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C Y Chai

Publications and source records attributed to C Y Chai.

At least 55 records · Page 3Linked to original sources

GABAergic inhibition of neonatal rat phrenic motoneurons.

Phrenic motoneurons (PMNs) receive intermittently glutaminergic inspiratory drives and GABAergic inhibition in adult mammals. Since gamma-amino-butyric acid (GABA) might act as an excitatory amino acid in early stages of development, we here investigated if GABA(A) receptors inhibit PMNs in neonates. Using in vitro neonatal rat brainstem-spinal cord preparation, local application of GABA and muscimol (a GABA(A) receptor agonist) to the vicinity of PMNs consistently reduced the inspiratory activity of C4 ventral roots. Under whole-cell patch-clamp conditions and in the presence of 0.5 microM TTX to block synaptic transmission, muscimol (10 microM) decreased whole-cell input resistance, and surprisingly, when PMNs were voltage-clamped at their resting membrane potential, muscimol induced depolarizing-inward, rather than hyperpolarizing-outward membrane current. Our findings indicate that GABA(A) receptors mediate a depolarizing blockade of the glutaminergic excitatory inputs to neonatal rat PMNs.

Animals↗

Vagal innervation of the gastrointestinal tract arises from dorsal motor nucleus while that of the heart largely from nucleus ambiguus in the cat.

The origin of medullary cells that form the cardiac vagal branch and the vagal branches in the lower thorax innervating the gastrointestinal (GI) tract was studied using horseradish peroxidase (HRP), a retrograde transport tracer in the cat. The distributions of parasympathetic postganglionic neurons of the heart were studied with acetylcholinesterase histochemistry. Intracardiac ganglionic neurons were found mainly in the connective tissue surrounding the base of the pulmonary arteries and in an area in and dorsal to the interatrial septum. Following injection of HRP into the subepicardum where most of the cardiac postganglionic neurons reside, 91% of the labelled neurons were found bilaterally distributed in the nucleus ambiguus (NA). A small population of labelled neurons was found in the dorsal motor nucleus of the vagus (DMV) and an intermediate zone (IZ) between the two nuclei. When HRP was injected into the left or right cardiopulmonary vagus branch, labelled neurons were found exclusively in the ipsilateral NA, DMV and IZ with a predominance in the NA. In the thorax, after they course around the heart, the left and right thoracic vagus nerves divides into a left and a right branch, respectively. The left branch of the left thoracic vagus joins the left branch of the right thoracic vagus to form the anterior vagus nerve at 3 cm above the diaphragm. The right branch of the right thoracic vagus nerve joins the right branch of the left thoracic vagus to form the posterior vagus nerve. After application of HRP into the right or the left branch of the left thoracic vagus, HRP labelled cells were found in the left DMV. Similarly, after application of HRP into the left or the right branch of the right thoracic vagus, labelled cells were found in the right DMV. On the other hand, when HRP was injected into the anterior vagus, labelled neurons were found bilaterally in the DMV. This suggests that all rostral branches of the thoracic vagus have their origin in the ipsilateral DMV, and intermixing occurs only at the caudal level near the diaphragm. Findings of the present experiments suggest that parasympathetic preganglionic neurons innervating the GI tract are located exclusively in the DMV while those of the heart are located mainly in the NA. Within the DMV, GI vagal neurons were found medially from the level 0-2.5 mm rostral to the obex. In contrast, cardiac vagal neurons were found in the lateral edge of the DMV at the level 0-1 mm rostral to the obex.

Animals↗

The depressor caudal ventrolateral medulla: its correlation with the pressor dorsomedial and ventrolateral medulla and the depressor paramedian reticular nucleus.

