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Biomedical subjects

P J Zhu

Publications and source records attributed to P J Zhu.

At least 19 recordsLinked to original sources
PubMed2002

Nicotinic receptors mediate increased GABA release in brain through a tetrodotoxin-insensitive mechanism during prolonged exposure to nicotine.

The effects of nicotine on the spontaneous release of GABA from nerve terminals in the chick lateral spiriform nucleus were examined using whole cell patch-clamp recording in brain slices. Exposure to 1 microM nicotine produced an early immediate increase in the frequency of spontaneous postsynaptic GABAergic currents. This effect was blocked in the presence of 0.5 microM tetrodotoxin. However, a prolonged application of 0.1-1 microM nicotine (>3 min) caused a tetrodotoxin-insensitive increase in the frequency of spontaneous GABAergic currents. This late tetrodotoxin-insensitive effect was blocked by the nicotinic antagonists dihydro-beta-erythroidine (30 microM) and mecamylamine (10 microM), but not by methyllycaconitine (50-100 nM), indicating that activation of high affinity nicotine receptors was mainly responsible for this effect. This enhancement was inhibited by the high threshold Ca(2+) channel blocker Cd(2+) (100 microM), but not by dantrolene or ryanodine. The tetrodotoxin-insensitive enhancement of the frequency of GABA currents by nicotine was reduced by inhibition of cAMP-dependent protein kinase with HA1004 (30 microM), but not by inhibition of protein kinase C with staurosporine (1 microM), and was facilitated by forskolin (10 microM) or bromo-cAMP (50 microM). The results indicate that nicotine-enhanced GABA release can operate through both tetrodotoxin-sensitive and -insensitive mechanisms in a single brain region and that a second messenger cascade may be involved in the tetrodotoxin-insensitive enhancement by nicotine.

Animals↗
PubMed1999

Persistent block of CA1 synaptic function by prolonged hypoxia.

The effects of prolonged hypoxia were studied by field and intracellular recordings from hippocampal slices of the rat, kept submerged at 34 degrees C. When artificial cerebrospinal fluid contained 10 mM glucose, even very long exposures to hypoxia or 300 microM cyanide (21-25 min) did not block field excitatory postsynaptic potentials and population spikes irreversibly. By contrast, in the presence of 4 mM glucose, hypoxia lasting only 9-13 min-ending 2-3 min after the characteristic transient recovery ("hypoxic injury potential")-resulted in irreversible block of synaptic responses. Voltage-dependent sodium channels and N-methyl-D-aspartate receptors are involved, because irreversible block was prevented by tetrodotoxin (0.5 microM), kynurenate (2 mM) or DL-aminophosphonovalerate (50 microM), whereas 6,7-dinitroquinoxaline-2,3-dione (25 microM) suppressed only the transient recovery. The hypoxic suppression of afferent volleys in slices kept in 4 mM glucose was also prevented by kynurenate or aminophosphonovalerate. Intracellular recordings revealed opposite effects of hypoxia according to glucose concentration: in 10 mM glucose, mainly hyperpolarization; in 4 mM glucose, after a brief hyperpolarization, a major and usually irreversible depolarization. In the presence of kynurenate or tetrodotoxin, major depolarizations also occurred, but they were reversible. Thus, large depolarizations of hippocampal neurons do not necessarily lead to irreversible block of synaptic transmission: there is lasting damage only when hypoxia is combined with low glucose, presumably because a reduced supply of glycolytically generated ATP limits the Na+/K+ pump's ability to maintain or restore membrane potentials and thus prevent excessive activation of N-methyl-D-aspartate receptors.

Afferent Pathways↗
PubMed1999

Nicotine modulates evoked GABAergic transmission in the brain.

