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J Zhai

Publications and source records attributed to J Zhai.

30 records · Page 2Linked to original sources
PubMed1998

Effects of ethanol on rat somatosensory cortical neurons.

In this study, we characterized the local effects of ethanol (EtOH) on postsynaptic potentials (PSPs) and membrane properties of layer II-III (L2-3) and layer V (L5) somatosensory cortical neurons. Intracellular recordings were done using the in vitro slice preparation of rat somatosensory cortex. Our results show that EtOH exerts local effects on cortical cell membrane at physiologically relevant concentrations. A predominant effect of EtOH was to reduce excitability of L2-3 and L5 neurons by increasing the rheobase, decreasing input resistance and repetitive firing, reducing PSPs amplitude and the probability of evoking action potentials. Early (6 ms) and late (18 ms) PSP components were affected differentially by EtOH, the late components being more suppressed. Overall, EtOH-mediated suppression of PSPs was stronger in L5 neurons. Cortical neurons were divided into three subtypes: regular spiking adapting (RS-A), regular spiking non-adapting (RS-NA) and bursting (D-IB) neurons. PSPs evoked in RS-A neurons were more sensitive to EtOH suppressant effects. EtOH effects on input resistance were distributed differentially among the three groups of neurons. These results support the notion that EtOH disrupts higher processing of somatosensory information via a differential alteration of cortical neuron's membrane properties and synaptic transmission.

Animals↗
PubMed1998

Proton inhibition of GABA-activated current in rat primary sensory neurons.

The modulation of the Cl- current activated by gamma-aminobutyric acid (GABA) by changes in extracellular pH in freshly isolated rat dorsal root ganglia (DRG) neurons was studied using the whole-cell patch-clamp technique. In the pH range of 5.0-9.0, increased extracellular pH enhanced, and decreased extracellular pH suppressed, current activated by 10 microM GABA in a reversible and concentration-dependent manner with an IC50 of pH 7.1 in these neurons. Acidification to pH 6.5 inhibited currents activated by the GABAA-selective agonist muscimol in all neurons tested. The antagonism of GABA-activated current by lowering the pH was equivalent at holding potentials between -80 and +40 mV and did not involve a significant alteration in reversal potential. Acidification shifted the GABA concentration/response curve to the right, significantly increasing the EC50 for GABA without appreciably changing the slope or maximal value of the curve. Inhibition of the GABA-activated current by protons was not significantly different when the patch-pipette solution was buffered at pH 7.4 or pH 6.5. These results suggest that extracellular protons inhibit GABAA receptor channels in primary sensory neurons by decreasing the apparent affinity of the receptor for GABA. This represents a novel mechanism of inhibition by protons of a neurotransmitter-gated ion channel. Proton inhibition of GABAA receptor channels may account in part for the modulation by protons of sensory information transmission under certain pathophysiological conditions.

Animals↗
PubMed1998

Gene expression of luteinizing hormone receptor and steroidogenic enzymes during Leydig cell development.

