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

AIMIn order to explore the neurobiological mechanism of morphine addiction and treatment methods, the acute and chronic effects of morphine on the intracellular free calcium concentration ([Ca2+]i) in cultured hippocampal neurons were investigated.

METHODSChanges of [Ca2+]i induced by morphine in primarily cultured hippocampal neurons were measured by confocal laser scanning microscopy using Ca(2+) -sensitive dye fluo-4 as the calcium fluorescent probe.

RESULTSMorphine actually induced the increase in [Ca2+]i of hippocampal neurons. This process could be blocked by naltrindole (delta opioid receptor antagonist) pretreatment, but not by CTOP (micro opioid receptor antagonist) pretreatment. Pretreatment of the cells with thapsigargin almost completely blocked morphine-evoked response; while pretreatment of the cells with verapamil partially inhibited this response. After exposure to 100 micromol/L morphine for 24 h, intracellular [Ca2+]i increased and the increase could be intensified after adding 10 micromol/L naloxone to the medium.

CONCLUSIONMorphine induced the release of Ca2+ is mainly from inositol 1, 4, 5-trisphosphate (IP3) sensitive stores in hippocampal neuron of rats through activation of delta2 subtype opioid receptor.

Animals ; Calcium ; metabolism ; Cells, Cultured ; Hippocampus ; cytology ; Male ; Microscopy, Confocal ; Morphine ; pharmacology ; Neurons ; cytology ; drug effects ; Rats ; Rats, Wistar

OBJECTIVETo explore the effects of manganese poisoning on the proliferation of neural stem cells (NSCs) in mice's hippocampus.

METHODSThe mice (weight 8 approximately 10 g) were divided into control group(CG) low-dose group(LDG) middle-dose group(MDG) and high-dose group(HDG)by intraperitoneal injection of 0, 5, 20, 50 mg x kg(-1) x d(-1) of manganese chloride dissolved in physiological saline. The ability of learning and memory was detected by Morris Water Maze, and the proliferation of NSCs in subgranular zone (SGZ) in these mice's hippocampus was also detected by immunohistochemistry.

RESULTS1) Compared with the CG, the ability of learning and memory in all manganism group decreased significantly (P < 0.01) and this phenomenon in HDG was most notable (P < 0.01). Meanwhile, the ability of memory was negatively correlated with the dose of manganese chloride (r(s) = -0.598, P < 0.01), but the difference of swimming speed in every group was of no statistic significance. (2) The numbers of NSCs in proliferation period in SGZ of all manganism groups was much lower than that of CG (P < 0.01) negatively correlated with the dose of manganese chloride (r(s) = -0.666, P < 0.01). (3) The reduction of NSCs had a positive correlation to the depression of learning and memory (r(s) = 0.734, P < 0.01).

CONCLUSIONSManganismus can affect the ability of learning and memory, which is probably caused by the inhalation of manganese on NSCs in hippocampus.

Animals ; Cell Proliferation ; drug effects ; Cells, Cultured ; Disease Models, Animal ; Hippocampus ; cytology ; drug effects ; Male ; Manganese Poisoning ; pathology ; Maze Learning ; drug effects ; Memory ; drug effects ; Mice ; Neural Stem Cells ; cytology ; drug effects

Animals ; Apoptosis ; drug effects ; Cell Hypoxia ; Cells, Cultured ; Hippocampus ; cytology ; Neurons ; cytology ; drug effects ; Propofol ; pharmacology ; Proto-Oncogene Proteins c-fos ; metabolism ; Rats

Animals ; Apoptosis ; drug effects ; Brain Ischemia ; pathology ; Hippocampus ; cytology ; drug effects ; pathology ; Neurons ; drug effects ; pathology ; Rats ; Rats, Wistar ; Reperfusion Injury ; pathology ; Sulfinic Acids ; pharmacology

OBJECTIVETo study the protective effect of MG-132 on hippocampus cells apoptosis induced by deltamethrin (DM), one kind of pyrethroid pesticide.

METHODS40 Male wistar rats were randomly divided into four groups: olive oil control, DM treated alone (12.5 mg/kg), MG-132 (0.5 mg/kg) plus DM group, MG-132 treated 2h plus olive oil. After 24h treatment of DM, the hippocampus was taken out to detect the apoptotic cell rate, the level of bcl-2 and Caspase-3 activity.

RESULTSCompared with DM treated alone group (27.29% +/- 2.41%), the apoptotic cell rate in MG-132 + DM group (19.94% +/- 2.07%) was increased (P < 0.05), bcl-2 expression was enhanced [(0.43 +/- 0.06) vs. (2.01 +/- 0.23)] (P < 0.05) and the activity of Caspase-3 was decreased significantly (P < 0.05) in MG-132 treated 2h plus DM group [(4.55 +/- 0.46) vs.(3.73 +/- 0.35)].