The functional correlation of the depressor caudal ventrolateral medulla (CVLM) with the two pressor regions, i.e. rostral ventrolateral medulla (RVLM) and dorsomedial medulla (DM), and with another inhibitory region, i.e. the paramedian reticular nucleus (PRN), were studied in cats anesthetized intraperitoneally with chloralose (40 mg/kg) and urethane (400 mg/kg). Systemic arterial pressure (SAP), heart rate (HR) and the sympathetic vertebral nerve activity (VNA) were recorded. The correct location of CVLM, RVLM or DM was determined by their specific responses, i.e. decreases of SAP, HR and VNA, for CVLM increases of these parameters for RVLM and DM, elicited first by electrical stimulation (80 Hz, 0.5 ms, 50-100 microA) then followed by microinjection of glutamate (Glu, 0.25 M, 70 nl). The depressor action of PRN was produced by electrical stimulation only. It was found that the depressor responses caused by the CVLM stimulation were greatly reduced 2 h after lesioning either the RVLM or DM by microinjection of kainic acid (KA, 24 mM, 200 nl) ipsilateral to the side of CVLM stimulation. The CVLM responses were further reduced after the remaining side of RVLM or DM was lesioned. The reduction of the CVLM-depressor responses was more apparent after the RVLM than DM lesioning. Data suggest that the CVLM-depressor responses are mediated through inhibition of the sympathetic-pressor neurons in both RVLM and DM with predominance of the former. Lesioning the PRN by KA and/or combination with DC electrolytic lesion reduced the CVLM-induced depressor responses. In turn, lesioning the CVLM by KA reduced the PRN-induced depressor responses. The reduction in the later manipulation was more apparent in the PRN-depressor responses than the CVLM-depressor responses. Data suggest that part of the PRN depressor action is mediated through activation of the CVLM.

Animals↗

Role of dopamine uptake in NMDA-modulated K(+)-evoked dopamine overflow in rat striatum: an in vivo electrochemical study.

An involvement of dopamine uptake in the N-methyl-D-aspartate (NMDA)-modulated dopaminergic transmission in rat striatum was studied using the technique of in vivo electrochemical detection. Microinjection of potassium (K+) evoked dopamine overflows from the dopamine-containing nerve terminals in the striatum. While application of NMDA did not evoke any dopamine overflow, co-application of NMDA and K+ induced larger dopamine overflows than those by K+ alone. Furthermore, dynamic analysis showed that the rate of clearance (Tc) was reduced by NMDA. Indeed, our uptake study demonstrated an NMDA-induced inhibition of dopamine clearance. The time course of electrochemical signals evoked by microinjection of exogenous dopamine was increased and Tc was reduced following NMDA application. In order to delineate the effects of NMDA on K(+)-evoked dopamine overflows and/or on dopamine uptake, nomifensine, a dopamine uptake inhibitor was used. Application of nomifensine potentiated K(+)-evoked dopamine overflows. Co-administration of NMDA further augmented dopamine overflows by the K+ and nomifensine mixture. Taken together, our data suggest that NMDA concomitantly potentiated dopamine overflows in response to depolarizing stimuli and attenuated dopamine uptake. The increment by NMDA of K(+)-evoked dopamine overflows may partially result from an attenuated dopamine uptake in rat striatum.

Animals↗

Striatal dopamine dynamics are altered following an intranigral infusion of iron in adult rats.

In vivo electrochemical detection was employed to examine iron-induced oxidative injury on dopamine dynamics in the nigrostriatal system of urethane-anesthetized rats. Seven days after an intranigral infusion of iron, oxidative stress was confirmed by an elevated lipid peroxidation in lesioned substantia nigra (SN). Local application of potassium (K+) evoked dopamine releases from the dopamine-containing nerve terminals in the striatum. Both amplitude and rate of clearance (Tc) of evoked dopamine releases were lower in striatum with lesioned SN; however, the time course parameters of dopamine release in the lesioned group were not different from those of the intact group, indicating a reduction in dopamine clearance. Indeed, iron-induced oxidative stress attenuated the effect of nomifensine, a high-affinity dopamine uptake blocker, on dopamine clearance. In striatum with intact SN, the amplitude and time course parameters of signals by exogenous dopamine were increased and Tc was decreased by nomifensine. In contrast, nomifensine did not significantly alter the dopamine signals of the lesioned group. Taken together, in addition to the increased lipid peroxidation in SN, our in vivo electrochemical data demonstrates that iron-induced oxidative injury attenuates K+-evoked dopamine release and dopamine uptake in the ipsilateral striatum. The diminished nomifensine effect implies a lack of high-affinity dopamine uptake sites.

