Child ; Epiphyses ; Fracture Fixation, Internal ; Humans ; Lower Extremity

OBJECTIVEThe present study investigated the effects of rapamycin on Aβ1-42-induced deficits in working memory and synaptic plasticity.

METHODSAfter bilateral hippocampal injection of Aβ1-42 and rapamycinin rats, spontaneous alternation in Y-maze and in vivo hippocampal long-term potentiation (LTP) of rats were recorded. All data were analized by two-way repeated measures analysis of variance (ANOVA).

RESULTS(Hippocampal injection of Aβ1-42 alone impaired working memory of rats; (2) Rapamycin did not affect working memory of rats, but alleviated Aβ1-42-induced working memory deficits, compared with Aβ1-42 alone group; (Aβ1-42 remarkably suppressed in vivo hippocampal LTP of fEPSPs in the CA1 region; (4) Pretreatment with rapamycin prevented Aβ1-42-induced suppression of LTP.

CONCLUSIONThese data indicates that rapamycin could protect against Aβ1-42-induced impairments in working memory and synaptic plasticity in rats.

Amyloid beta-Peptides ; adverse effects ; Animals ; Hippocampus ; drug effects ; Long-Term Potentiation ; Maze Learning ; Memory, Short-Term ; drug effects ; Neuronal Plasticity ; drug effects ; Peptide Fragments ; adverse effects ; Rats ; Sirolimus ; pharmacology

AIMTo study the feasibility of long-term potentiation(LTP) recording in the CA1 area of the rat in vivo with electrodes-binding technique.

METHODSAnesthetizing Wistar rats with urethane and fixing the animal on the stereotaxic device for acute surgery; implanting cannula into lateral cerebral ventricle; inserting self-made bound stimulating/recording electrodes into hippocampal CA1 area; recording basal field excitatory postsynaptic potential (fEPSP) and tetanus-induced long term potentiation (LTP).

RESULTSfEPSPs were reliably induced by using the stimulating/recording electrodes-binding technique, and the appearance rate of fEPSP was nearly 100%; basal fEPSP recording was very stable, lasting for long time enough to finish all experiment; high frequency stimulation (HFS) successfully induced LTP, which maintained more than three hours, the inductivity is about 67%; paired-pulse facilitation (PPF) recording was also stable; intracerebroventricular (i c v) injection of amyloid beta suppressed HFSinduced LTP evidently.

CONCLUSIONThe electrodes-binding technique for recording hippocampal LTP in vivo is quite simple and convenient. The experimental resource can be saved, and the rates of fEPSP appearance and LTP induction are kept high. Therefore, it is promising for this technique to be one electrophysiological auxiliary method in the research of learning and memory.

Animals ; Electric Stimulation ; methods ; Electrodes ; Excitatory Postsynaptic Potentials ; physiology ; Feasibility Studies ; Hippocampus ; physiology ; Long-Term Potentiation ; physiology ; Male ; Rats ; Rats, Wistar

The recombinant adenoviruses containing pGH cDNA and pGH cDNA with the first intron under the control of CMV promoter were constructed respectively by homogenous recombination method. The results showed that the recombinant adenoviruses could mediate pGH cDNA expression in CHO cells infected with the recombinant adenoviruses. The expression level of pGH cDNA with the first intron increased by 117% compared with pGH cDNA without intron. This indicate that the first intron of pGH gene have the function of improving the expression of the pGH gene.
Adenoviridae ; genetics ; Animals ; CHO Cells ; Cricetinae ; Cytomegalovirus ; genetics ; Gene Expression ; Genetic Engineering ; Genetic Vectors ; genetics ; Growth Hormone ; genetics ; Introns ; Promoter Regions, Genetic ; Recombinant Fusion Proteins ; genetics ; Swine