The effects of nicotine on evoked GABAergic synaptic transmission were examined using whole cell recordings from neurons of the lateral spiriform nucleus in embryonic chick brain slices. All synaptic activities were abolished by the GABA(A) receptor antagonist, bicuculline (20 microM). Under voltage-clamp with KCl-filled pipettes (holding potential -70 mV), nicotine (0.1-1.0 microM) increased the frequency of spontaneous GABAergic currents in a dose-dependent manner. Nicotine enhanced electrically evoked GABAergic transmission only at relatively low concentrations of 50-100 nM (but not 25 nM), which approximate the concentrations of nicotine in the blood produced by cigarette smoking. At higher concentrations nicotine had either no effect (0.25 microM) or diminished (0.5-1.0 microM) evoked GABAergic neurotransmission. Nicotine had no significant effect on the postsynaptic current induced by exogenous GABA (30-50 microM). These data imply that nicotine levels attained in smokers are sufficient to enhance evoked GABAergic transmission in the brain, and that this effect is most likely mediated through activation of presynaptic nicotinic receptors.

Animals↗
PubMed1997

Adenosine release mediates cyanide-induced suppression of CA1 neuronal activity.

The rapid suppression of CNS function produced by cyanide (CN) was studied by field, intracellular, and whole-cell recording in hippocampal slices (at 33-34 degrees C). Population spikes and field EPSPs were depressed by 4-5 min bath applications of 50-100 microM CN (IC50 was 18 miroM for spikes and 72 microM for EPSPs). The actions of CN were reversibly suppressed by the adenosine antagonists 8-sulfophenyltheophylline (8-SPT; 10 microM) and 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; 0.2 microM), potentiated by the adenosine transport inhibitor dipyridamole (0.5 microM), but unaffected by the KATP channel blocker glyburide (10 microM). Therefore the CN-induced reductions of synaptic efficacy and postsynaptic excitability-demonstrated by synaptic input:output plots-are mediated mainly by adenosine. In whole-cell or intracellular recordings, CN depressed EPSCs and elicited an increase in input conductance and an outward current, the reversal potential of which was approximately -90 mV (indicating that K+ was the major carrier). These effects also were attenuated by 8-SPT. In the presence of 1 mM Ba, CN had no significant postsynaptic action; Cs (2 mM) also prevented CN-induced outward currents but only partly blocked the increase in conductance. Another 8-SPT-sensitive action of CN was to depress hyperpolarization-activated slow inward relaxations (Q current). At room temperature (22-24 degrees C), although it did not change holding current and slow inward relaxations, CN raised the input conductance; this effect also was prevented by 8-SPT (10 microM), but not by glyburide (10 microM). Adenosine release thus appears to be the major link between acute CN poisoning and early depression of CNS synaptic function.

Adenosine↗
PubMed1997

Endogenous adenosine on membrane properties of CA1 neurons in rat hippocampal slices during normoxia and hypoxia.

The effects of endogenous adenosine release on CA1 neurons in hippocampal slices were studied under normoxic and hypoxic conditions, by using extra-/intracellular and whole-cell recordings. During normoxia, the adenosine antagonist, 8-(p-sulphophenyl) theophylline (8-SPT) or adenosine deaminase (ADA) potentiated both evoked CA1 EPSPs and spontaneous synaptic activity, but not monosynaptic IPSPs; there was a minimal depolarization (by 1 mV), probably caused by the enhanced synaptic activity, but no increase in input conductance. Under voltage-clamp with KCl electrodes (with holding potential (VH) near -70 mV), hypoxia (4-5 min) elicited a rise in input conductance and an outward current that reversed near -90 mV, in keeping with the activation of K conductance. These effects of hypoxia were partly attenuated by 8-SPT (10 microM). The hypoxia-induced outward current and conductance increase were abolished by 1 mM Ba, being replaced by a small inward current and a conductance decrease. These data indicate that adenosine tonically inhibits excitatory, but not inhibitory, synaptic transmission, has no direct effect on input conductance, and contributes to the hyperpolarization and fall in input resistance induced by hypoxia.