Animals↗

Corticotrophin-releasing factor produces a long-lasting enhancement of synaptic efficacy in the hippocampus.

We have previously demonstrated that intra-hippocampal injection of corticotrophin-releasing factor improved memory retention of an inhibitory avoidance learning in rats; while the electrophysiological effects corticotrophin-releasing factor produces on hippocampal neurons are largely uncharacterized. In the present study, we found that corticotrophin-releasing factor injected into the dentate gyrus of hippocampus produced a dose-dependent and long-lasting enhancement in synaptic efficacy of these neurons, as measured by an increase in the amplitude and slope of population excitatory postsynaptic potentials, as well as the amplitude of population spike. The onset of corticotrophin-releasing factor-induced potentiation was slow. It was observed approximately 40-60 min after corticotrophin-releasing factor administration and lasted for more than 5 h. This effect of corticotrophin-releasing factor was blocked by pretreatment with the cyclase-adenosine-3,5-monophosphate (cAMP) inhibitor Rp-adenosine-3,5-cyclic monophosphothiolate triethylamine (Rp-cAMPS) and partially blocked by the N-methyl-D-aspartate receptor antagonist MK-801. Further, pretreatment with corticotrophin-releasing factor receptor antagonist dose-dependently diminished tetanization-induced long-term potentiation, and corticotrophin-releasing factor and tetanic stimuli had an additive effect on hippocampal neuron excitation. Moreover, direct injection of corticotrophin-releasing factor increased cAMP level in the dentate gyrus. These results together suggest that corticotrophin-releasing factor-induced potentiation simulates the late phase of tetanization-induced long-term potentiation and cAMP seems to be the messenger mediating this effect. Moreover, corticotrophin-releasing factor-induced potentiation and long-term potentiation may share some similar mechanisms, and corticotrophin-releasing factor is probably involved in the neural circuits underlying long-term potentiation. Thus, corticotrophin-releasing factor may play an important role in modulating synaptic plasticity in the hippocampus.

Action Potentials↗

Expression of bcl-2, p53 and Ki-67 in arsenical skin cancers.

To investigate the regulation of apoptosis and proliferation in arsenic-induced skin cancers, we examined the expression of bcl-2, p53, and Ki-67 using immunohistochemical staining. Thirty patients with Bowen's disease (BD), ten with basal cell carcinoma (BCC), eight with squamous cell carcinoma (SCC) and eleven of perilesional normal skin (PLN) of the non-sun exposure sites from endemic area were examined. The results showed that: 1) bcl-2 was expressed in all of the BCC homogeneously, in none of the SCC, and in 12/30 of the BD focally or homogeneously; 2) p53 was expressed in all of the arsenical skin cancers with a labelling index of 75 +/- 14% of BD, 50 +/- 17% of BCC, 61 +/- 15% of SCC, and also in all of the perilesional normal skin with a labelling index of 55 +/- 24%; 3) Ki-67 was expressed in all of the skin cancers with labelling index of 58 +/- 17% of BD, 12 +/- 7% of BCC, 47 +/- 21% of SCC, and in 9/11 of PLN with a labelling index of 41 +/- 24%. Expression of bcl-2 in BCC or BD is related to the phenotype of germinative basal cell. The constant expression of bcl-2 i early dysplastic cells of BD and the earliest expression of P53 in the basal cells of perilesional normal skin indicate that the initial step of arsenic-induced carcinogenesis is from the basal germinative cells. There is no mutual relationship between bcl-2, p53 or Ki-67 expression in any type of the arsenical skin cancers, but there is a positive correlation between p53 and Ki-67 expression identified in perilesional normal skin. BD had the highest labelling index of p53 and Ki-67.

Aged↗

Radiation-induced muscle damage in rats after fractionated high-dose irradiation.