It has been known that locus coeruleus (LC) stimulation suppresses nociceptive discharges of the thalamic parafascicular (PF) neurons through the spinally descending adrenergic terminals which inhibit the transmission of nociceptive signals in the spinal dorsal horn. This experimental model was used in the present study to analyze the detailed processes that happened in the dorsal horn following norepinephrine release by preemptive intrathecal (i.t.) administration of related drugs in lightly urethane-anesthetized rats. The results showed that: (1) LC stimulation significantly inhibited the noxiously-evoked discharges of PF neurons; (2) the LC stimulation-produced antinociception in PF neurons could be blocked either by i.t. glibenclamide, an ATP-sensitive potassium (K(+)(ATP)) channel blocker, or by i.t. aminophylline, an adenosine receptor antagonist; (3) nociceptive discharges of PF neurons were also suppressed both by i.t. 5 -N-ethylcarboxamido-adenosine (NECA, an adenosine receptor agonist) and by i.t. nicorandil (a K(+)(ATP) channel opener); and (4) i.t. aminophylline blocked the suppression of PF nociceptive discharges induced by i.t. nicorandil, while i.t. glibenclamide showed no effect on the suppression of nociceptive discharges induced by i.t. NECA. These results suggest that: (1) K(+)(ATP) channels and endogenous adenosine may be involved in the mediation of spinal antinociception induced by descending adrenergic fibers originating from the LC; and (2) the opening of K(+)(ATP) channels precedes the release of adenosine in the cascade of mediation.
Adenosine ; metabolism ; physiology ; Adenosine Triphosphate ; physiology ; Animals ; Electric Stimulation ; Female ; Injections, Spinal ; Locus Coeruleus ; physiology ; Male ; Pain ; physiopathology ; Potassium Channels ; physiology ; Rats ; Rats, Wistar

Although the impairing effects of beta-amyloid (Aβ) protein on synaptic plasticity and cognitive function have been widely reported, the mechanisms underlying the neurotoxicity of Aβ are still not well known. The present study observed the effects of intracerebroventricular (i.c.v.) injection of both Aβ(23-35) and genistein (a specific tyrosine kinase inhibitor at high concentration) on the hippocampal long-term potentiation (LTP) in the CA1 region, and investigated its possible protein tyrosine kinase (PTK) mechanism. Male Wistar rats were surgically prepared for acute LTP recordings in vivo. Two parallel bond electrodes for stimulating and recording were simultaneously inserted into the right hippocampus of rats. The field excitatory postsynaptic potentials (fEPSPs), paired-pulse facilitation (PPF) and high-frequency stimuli (HFS)-induced LTP were recorded by delivering test stimuli, paired pulses and HFS to the Schaffer-collateral/commissural pathway. The results showed that: (1) i.c.v. injection of Aβ(23-35) did not affect the baseline synaptic transmission, but significantly suppressed the HFS-induced LTP, with a decreased average amplitude of fEPSPs [(129.2+/-6.7)% in 10 nmol Aβ(23-35) group; (110.6+/-8.6)% in 20 nmol Aβ(23-35) group; P<0.01] at 1 h post-HFS when compared to that in the control group [(163.1+/-8.1)%]; (2) Similarly, i.c.v. injection of genistein (200 nmol) did not change the basic synaptic transmission, but significantly suppressed HFS-induced LTP, with the similar average amplitude of fEPSPs [(114.0+/-7.2)%] at 1 h post-HFS to that in 20 nmol Aβ(23-35) group; (3) Co-application of Aβ(23-35) (20 nmol) and genistein (200 nmol) caused no additive suppression of LTP, and the average amplitude of fEPSPs was (113.0+/-8.8)% at 1 h post-HFS, showing no significant difference when compared with that in Aβ(23-35) or genistein alone groups (P>0.05); (4) There was no significant change in the PPF following genistein and Aβ(23-35) alone or co-injection (P>0.05). These experimental results indicate that i.c.v. injection of Aβ(23-35) can significantly suppress the HFS-induced LTP in the CA1 area of rat hippocampus in vivo, implying that the Aβ deposited in the brain of patients with Alzheimer's disease may impair the function of learning and memory by suppressing the hippocampal LTP. The facts that the extent of inhibition of Aβ(23-35) and genistein on LTP was similar and no further potentiation of the suppression was observed when Aβ(23-35) and genistein were co-applied suggest that PTK is probably involved in the Aβ-induced suppression of hippocampal LTP.
Amyloid beta-Peptides ; pharmacology ; Animals ; CA1 Region, Hippocampal ; drug effects ; enzymology ; Excitatory Postsynaptic Potentials ; Genistein ; pharmacology ; Long-Term Potentiation ; Male ; Neuronal Plasticity ; Peptide Fragments ; pharmacology ; Protein Kinase Inhibitors ; pharmacology ; Protein-Tyrosine Kinases ; metabolism ; Rats ; Rats, Wistar ; Synaptic Transmission