Testicular Leydig cells (LC) are rapidly and selectively destroyed by an injection of ethane dimethane sulfonate (EDS). LC regeneration occurs in the testis of the EDS-treated rats from the differentiation of the precursor Leydig cells (PLC). This study was designed to investigate the patterns of change in the mRNAs for the luteinizing hormone receptor (LHR) and the steroidogenic enzymes, cholesterol side chain cleavage (P-450scc) and 17 alpha-hydroxylase (P-450(17 alpha)) during LC regeneration from PLCs. Mature (60 days of age) Sprague-Dawley male rats received a single intraperitoneal injection of EDS and were killed at different times between days 2 and 60 post-treatment. PLC- and LC-enriched fractions were isolated from the testes of the EDS-treated rats and age-matched control rats using a collagenase digestion-Percoll gradient method. Total RNA was extracted from these cell populations and subjected to Northern blot analysis. The LC fraction isolated from testes of control rats expressed four major transcripts of the LHR, sized 1.8, 2.5, 4.2 and 7.0 kb. The undifferentiated PLC fraction from controls expressed only a truncated form, the 1.8 kb transcript. This truncated LHR transcript was also the only LHR mRNA species detected in PLCs at day 2 post-EDS treatment. In contrast, all four transcripts of the LHR were detected in the PLC fraction at day 10 post-EDS treatment. The levels of the full length 7.0 kb transcript increased thereafter and reached a peak between days 24 and 36 post-EDS treatment in the PLC fraction. Concomitant with the increase in the 7.0 kb transcript, the truncated 1.8 kb transcript decreased in amount and reached a nadir between days 16 and 36 post-treatment. The changes observed in this cell fraction reflect the process of differentiation of PLCs into LCs. At day 45 post-EDS treatment, the level of the 7.0 kb transcript decreased while the 1.8 kb form increased in the PLC fraction, reflecting the completion of LC regeneration from this cell fraction. By day 60 post-EDS treatment, the levels of the 1.8 kb transcript rose to the value observed in undifferentiated control PLCs and the other transcripts were no longer detected in the PLC fraction, indicating that cells in the PLC fraction were again in an undifferentiated stage. Messenger RNAs for both the steroidogenic enzymes, P-450scc and P-450(17 alpha) were expressed in the control LC fraction. Neither of these two mRNAs were detected in the PLC fraction of the control rats. P-450scc and P-450(17 alpha) mRNAs were first expressed in the PLC fraction at day 10 post-EDS treatment. Thereafter, the levels of P-450scc and P-450(17 alpha) mRNAs increased in the PLC fraction and reached a peak between days 24 and 36 and days 24 and 45 post-EDS treatment respectively. P-450scc and P-450(17 alpha) mRNAs were no longer expressed in the PLC fraction at day 60 post-EDS treatment. These patterns also reflect the process of differentiation of PLCs into functional LCs. These results demonstrate for the first time that PLCs in the control testis are undifferentiated and do not express functional LHR and steroidogenic enzymes or their mRNAs. The PLCs are characterized, however, by the expression of a truncated 1.8 kb transcript of the LHR mRNA. Functional LHR and steroidogenic enzymes are expressed in PLCs only during their differentiation into LCs after EDS treatment. Subsequent to LC regeneration, the PLCs return to an undifferentiated stage.

Animals↗
PubMed1998

Aqua-Reslin droplet analysis.

Aerosol droplets were collected, counted, and sorted using a laser system, the Army Insecticide Measuring System, Teflon-coated slides, and magnesium oxide-coated slides. All droplets, for each method and replication, were generated by a London Aire 1820 or a Leco Model 1600. These data indicate that the Army Insecticide Measuring System or Teflon-coated slides are so closely similar to the laser that they could effectively be used in the field without an overwhelming loss in precision.

Aerosols↗
PubMed1997

Chronic cocaine intoxication alters hippocampal sodium channel function.

Repeated daily administration of subconvulsive doses of cocaine results in the appearance and increase in convulsive responsiveness to the drug and its lethal effects. The mechanisms involved in this increased susceptibility to cocaine-induced seizure are yet unknown. In this study, we used whole cell patch-clamp recording techniques to examine the functional changes in voltage-dependent Na+ channels produced by subconvulsive doses of cocaine (45 mg/kg per day, i.p.) in rat hippocampal CA1 pyramidal neurons. Intact animals were injected with cocaine for 5-6 days. Acutely dissociated hippocampal neurons were then recorded in vitro. Our results show that an augmentation of peak Na+ currents and a shift in depolarizing direction of the steady-state inactivation were present in neurons from drug-treated rats. These changes, by making a larger proportion of Na+ channels available for opening, could increase the excitability of CA1 neurons and may contribute to the increase in convulsive responsiveness to cocaine.

Animals↗
PubMed1997

DNA based biosensors.