Muscle damage in the legs of male Wistar rats after exposure to high-dose radiation was evaluated by observations of biopsied tissue made with light and transmission electron microscopy. Both legs of about 40 mature male Wistar rats were exposed to 80 Gy 6 MV X rays from a linear accelerator given in 40 fractions of 2 Gy. At intervals starting from the first day to 12 months after irradiation, serial muscle biopsies were obtained by sacrificing the rats on different days according to the experimental design. The irradiated gastrocnemius muscle displayed a progressive structural change that began immediately after the completion of the exposures. Morphological changes in irradiated muscles were characterized by hemorrhage, lymphocytic infiltration and obvious vascular destruction. Increased amounts of collagen between the muscle fibers were present even at 12 months after irradiation. There were significant changes in the number, size and structure of mitochondria in the muscle cells from the first day until 1 year after irradiation. Even 12 months after the final exposure, no recovery of muscle tissue was seen by light and transmission electron microscopy.

Animals↗

Prostatic carcinoma with brain metastasis presenting as a tumor hemorrhage.

Adenocarcinoma of the prostate commonly metastasizes to the lymph nodes and bones, with occasional visceral deposits, however, metastasis to the brain is rare. A case of prostatic carcinoma with brain metastasis presenting as a tumor hemorrhage is reported. The pertinent literature is also reviewed.

Adenocarcinoma↗

Spike responses of sympathetic vertebral nerve activities during stimulation of the pressor dorsomedial and rostral ventrolateral medulla differ in cats.

In this study, we developed a differential integrator unit containing a window discriminator (WPI-121) and three integrators (sample/hold, Gould) to characterize the difference in spikes involved in sympathetic vertebral nerve activity (VNA) and integrated VNA (Int. VNA) during stimulation of the dorsomedial (DM) and rostral ventrolateral (RVLM) medullar. The upper level (UL) in the window discriminator was set at a value, 80% of the VNA amplitude above the zero. The low level (LL) was set at a value 10% above the zero. The number of VNA spikes above the UL in the window discriminator was defined as Fa, while the number of VNA spikes within the UL and LL as Fw. In 26 cats anesthetized with urethane and alpha-chloralose, results showed that electrical stimulation and microinjections of glutamate (Glu, 0.25 M, 50 nl) or glycine (Gly, 1.0 M, 50 nl) at the same point in DM or RVLM increased both systemic arterial pressure (SAP) and Int. VNA. However, the increase of Int.VNA on DM stimulation was contributed by increases of both Fa and Fw, while on RVLM stimulation the increase of Int.VNA was mainly contributed by the increase of Fa, against a decrease of Fw. As compared to Glu, stimulation of DM by Gly produced more increase in Fw, while stimulation of RVLM by Gly produced more decrease in Fw. During RVLM stimulation the VNA was usually transferred to a huge synchronized oscillation. These findings suggest that although stimulations of the sympathetic-pressor neurons in DM and RVLM produce similar increases in SAP and VNA, the nature of these neurons is different.

Action Potentials↗

The role of CD8+ cells and CD11a in the rejection-reaction of the allogeneic microskin grafting.

By using histological tissue sections and immunohistochemical stains, the rejection-reaction of the allogeneic microskin grafting of rabbit-skin wounds was studied. The results revealed that the rejection started early in the days following transplantation. In the second week following transplantation, severe graft rejection with epithelial destruction was noted. In addition, an increase of CD8+ cells and expression of the adhesion molecule-CD11a-were also noticed and persisted throughout the days following transplantation. These findings suggest that the CD8+ cells and CD11a may play a major role in the rejection of allogeneic skin grafting.

Animals↗

Contralateral recurrent cerebellar hemangioblastoma--a case report.

Hemangioblastomas are regarded as benign neoplasms. They may recur in 3 to 10% of cases after apparently total excision. The opposite site recurrence is not found in the reported literature. A case is described in which, after successful removal of a cerebellar hemangioblastoma followed by two years of freedom from symptoms, developed a new growth of cerebellar hemangioblastoma contralaterally again. The histology of the tumor tissue is in no way different from that of a conventional hemangioblastoma. This case gives us some insights into the biological multipotentiality of cerebellar hemangioblastoma. We stress that close observation is absolutely necessary for this unique group of tumors, even after total removal.