Adenosine↗
PubMed1997

[Effect of boayuan qiangshen II tablet on plasma and urine superoxide dismutase and malondialdehyde in patients with chronic renal failure].

OBJECTIVE: To observe the effect of Chinese herbs of replenishing Kidney in treating chronic renal failure (CRF). METHODS: Forty patients with CRF wrer randomly divided into two groups, Baoyuan Qiangshen (BQ) II tablet group and essential amino acid added capoten group. The changes of plasma and urine superoxide dismutase (SOD) and malondialdehyde (MDA) and the kidney function indices were investigated before and after treatment. RESULTS: Before treatment, SOD reduced and MDA of both groups increased (P < 0.01), while urine SOD and MDA increased (P < 0.01). After treatment, plasma SOD increased but MDA was reduced and urine SOD, MDA were also reduced (P < 0.01). Although the BUN and serum creatinine reduced significantly, creatinine clearance rate elevated significantly (P < 0.01). CONCLUSIONS: The BQ II tablet could strengthen antioxidation and inhibit lipid peroxidation, so it was effective to improve kidney function.

Adult↗
PubMed1996

[Study on effect of baoyuan qiangshen tablet no. I in prolongating interval of hemodialysis in patients of terminal-stage of renal disease].

Twenty cases of terminal stage of renal disease (TSRD) were treated with Baoyuan Qiangshen Tablet No. I(BYQS I) combined with hemodialysis once every 5 days (TCM-WM group) was observed and compared with patients treated with routine hemodialysis (once every 3 days) only (control group). Results showed that the increasing extents of serum creatinine, blood urea nitrogen of TCM-WM group at dialysis interval were all lower than that of control group (P < 0.01). After 3 months' treatment, serum creatinine, blood urea nitrogen of TCM-WM group were lower than that before treatment, plasma albumin, lipoprotein, urine level of prostaglandin and anemia were all improved to varies extent, but the creatinine clearance rate was unchanged. The author considered that BYQS I could prolong the interval and reduce the times of dialysis by way of regulating the lipid metabolism disorder, improving pathological change of kidney and protect function of residual kidney unit, and above-mentioned therapeutic method is a good programm of integrated TCM-WM in treating TSRD.

Adult↗
PubMed1995

Nitric oxide may be a mediator of effects of prolonged but not brief anoxia in CA1 neurons in slices.

As a known vasodilator, nitric oxide (NO) probably acts by hyperpolarizing smooth muscle by increasing K conductance (GK). Therefore NO could mediate the anoxic hyperpolarizations of brain neurons that are also mediated by GK. We investigated this question by recording from CA1 neurons in submerged hippocampal slices (from rats), kept at 33 degrees C. Incubation with the NO synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME; 200 microM) had no significant effect on CA1 population spikes (delta = 2.5%, SEM +/- 3.1%, n = 7) or on the time course of their suppression by brief exposure to anoxia (2-3 min). In intracellular recordings, L-NAME did not change the resting membrane potential or input resistance (n = 10). In the presence of L-NAME, anoxic changes were not significantly different: the cells were hyperpolarized by 6.4 +/- 0.74 mV (6.3 +/- 0.82 mV for controls) and their resistance decreased by 16 +/- 3.2% (18 +/- 1.4% for controls, n = 10). In whole-cell recordings from another 15 cells (clamped at approximately -50 mV, near resting level), L-NAME also had no consistent effect on input conductase (GN) or holding current (IH); and the anoxic increased in GN were unchanged (44 +/- 12% before and 48 +/- 20% after, for n = 10). Thus NO does not appear to be a significant element in the mechanism of membrane and synaptic changes during brief anoxia in CA1 neurons in slices.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Anoxia selectively depresses excitatory synaptic transmission in hippocampal slices.