For expressing the condolences on the passing away of Dr. Hsiang-Tung Chang, one of the distinguished members of the Chinese Academia of Sciences, the pioneer studies on cortical dendritic potentials that Dr. Chang carried out in the 1950s and the prosperous progresses since then, especially, concerning the modifications of synaptic plasticity by the dendritic back-propagating action potentials were briefly reviewed.
Action Potentials ; Dendrites ; physiology ; Humans ; Neuronal Plasticity

OBJECTIVETo investigate the intervening effect of Liuwei Dihuang pill (LWDH) on lupus nephropathy (LN) treated with glucocorticoids and cyclophosphamide (CTX).

METHODSSixty-four patients were randomly divided into two groups, all patients were treated by conventional treatment, using prednisone in standard program, and CTX in a daily dose of 8 - 12 mg/kg, accumulated dose < or = 150 mg/kg, by adding into 500 ml of 5% glucose in saline through intravenous dripping, as well as the symptomatic treatment. Patients in the treated group were given LWDH additionally.

RESULTSThe curative effect in the treated group was significantly superior to that in the control group (P < 0.05). Laboratory indexes, including urinary protein, plasma protein and serum creatinine (SCr), erythrocyte sedimentation rate (ESR), complement C3, etc. were significantly improved in both groups (P < 0.01), but all the improvement, except that of SCr, in the treated group were superior to those in the control group respectively (P <0.05 or P <0.01). Besides, the recurrent rate and incidence rate of adverse reaction in the treated group was significant lower than those in the control group (P < 0.05 and P < 0.01).

CONCLUSIONLWDH can significantly enhance the therapeutic effect of CTX and glucocorticoids on LN, decrease the recurrence and shows advantage in counteracting against the adverse effects of glucocorticoids and CTX.

Adolescent ; Adult ; Cyclophosphamide ; administration & dosage ; adverse effects ; Drug Therapy, Combination ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Humans ; Lupus Nephritis ; drug therapy ; Male ; Middle Aged ; Phytotherapy ; Prednisone ; administration & dosage ; adverse effects ; Secondary Prevention

Craniofacial Dysostosis ; Humans ; Receptors, Fibroblast Growth Factor

The accumulation of amyloid β-protein (Aβ) plaques is identified as a major pathological feature of Alzheimer's disease (AD). Recent studies show that soluble species of Aβ are involved in the early memory dysfunction long before neurodegenerative changes. However, the mechanism underlying the neurotoxicity of soluble Aβ is still unclear. Long-term potentiation (LTP) has been thought as an important cellular model of synaptic plasticity for many years. The studies on the hippocampal LTP and Aβ, especially those using AD transgenic models, provided more evidence for the Aβ-induced dysfunction of learning and memory. Based on the recent researches on AD, this article reviewed the effects of Aβ, especially soluble Aβ and its active fragments, on the hippocampal LTP. The possible mechanisms by which Aβ impairs hippocampal LTP are also discussed.
Alzheimer Disease ; physiopathology ; Amyloid beta-Peptides ; physiology ; Animals ; Hippocampus ; physiology ; Humans ; Learning Disorders ; physiopathology ; Long-Term Potentiation ; physiology ; Memory Disorders ; physiopathology ; Neuronal Plasticity ; Synapses ; physiology