Adult↗

Prognostic evaluation in supratentorial astrocytic tumors using p53, epidermal growth factor receptor, c-erbB-2 immunostaining.

Molecular pathology may play an important role in predicting the tumor prognosis, particularly p53, epidermal growth factor receptor (EGFR), and c-erbB-2. We investigated six variables (age, sex, histopathological grade, p53, EGFR, and c-erbB-2) to identify the role of such factors in predicting the outcome of patients with supratentorial astrocytic tumors. Thirty-seven tumors were studied including 9 well-differentiated astrocytomas (WHO grade 2), 19 anaplastic astrocytomas (WHO grade 3), and 9 glioblastomas multiforme (WHO grade 4). In univariate analysis, no statistical significance was found for the prognostic value of the sex (p = 0.2188), age (p = 0.5530), p53 immunostain (p = 0.2194), and c-erbB-2 immunostain (p = 0.4203). A significant correlation with the prognosis was found with respect to the histopathological grade (p = 0.0049) and EGFR expression (p = 0.0284). In multivariate analysis, the histopathological grade was shown to be significant independent variable (p = 0.0152). In WHO grade 2 and 3 astrocytomas, expression of p53 or EGFR was associated with poorer patient outcome. In glioblastomas, expression of p53 was also associated with poorer prognosis. Our studies suggested that conventional histological assessment of supratentorial astrocytic tumors remains the best guide to prognosis. Although no statistical significance was found between the immunostains and survival in variant grades of astrocytomas, there was a trend between p53 or EGFR proteins expression and the decrease of survival time.

Adult↗

Hypothalamic juvenile pilocytic astrocytoma presenting with intracerebral hemorrhage.

Hemorrhage of juvenile pilocytic astrocytomas is very rare. However, it is clinically important because a high probability of a fatal outcome exists if hemorrhage occurs outside the optic nerve. Hemorrhage of a hypothalamic juvenile pilocytic astrocytoma has been reported only once, from an autopsy examination. We present a successfully managed case. The patient, a 34-year-old man, presented with sudden loss of consciousness. Computed tomography (CT) and magnetic resonance imaging demonstrated an exophytic hypothalamic tumor with a hemorrhage. Craniotomy with total removal of the tumor and the hematoma was performed. Histopathologic examination revealed that the tumor was a juvenile pilocytic astrocytoma. Brain CT examination 18 months later revealed no evidence of tumor recurrence. The patient was well, without neurologic deficit, and had a normal social life as of the last follow-up examination 22 months after craniotomy.

Adult↗

Glycine increases arterial pressure and augments NMDA-induced pressor responses in the dorsomedial and ventrolateral medulla of cats.

The present study is designed to determine and characterize two neurobiological events. Firstly, we investigated whether increases of systemic arterial pressure (SAP) and sympathetic vertebral nerve activity (VNA) produced by microinjection of glycine (Gly) in the dorsomedial (DM) or rostral ventrolateral medulla (RVLM) are mediated by pressor neurons in DM or RVLM. Secondly, we assessed whether simultaneous microinjections of Gly and N-methyl-D-aspartate (NMDA) in DM or RVLM potentiate the NMDA-pressor effects. Changes in SAP and VNA were recorded in 33 cats under alpha-chloralose and urethane anesthesia. Microinjection of sodium glutamate (Glu, 0.25 M, 30 nl) or Gly (1.0 M, 30 nl) into the DM or RVLM increased SAP and VNA in similar magnitude. Latencies of changes in SAP and VNA induced by Gly, however, were longer (3 s) than those induced by Glu. Prior microinjection of the following antagonists blocked the Gly-induced pressor responses: 2-amino-5-phosphonopentanoate (AP-5, 25 mM, 30 nl), a specific NMDA receptor antagonist; or glutamate diethyl ester (GDEE, 0.5 M, 30 nl), a quisqualate receptor antagonist; or kynurenic acid (KYN, 10 mM, 30 nl), a broad spectrum competitive Glu antagonist. Prior treatment with strychnine (3 mM, 30 nl), a specific Gly antagonist, also blocked the Gly-induced pressor responses. Since Gly is believed to be an inhibitory neurotransmitter, these data suggest that Gly may produce pressor actions via an inhibition on specific inhibitory neurons synapsing with the pressor neurons. NMDA (0.1 M, 30 nl) and Gly (1.0 M, 30 nl) microinjected simultaneously in DM or RVLM produced a greater pressor action than NMDA alone. This potentiation was blocked by KYN, another known antagonist for such potentiation, but was only partially blocked by strychnine.