Compared to advances in enzyme sensors, immunosensors, and microbial biosensors, relatively little work exists on DNA based biosensors. Here we review the DNA based biosensors that rely on nucleic acid hybridization. Major types DNA biosensors--electrochemical, optical, acoustic, and piezoelectric--are introduced and compared. The specificity and response characteristics of DNA biosensors are discussed. Overall, a promising future is foreseen for the DNA based sensor technology.

Journal Article↗
PubMed1996

Estrogen receptor messenger ribonucleic acid changes during Leydig cell development.

Mature (60-65 days old) male Sprague-Dawley rats received a single i.p. injection of ethane dimethane sulfonate (EDS, 100 mg/kg BW) and were killed at different times from Days 2 to 60 posttreatment. Bands of cells enriched in precursor Leydig cells (PLCs) and Leydig cells (LCs) were isolated from the testis of EDS-treated rats and age-matched controls using a collagenase digestion-Percoll gradient method. Total RNA extracted from the PLC and LC fractions was subjected to reverse transcriptase polymerase chain reaction (RT-PCR) to detect estrogen receptor (ER) mRNA. The RT-PCR results demonstrated that ER mRNA was present in both LC and PLC fractions. Quantitative RT-PCR analysis, using rabbit beta-globin mRNA as the internal standard, showed that ER mRNA in the PLC fraction was 20-fold higher than in the LC fraction in control testis. After EDS treatment, ER mRNA levels in the PLC fraction decreased and reached a nadir at Day 16 posttreatment. Thereafter, ER mRNA in the PLC fraction gradually increased and returned to control PLC levels. In contrast, ER mRNA levels in the LC fraction in controls and at Days 16-45 posttreatment remained constant. To correlate the changes in ER mRNA levels with LC differentiation, in vitro testosterone (T) production by PLC- and LC-enriched fractions in the presence or absence of 50 mIU hCG was measured by RIA. T production in the control PLC fraction was low (1/10th that in the control LC fraction), and hCG addition resulted in only a 1.5-fold stimulation (relative to a 7.5-fold stimulation in LCs). In the PLC fraction, T production was not detectable at Days 2 and 10 after EDS treatments, began to respond to hCG stimulation with increased T production at Day 16, and reached a maximum between 4 and 6 wk after EDS treatment. By Day 60 posttreatment, T production in the PLC fraction decreased and returned to control PLC levels. Testosterone production in the LC fraction was not detectable at Days 2 and 10 posttreatment. From Days 16 to 60 posttreatment, LC basal and hCG-responsive T production increased gradually and returned to control LC levels. It is concluded that functional LCs are regenerated from the PLCs and that both these cell types possess ER mRNA. It is interesting to note that PLCs exhibit higher levels of ER mRNA than do LCs. A decrease in ER mRNA in PLCs appears to coincide with the early differentiation process to yield LCs. Thus, estradiol-17 beta produced locally in the testis by the LCs might act via its receptor as a paracrine substance to impede PLC development into LCs. It is therefore possible that either a decrease in E2 production or a decrease in ER and its mRNA in PLCs would then release the PLCs to begin the regeneration process.

Animals↗
PubMed1992

Measuring cypermethrin resistance in the German cockroach (Orthoptera: Blattellidae).

Cypermethrin resistance in the German cockroach, Blattella germanica (L.), was assessed by tests of surface contact and topical application. Topical application provided the most sensitive measure of resistance in a field strain. The resistance ratio (RR) measured by topical application was 122.6 for cypermethrin at LD50. As measured by surface contact, the resistance ratio at KT50 was 2.9. Differences between the walking movement of cockroaches of susceptible (VPI) and field (RHA) strains on deposits of cypermethrin influenced KT50 values. A bioassay with unrestricted movement resulted in RHA strain cockroaches accumulating a larger dose on the tarsal pads and subsequent reduction of the resistance ratio at KT50. Less walking by the VPI strain resulted in less insecticide accumulation on their tarsal pads. On a bioassay in which movement was restricted, the amount of insecticide accumulating on the tarsi was equalized, resulting in an increased resistance ratio at KT50. Differences in susceptibility were more accurately measured when the two strains were topically treated (either on the thorax or the tarsal pads) with known doses of insecticide.

