OBJECTIVETo investigate the effect of ginsenoside Rg1 (G-Rg1) on the morphology of the hippocampal neurons of rats with electrical hippocampal injuries and evaluate its protective effects on the learning and memory function.

METHODSForty female SD rats were randomly divided into G-Rg1 group, saline group, sham-operated group and G-Rg1+Sham operation group. Using the stereotactic apparatus, electrical hippocampal injury was induced, not in the two sham groups, by application of direct electrical current, followed by treatments with intragastric administration of G-Rg1 or saline for 14 consecutive days. The learning and memory function of the rats was assessed with Morris water maze test. The viability and arrangement of the hippocampal neurons and the number of Nissl bodies were observed after the treatments.

RESULTSTreatment with G-Rg1 significantly improved the learning and memory function of rats with electrical hippocampal injury. The viability of the hippocampal neurons showed no significant changes in the two sham-operated groups (P>0.05), and the number of Nissl bodies was much lower in saline group than in the other groups (P<0.05).

CONCLUSIONSG-Rg1 can improve the learning and memory function of rats with electrical hippocampal injury, the mechanism of which is probably associated with its protective effect on the hippocampal neurons against electrical injury.

Animals ; Female ; Ginsenosides ; pharmacology ; Hippocampus ; cytology ; drug effects ; pathology ; Maze Learning ; drug effects ; Memory ; drug effects ; Neurons ; drug effects ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate the relationship between the effects of zinc on hippocampal cholecystokinin (CCK) positive neurons and learning and memory ability of lead-exposed rats.

METHODSThirty-six Wistar rats were divided into control group, lead-exposed group (drunk 6.15 mmol/L of lead solution) and lead-zinc group (drunk 6.15 mmol/L of lead + 3.10 mmol/L of ZnSO(4) solution) randomly. Y-maze test was used to study learning and memory ability in rats; Atomic absorption method was used to determine serum and hippocampal lead content; ABC immunohistochemistry and quantitative graphic analysis were used to investigate the changes of CCK positive neurons in different hippocampal subfields in lead-exposed rats.

RESULTSThe learning and memory ability in lead-exposed rats were significantly lower (P < 0.05) while the serum and hippocampal lead content in lead-exposed rat were significantly higher (P < 0.05) than those in control and lead-zinc group. The number and optical density of CCK positive neurons in CA(1) and CA(3) areas of lead-exposed rats were significantly lower (P < 0.05) than those in control and lead-zinc group. No differences in these indexes between the control and lead-zinc group were found (P > 0.05).

CONCLUSIONLead may damage the learning and memory ability and affect the number of CCK positive neurons in lead-exposed rats. Zinc might play an important role in preventing lead-induced damages.

Animals ; Cholecystokinin ; metabolism ; Hippocampus ; drug effects ; metabolism ; Lead ; toxicity ; Maze Learning ; drug effects ; Memory ; drug effects ; Neurons ; drug effects ; metabolism ; Rats ; Rats, Wistar ; Zinc ; pharmacology

OBJECTIVETo investigate the effects of calcium on learning and memory ability of rats exposed to low level lead before and after birth.

METHODSWistar dam rats were randomly divided into normal group, lead-contaminated group and lead with Ca group. Corresponding food and water were given to pregnant rats from d 15 of gestation and to young rats till 7 w after birth. The weight of brain and hippocampus, blood lead content, serum calcium content, learning and memory ability of young rats were tested.

RESULTThe blood lead concentrations: lead-contaminated group was the highest, lead with Ca group the second and normal group the lowest. Serum calcium concentrations: normal group and lead with Ca group were both higher than lead contaminated group. Ability of learning and memory: lead with Ca group was better than lead-contaminated group, but poorer than normal group. No differences were found upon the weight of brain and hippocampus in all groups.

CONCLUSIONA minilaparotomy approach for curative resection of rectal cancer may be an ideal alternative approach to conventional laparotomy.

Animals ; Calcium ; pharmacology ; Female ; Fetus ; drug effects ; Hippocampus ; drug effects ; pathology ; Lead ; blood ; toxicity ; Learning ; drug effects ; Male ; Memory ; drug effects ; Rats ; Rats, Wistar

Amyloid beta-Peptides ; analysis ; Animals ; Frontal Lobe ; drug effects ; physiology ; Hippocampus ; drug effects ; physiology ; Learning ; drug effects ; Memory ; drug effects ; Rats ; Rats, Wistar ; Sodium Azide ; pharmacology ; Space Perception

OBJECTIVETo investigate the effect of ketamine on the high-voltage-activated calcium currents (ICa(HVA)) in rat hippocampal neurons.

METHODSNeurons were cultured from Wistar rat hippocampus. ICa(HVA) was recorded using whole-cell patch clamp technique. After application with ketamine at different concentrations (10, 30, 100, 300, and 1000 μmol/L), the effect of ketamine on ICa(HVA) was evaluated.

