些结果表明，用犬尿酸预处理有助于自主神经症状的恢复以及UL后的行为反应。
{"title":"Role of kynurenic acid on vestibulo-autonomic symptoms following unilateral labyrinthectomy in rats","authors":"B. Park, M. S. Kim, M. Lee, M. Choi, D. Choi, Nam-Yong Doh","doi":"10.1002/NRC.10099","DOIUrl":"https://doi.org/10.1002/NRC.10099","url":null,"abstract":"Unilateral labyrinthectomy produces vestibular symptoms that abate over time in a process of behavioral recovery known as vestibular compensation. To investigate the role of glutamate receptors in vestibulo-autonomic symptoms, we measured spontaneous nystagmus and c-Fos expression in the medial vestibular nucleus (MVN) and the solitary tract nucleus (STN) in unilateral labyrinthectomized Sprague-Dawley rats treated with kynurenic acid, a broad spectrum glutamate receptor antagonist, 30 min before labyrinthectomy. Spontaneous nystagmus occurred after unilateral labyrinthectomy (UL), and nystagmus decreased gradually over time. Spatial expression of c-Fos in the MVN following UL corresponded to disappearance of spontaneous nystagmus. Expression of c-Fos in the STN decreased 24 h after UL. Pretreatment with kynurenic acid decreased c-Fos expression in both the MVN and STN and decreased spontaneous nystagmus. These results suggest that pretreatment with kynurenic acid facilitates recovery of autonomic symptoms as well as behavioral response following UL.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"11 1","pages":"227-234"},"PeriodicalIF":0.0,"publicationDate":"2003-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81216934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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