Animals↗
PubMed1991

Effect of nifedipine on neurons of guinea pig celiac ganglion.

The effect of nifedipine on electrophysiological membrane properties and nicotinic neurotransmission of guinea pig celiac ganglion neurons was studied using intracellular recordings in vitro. Nifedipine in concentrations of 0.1-10 microM did not affect membrane potential, membrane input resistance or the amplitude and duration of action potentials induced by intracellular current injection. Higher doses of nifedipine (0.1-1 mM) significantly reduced the amplitude and extended the duration of action potentials induced by intracellular current injection. Superfusion of the ganglia with nifedipine in concentrations of 0.1-10 microM significantly inhibited nicotinic fast excitatory postsynaptic potentials (f-EPSPs) and orthodromic action potentials evoked by nerve stimulation. This depressant effect of nifedipine on synaptic transmission was eliminated with high Ca2+ (12.5 mM). Nifedipine (10 microM) did not affect the postsynaptic effect of exogenous acetylcholine (ACh), but significantly reduced the quantal content but not the quantal size of evoked f-EPSPs in a low Ca2+ (0.5 mM), high Mg2+ (5.5 mM) Krebs solution. Nifedipine in concentration of 10 microM did not affect afterspike hyperpolarization (AH) and post-tetanic hyperpolarization (PTH), which have been recognized to be generated mainly by an increase of calcium-dependent potassium conductance. Higher doses of nifedipine (0.1-1 mM) significantly depressed AH and PTH. These experimental results suggest that nifedipine in concentrations of 0.1-10 microM exerts an inhibitory effect on nicotinic neurotransmission without affecting the membrane properties of the guinea pig celiac ganglion neurons. This inhibitory effect of nifedipine on synaptic transmission may result from blocking L-type calcium channels and reducing the quantal release of ACh from the presynaptic nerve terminals.

Animals↗
PubMed1991

[Nifedipine inhibits calcium-dependent potentials in guinea pig sympathetic neurons].

Reversible effects of nifedipine, a calcium channel blocker, on 3 types of calcium-dependent potentials in the celiac ganglion cells of the guinea pigs in vitro were investigated by means of intracellular recordings. Nifedipine (0.1-1 mmol/L) inhibited the spike afterhyperpolarization, the post-tetanic membrane potential in dose-dependent manner. Nifedipine (0.1 mumol/L) also depressed the Ca2+ spike potential in a Na(+)-free/high Ca2+ solution plus TEA. Thus the results indicate that nifedipine in clinical therapeutic dosage may directly reduce Ca2+ conductance and then in higher concentration may also depress secondarily Ca(2+)-dependent potassium conductance. These actions of nifedipine may underlie the mechanism of blockade of quantal release of ACh from presynaptic membrane as well as the modulation of excitability of sympathetic postganglionic neuron.

Animals↗
PubMed1990

[Depressant effect of nifedipine on synaptic transmission in celiac ganglion].

The effect of nifedipine, a calcium channel blocker, on nicotinic transmission, was studied in the isolated celiac ganglia of the guinea pig by means of intracellular recordings. Nifedipine in concentration of 0.1-10 mumol/L did not affect resting membrane potential, input membrane resistance and action potential induced by intracellular stimulation in all cells tested, but obviously inhibited nicotinic transmission. The depressant effect of nifedipine on synaptic transmission could be limited by low Ca2+ and antagonized by high Ca2+. Nifedipine did not affect acetylcholine (ACh) sensitivity of postsynaptic membrane, but decreased frequency of miniature excitatory postsynaptic potentials (mEPSPs) in high K+ Kreb's solution and reduced quantal content without effect on quantal size of evoked EPSPs in low Ca2+ /high Mg2+ kreb's solution. The results indicate that nifedipine in therapeutic dose exerts depressant effect on synaptic transmission through blocking Ca2+ entry into presynaptic membrane and reducing quantal release of ACh from presynaptic nerve terminals.

Acetylcholine↗