EPSPs/IPSPs were recorded with intracellular electrodes from CA1 neurons close to site of stimulation. Brief anoxia (3 min) abolished EPSPs but reduced IPSPs by 64.8 +/- 4.0% (n = 10); the remaining IPSP was presumed to be monosynaptic. The effects of anoxia on purely monosynaptic IPSPs were examined after pharmacological blockade of excitatory synaptic transmission with 2 mM kynurenate or 20 microM CNQX + 20 microM APV. In these tests, after 3 min of anoxia the slopes of IPSPs vs. membrane potential were reduced by only 38.2 +/- 4.3% (n = 12). The present study demonstrates that, contrary to previous reports, inhibitory synaptic transmission is quite resistant to anoxia.

2-Amino-5-phosphonovalerate↗
PubMed1994

Endogenous adenosine deaminase does not modulate synaptic transmission in rat hippocampal slices under normoxic or hypoxic conditions.

Field and intracellular potentials were recorded from CA1 pyramidal stratum in submerged slices (at 33 degrees). During "normal" oxygenation (95% O2 + 5% CO2), tonic depression of population spikes and field excitatory postsynaptic potentials by endogenous adenosine was demonstrated by (i) the marked enhancement by the adenosine antagonists 8-(p-sulfophenyl)theophylline (10 microM) and caffeine (0.2 mM), (ii) depression by the transport blocker dipyridamole (5 microM), and (iii) enhancement by exogenous adenosine deaminase (all tested by bath application). Thus, adenosine deaminase (0.5 units/ml) reduced by 10.7 +/- 3.0% (S.E.) the half-maximal stimulus intensity (for population spikes). The effects of adenosine deaminase were prevented by the specific inhibitor, deoxycoformycin (30 microM). In intracellular recordings, excitatory postsynaptic potentials were enhanced in a comparable manner by adenosine deaminase. By contrast, neither deoxycoformycin (5 and 30 microM) nor erythro-9-(2-hydroxy-3-nonyl)adenine (another adenosine deaminase inhibitor; 10 and 50 microM) had significant effects on population spikes. Superfusion with anoxic medium (saturated with 95% N2 + 5% CO2) for 2-3 min suppressed population spikes reversibly, by a mechanism involving adenosine, because 8-(p-sulfophenyl)theophylline (10 microM) and caffeine (0.2 mM) delayed the onset of anoxic block and accelerated the subsequent recovery, and the recovery was much slower or incomplete in the presence of dipyramidole (0.5 microM). However, the anoxic suppression of population spikes was not affected by deoxycoformycin (30 microM) or erythro-9-(2-hydroxy-3-nonyl)adenine (10 microM); the corresponding 50% postanoxic recovery times were also unchanged (e.g. 4.0 +/- 0.2 min for controls and 4.1 +/- 0.3 min in deoxycoformycin).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenine↗
PubMed1993

Adenosine release is a major cause of failure of synaptic transmission during hypoglycaemia in rat hippocampal slices.

Glucose-free medium (aglycaemia) caused a complete failure of CA1 population spikes (after 14.5 +/- 0.8 min) and field EPSPs (after 18.1 +/- 0.5 min). In the presence of the selective adenosine A1 antagonist, 8-(p-sulfophenyl)theophylline (10 microM), population spikes and EPSPs were decreased by only 13.8 +/- 11.9% and 32.4 +/- 11.6% at the end of 17.0 +/- 3.0 min and 19.8 +/- 1.7 min of aglycaemia, respectively. A similar effect was produced by caffeine (0.2 mM). The ATP-sensitive K+ channel blockers tolbutamide (1 mM) and glibenclamide (10 microM) had no significant effect on aglycaemic suppression of synaptic transmission. These observations indicate that endogenous adenosine, but not ATP-sensitive K+ conductance, plays a major role in hypoglycaemia failure of transmission.

Action Potentials↗
PubMed1993

Effects of bretylium tosylate on electrophysiologic properties of normal and digitalized papillary muscles of guinea pigs.