2-Amino-5-phosphonovalerate↗

Paramedian reticular nucleus may be unrelated to the development of hypertension in spontaneously hypertensive rats.

The role of paramedian reticular nucleus (PRN), a structure effecting sympathetic inhibition, in the development of hypertension was investigated in young spontaneously hypertensive rats (SHR) and two age-matched normotensive rats, Wistar-Kyoto (WKY) and Sprague-Dawley rats (SD). Three different experimental manipulations, including electrical-lesioning, sham-operated and intact control, were performed in SHR, WKY and SD rats 7 weeks after birth. In the control groups, the systolic arterial blood pressure (SABP) of SHR increased abruptly from 160 mmHg to 230 mmHg from the 6th to 13th week after birth, whereas those of WKY and SD maintained a normal range of SABP. In the lesioned groups, a hypotension and/or bradycardia was evoked by electrical stimulation to verify the location of PRN. Following the verification, a direct current was delivered to lesion the PRN in situ. The effect of PRN lesioning on the subsequent development of hypertension was illustrated by comparing SABP in three experimental groups of age-matched conscious SHR, WKY and SD during 8-13 weeks after birth. We found that the average SABP in the lesioned SHR was consistently elevated and was not significantly different from those of the sham-operated and the control. In contrast, in the normotensive rats, there was no significant increase in SABP within the three experimental groups, i.e., the average SABP of the lesioned, the shamed-operated and the control group maintained a normal range. Our results support the contention that the hypertension of SHR developed within 6-13 weeks after birth. In addition, the sympatho-inhibitory mechanism of PRN was not directly related to the development of hypertension.

Aging↗

Attenuation of cardiovascular reactions of vocalized and non-vocalized defence areas of periaqueductal grey following lesions in dorsomedial or ventrolateral medulla of cats.

In the pretentorial periaqueductal grey (PAG), the region producing pressor responses, vocalization and other somatic and visceral signs (VPR) of the defence reaction and another region producing pressor responses (PR) were localized by electrical stimulation in adult cats, anesthetized with intraperitoneal chloralose (40 mg/kg) and urethane (400 mg/kg). The pressor responses included increases of systemic arterial pressure (SAP) and heart rate, increases of blood flow in the common carotid and femoral arteries and a decrease of blood flow in the superior mesenteric artery. The VPR was found in a relatively restricted region of the dorsolateral PAG, while PR was found scattered within the dorsal and ventral portions of the lateral PAG. The increase of SAP and the changes of blood flow in the sampled arteries were slightly greater during VPR than PR stimulation. Mild vocalization with a slight increase of SAP but marked increases of carotid and femoral blood flow (vasodilation) could be induced by microinjection of N-methyl D-aspartate (0.2 M, 200 nl) into the VPR and the blood flow increase, particularly that of the femoral artery, was greatly attenuated by atropine (1 mg/kg, i.v.). In order to ascertain the contribution of the medullary pressor areas to the VPR- and PR-induced responses, extensive lesions were made in the dorsomedial (DM) or vetrolateral medulla (VLM) by microinjections of kainic acid (KA, 0.024 M) in 27 of the 42 cats. The resting SAP and blood flow of the three arteries were reduced by lesioning of the VLM more than that of the DM. Responses of SAP and blood flow from activation of the PR and VPR, particularly the latter, were affected more after DM compared to VLM lesioning. These data suggest that, while the pretentorial PAG constitutes the 'defence area,' vocalization is confined exclusively to its dorsolateral region and that both the VLM and DM contribute to the cardiovascular components of defence reactions. The DM appears to have a greater contribution compared to the VLM.

Animals↗