CONCLUSIONMG-132 can protect hippocampus cells against apoptosis induced by deltamethrin.

Animals ; Apoptosis ; drug effects ; Hippocampus ; cytology ; drug effects ; Insecticides ; toxicity ; Leupeptins ; pharmacology ; Male ; Neurons ; drug effects ; Nitriles ; toxicity ; Pyrethrins ; toxicity ; Rats ; Rats, Wistar

AIMThe effect of stress hormone corticosterone on hippocampal neurons delayed rectified potassium currents was probed.

METHODSThe potassium currents of rat hippocampal neurons in primary culture were measured with patch clamp whole-cell recording.

RESULTSIt showed that the amplitudes of the potassium currents in hippocampal neurons decreased. However, the threshold potential of potassium currents increased.

CONCLUSIONIt is speculated that excessive corticosterone may hurt the hippocampal neurons via its effects on the potassium currents of rat hippocampal cells.

Animals ; Animals, Newborn ; Cells, Cultured ; Corticosterone ; pharmacology ; Delayed Rectifier Potassium Channels ; drug effects ; Hippocampus ; cytology ; drug effects ; Neurons ; drug effects ; physiology ; Patch-Clamp Techniques ; Rats ; Rats, Wistar

Angelica ; chemistry ; Animals ; Animals, Newborn ; Cell Count ; Female ; Fetal Hypoxia ; pathology ; Hippocampus ; cytology ; drug effects ; Male ; Neuroglia ; cytology ; Neurons ; cytology ; Pregnancy ; Rats ; Rats, Sprague-Dawley

The possible role of minocycline in microglial activation and neuronal death after cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) in mice was investigated in this study. The mice were given potassium chloride to stop the heart beating for 8 min to achieve CA, and they were subsequently resuscitated with epinephrine and chest compressions. Forty adult C57BL/6 male mice were divided into 4 groups (n=10 each): sham-operated group, CA/CPR group, CA/CPR+minocycline group, and CA/CPR+vehicle group. Animals in the latter two groups were intraperitoneally injected with minocycline (50 mg/kg) or vehicle (normal saline) 30 min after recovery of spontaneous circulation (ROSC). Twenty-four h after CA/CPR, the brains were removed for histological evaluation of the hippocampus. Microglial activation was evaluated by detecting the expression of ionized calcium-binding adapter molecule-1 (Iba1) by immunohistochemistry. Neuronal death was analyzed by hematoxylin and eosin (H&E) staining and the levels of tumor necrosis factor-alpha (TNF-α) in the hippocampus were measured by enzyme-linked immunosorbent assay (ELISA). The results showed that the neuronal death was aggravated, most microglia were activated and TNF-α levels were enhanced in the hippocampus CA1 region of mice subjected to CA/CPR as compared with those in the sham-operated group (P<0.05). Administration with minocycline 30 min after ROSC could significantly decrease the microglial response, TNF-α levels and neuronal death (P<0.05). It was concluded that early administration with minocycline has a strong therapeutic potential for CA/CPR-induced brain injury.
Animals ; Cardiopulmonary Resuscitation ; Cell Death ; drug effects ; Enzyme-Linked Immunosorbent Assay ; Heart Arrest ; pathology ; Hippocampus ; cytology ; drug effects ; metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Microglia ; cytology ; drug effects ; Minocycline ; pharmacology ; Neurons ; drug effects ; Tumor Necrosis Factor-alpha ; metabolism

AIMTo observe the effect and mechanism of scopolamine on morphine(Mor)-induced mice dependence.

METHODSThe Mor-dependent mice model was established by intraperitoneal (ip) administered Mor for seven days. Pain threshold, times of jump and hippocampus intracellular free calcium ion concentration ([Ca2+]i) were determined by the heat plate test, naloxone (Nal)-precipitated jumping response and flow cytometry, respectively.

RESULTSThe pain threshold of Mor-dependent mice decreased significantly while there was a marked increase in times of jump, the rate of jumping animals and hippocampus [Ca2+]i. Co-administered scopolamine, the pain threshold of Mor-dependent mice increased significantly; the number of jump, the rate of jumping animals and hippocampus [Ca2+]i all decreased significantly.

CONCLUSIONScopolamine could antagonize the Mor-induced mice dependence, which could be related to decreasing the levels of brain intracellular free calcium.

Animals ; Calcium ; metabolism ; Hippocampus ; cytology ; drug effects ; metabolism ; Mice ; Mice, Inbred Strains ; Morphine ; pharmacology ; Morphine Dependence ; metabolism ; Scopolamine Hydrobromide ; pharmacology