RESULTSICa(HVA) was inhibited by ketamine in a concentration-dependent manner. Ketamine at 10 μmol/L showed no effect on ICa(HVA). Four concentrations of ketamine (30, 100, 300,and 1000 μmol/L) reduced the peak ICa(HVA) currents by (17.5 ∓ 4.5)%, (25.5 ∓ 6.9)%, (38.5 ∓ 4.1)%, and (42.3 ∓ 4.6)% respectively,with a mean half maximal inhibitory concentration of 68.2 μmol/L and Hill coefficient of 0.47. The maximal activation membrane potential was shifted to (5.3 ∓ 0.8) from (5.4 ∓ 0.9). The half maximal activation membrane potential of inactivation curve was shifted from(-26.7 ∓ 3.9) mV to(-32.8 ∓ 4.2) mV.

CONCLUSIONKetamine can remarkably inhibit calcium currents in the central neurons,which may explain at least partly the action of ketamine on central nervous system.

Animals ; Calcium Channels ; drug effects ; physiology ; Cells, Cultured ; Hippocampus ; drug effects ; physiology ; Ketamine ; pharmacology ; Membrane Potentials ; drug effects ; Neurons ; drug effects ; physiology ; Rats ; Rats, Wistar

BACKGROUNDIt is a common phenomenon that children experience multiple general anesthesias in clinical practice, which raises the question whether repeated exposure to general anesthetics would interfere with the development of the central nervous system of children. The present study was designed to evaluate the effects of repeated treatment with ketamine or midazolam on postnatal dendrite development by examining the morphology of the dendritic spines of the pyramidal neurons in the hippocampal CA1 region in mice.

METHODSThe transgenic green fluorescent protein-M line (GFP-M) mice were used in this study. Ketamine (100 mg/kg), midazolam (50 mg/kg) or saline (10 ml/kg) was administered intraperitoneally once a day on consecutive days from postnatal day 8 (P8) to postnatal day 12 (P12). At postnatal day 13 (P13) and postnatal day 30 (P30), the density and length of the apical dendritic spines of the pyramidal neurons in the hippocampal CA1 region were examined under a confocal microscope.

RESULTSAt P13, for both the ketamine group and the midazolam group, the dendritic spines were found with a comparatively lower density and longer average length than in the control group. At P30, no significant difference in the density or average length of dendritic spines was found between the anesthetic group and control group.

CONCLUSIONSThis study indicated that repeated exposure to ketamine or midazolam in neonatal mice impaired dendritic spine maturation immediately afterwards, but this influence seemed to disappear during further postnatal development.

Animals ; Animals, Newborn ; Dendritic Spines ; drug effects ; Female ; Hippocampus ; drug effects ; Ketamine ; pharmacology ; Male ; Mice ; Microscopy, Confocal ; Midazolam ; pharmacology

Animals ; Corticosterone ; pharmacology ; Hippocampus ; drug effects ; physiology ; In Vitro Techniques ; Long-Term Potentiation ; drug effects ; physiology ; Male ; Rats ; Rats, Wistar

Voltage-gated sodium channels (VGSCs), which are widely distributed in the excitable cells, are the primary mediators of electrical signal amplification and propagation. They play important roles in the excitative conduction of the neurons and cardiac muscle cells. The abnormalities of the structures and functions of VGSCs can change the excitability of the cells, resulting in a variety of diseases such as neuropathic pain, epilepsy and arrhythmia. At present, some voltage-gated sodium channel blockers are used for treating those diseases. In the recent years, several neurotoxins have been purified from the venom of the animals, which could inhibit the current of the voltage-gated sodium channels. Usually, these neurotoxins are compounds or small peptides that have been further designed and modified for targeted drugs of sodium channelopathies in the clinical treatment. In addition, a novel cysteine-rich secretory protein (CRBGP) has been isolated and purified from the buccal gland of the lampreys (Lampetra japonica), and it could inhibit the Na+ current of the hippocampus and dorsal root neurons for the first time. In the present study, the progress of the sodium channelopathies and the biological functions of voltage-gated sodium channel blockers are analyzed and summarized.
Animals ; Channelopathies ; physiopathology ; Hippocampus ; drug effects ; Neurons ; drug effects ; Neurotoxins ; pharmacology ; Venoms ; chemistry ; Voltage-Gated Sodium Channel Blockers ; pharmacology

Animals ; Apoptosis ; drug effects ; Benzopyrenes ; administration & dosage ; toxicity ; Hippocampus ; drug effects ; pathology ; Injections, Intraventricular ; Male ; Rats ; Rats, Sprague-Dawley

Animals ; Cognitive Dysfunction ; metabolism ; Cystatin C ; pharmacology ; Hippocampus ; drug effects ; Insulin Resistance ; physiology ; Neurons ; drug effects ; Rats ; Rodentia