The effects of bretylium tosylate (BT) on the electrophysiologic properties of normal and digitalized papillary muscles isolated from guinea pigs were studied with regular glass microelectrode. BT prolonged effective refractory period (ERP) and action potential duration (APD) of normal papillary muscles. The ERP and APD of papillary muscles were shortened by perfusion with ouabain (Oua) 0.2 mumol.L-1. No recovery was seen in perfusion without drug for 30 min. In digitalized papillary muscles with Oua, ERP, APD90, and APD50 were prolonged by BT 120 mumol.L-1 form 175 +/- 20, 187 +/- 20, and 146 +/- 21 ms to 222 +/- 21, 220 +/- 19, and 190 +/- 19 ms, respectively. The results demonstrated that BT can prolong ERP and APD of papillary muscles digitalized with Oua.

Action Potentials↗
PubMed1993

[Oral and rectal administration of Chinese herbal and essential amino acids injection in 103 cases of chronic renal failure].

UNLABELLED: 103 cases of chronic renal failure (CRF), were treated by oral taken drugs for warming and replenishing Spleen and Kidney, rectal given drugs for expelling and purgating the pathogenic factor and injection of essential amino-acid (EAA). RESULTS: BUN and Scr of patients reduced obviously than that of pre-treatment (P < 0.05), but Ccr increased (P < 0.05), Scr of 43 cases normalized eventually, the total effective rate was 86.47%. 60 of 103 cases were observed for more than one year, the kidney function of 27 cases remained to be normal, Scr of 20 cases stabilized at the level of discharging from hospital. Although the Scr of 13 cases increased slightly, but 3 cases developed to the terminal stage of CRF only. It is considered that this program was effective not only for immediate efficacy, but also could delay the progress of CRF.

Administration, Rectal↗
PubMed1992

[Therapeutic changes in nephrotic syndrome treated with yiqi huoxue jiedu decoction and corticosteroid].

UNLABELLED: Plasmic and urinary TXB2 and 6-Keto-PGF1 alpha of 87 patients of nephrotic syndrome (NS) and 25 healthy subjects were measured by RIA, and the influence of Yiqi Huoxue Jiedu decoction (YHJ) and corticosteroid on above-mentioned parameters was investigated. RESULTS: Plasmic and urinary TXB2 as well as the ratio of TXB2/6-K-PGF1 alpha of both types of NS increased (P < 0.01-0.05). The plasmic TXB2 of II type was higher than that of I type of NS (P < 0.01), 6-K-PGF1 alpha increased as well (P < 0.05). After treatment, plasmic and urinary TXB2 of both types of NS were remarkably lower (P < 0.01), while urinary 6-K-PGF1 alpha increased significantly (P < 0.05). In comparing with pre-treatment investigation, the plasmic 6-K-PGF1 alpha of II type was reduced (P < 0.05). It was shown that YHJ would inhibit the synthesis of TXA2 and regulate the TXA2-PGI2 balance. YHJ was markedly effective in producing TXB2 and 6-K-PGF1 alpha increase, its therapeutical effects was better to patients with Yin Deficiency and both Qi-Yin Deficiency, but not so well with Yang Deficiency Syndrome.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

[Electrophysiologic effects of sophocarpine on papillary muscle in guinea pig].

Sophocarpine prolonged the action potential duration of guinea pig papillary muscle in a dose-dependent manner. After the preparations were exposed to sophocarpine 50 mumol/L for 30 min, APD50 and APD90 were prolonged from 189 +/- 21 and 216 +/- 24 ms to 205 +/- 27 and 241 +/- 25 ms (P less than 0.01). Simultaneously, ERP was prolonged from 202 +/- 14 to 211 +/- 16 ms, although the ERP/APD90 ratio was not changed. Sophocarpine had no significant effects on other AP parameters. Propranolol did not block sophocarpine effects.

Action Potentials↗