OBJECTIVETo investigate effect of chronic transauricular kindled seizures on passive-avoidance test memory retention in rats.

METHODSChronic transauricular kindled seizures was induced by repeated application of initially subconvulsive electrical stimulation through ear-clip electrodes once every 24 h until the occurrence of 3 consecutive clonic-tonic seizures. A passive avoidance test was used to measure memory retention ability. Morphological changes in neurons of hippocampal CA1 region was examined after HE staining. Histamine, gamma-aminobutyric acid (GABA) and glutamate levels in the hippocampus were measured by high performance liquid chromatography (HPLC).

RESULTChronic transauricular kindled seizures impaired passive-avoidance test memory retention in rats. The damaged CA1 neurons were observed and histamine content in the hippocampus markedly decreased 24 h after the end of kindling in the chronic transauricular kindled rats.

CONCLUSIONChronic transauricular kindled seizure impaired passive-avoidance test memory retention, and it might be due to the damaged CA1 neurons and a decrease of histamine in the hippocampus induced by epilepsy.

Animals ; Avoidance Learning ; Hippocampus ; metabolism ; pathology ; physiopathology ; Histamine ; metabolism ; Kindling, Neurologic ; Male ; Memory Disorders ; etiology ; physiopathology ; Rats ; Rats, Sprague-Dawley ; Seizures ; metabolism ; pathology ; physiopathology ; gamma-Aminobutyric Acid ; metabolism

AIMTo study the characteristics of neural information encoding of the epileptic networks involved caudate-putamen(CPu) and the hippocampi induced by tetanization of the right CPu in rats.

METHODSExperiments were performed on 59 SD rats. Acute or chronic tetanization of the right CPu (ATRC or CTRC) (60Hz,0.4-0.6 mA, 2 s) was used to induce rat epilepsy.

RESULTS(1) The bursting or primary unit afterdischarges of single neurons were asymmetric in dual hippocampi induced by the ATRC. (2) Continuous sharp waves were observed in ipsilateral or contralateral CPu induced by the CTRC. The oscillatory network seizures with phase shift appeared between two sharp waves in ipsilateral CPu. The frequency of oscillatory waves was negatively correlated with the time and fluctuated from 70 Hz to 110 Hz, then to 35 Hz, and finally to 30 Hz. (3) In the contralateral side primary network after discharges in the CPu were induced by the CTRC. Therefore, the characteristic primary network afterdischarges could be shifted from the CPu or to the HPC, but amplified. On the other hand, HPC sharp waves could be depressed when the CPu network seizures occurred.

CONCLUSIONThe reestablishment of CPu-hippocampal epileptic networks could be transhemispherically promoted by over-activation of the right CPu network, in which bilateral hippocampal neuronal network and CPu neural network were involved in some particular pathophysiological information encoding.

Animals ; Caudate Nucleus ; metabolism ; Epilepsy ; physiopathology ; Hippocampus ; metabolism ; Male ; Neurons ; metabolism ; Putamen ; metabolism ; Rats ; Rats, Sprague-Dawley

AIMTo observe the intracellular calcium ion spatio-temporal and dynamic changes in the hippocampal neuronal culture model of epilepsy induced by low magnesium ion medium, and to explore the relationship between calcium ion and epilepsy.

METHODSApplying both laser scanning confocal microscope and patch clamp to timely observe the changes of [Ca2+]i and electrophysiological in the hippocampal neuronal culture model of epilepsy, and the influence of NMDA receptor-gated channels retarder and non-NMDA receptor-gated channels retarder.

RESULTSAfter the hippocampal nerve cell broken into epileptiform discharges, [(Ca2+]i rapidly ascended to (620 +/- 70) nmol/L, NMIDA acceptor retarder (MK-801, 10 micromol/L) and non-NMDA acceptor retarder (NBQX, 10 micromol/L) reduced [Ca2+]i ascendance. Recovery of the elevated [Ca2+]i was obviously delay, after 90 min and 150 min epileptiform discharges, it took (114.8 +/- 5.2) min and (135.0 +/- 22.7) min (P < 0.05) respectively.

CONCLUSIONIn vitro status epilepticus causes sustained elevation of intracellular calcium levels in hippocampal neurons

Animals ; Animals, Newborn ; Calcium ; metabolism ; Cells, Cultured ; Hippocampus ; cytology ; metabolism ; Neurons ; metabolism ; Rats ; Rats, Sprague-Dawley ; Status Epilepticus ; metabolism ; physiopathology

OBJECTIVETo observe the changes in the learning and memory functions and the hippocampal expression of phosphorylated cAMP response element-binding protein (pCREB) in rats with status epilepticus and generalized nonconvulsive status epilepticus.

METHODSStatus epilepticus (SE) and generalized nonconvulsive status epilepticus (GNCSE) was induced by pentylenetetrazol kindling in SD rats, and the learning and memory function changes of the kindled rats were assessed by means of Morris water-maze test and Y-maze test with alternative electric stimulation. Immunocytochemistry was used for analysis pCREB protein expression in the hippocampus of the rats.

RESULTSIn Morris water-maze test, the rats with SE showed prolonged mean escape latency (P<0.05), shortened swimming time in the platform quadrant (P<0.05), and reduced number of times of platform crossing (P<0.05) in the short term after kindling. But these changes were reversed and became normal a month after the kindling (P>0.05). In the Y-maze test with alternative electric stimulation, the total error (TE) of SE rats increased significantly in the short term after epilepsy (P<0.05), but recovered the normal level a month after kindling (P>0.05). The GNCSE rats showed prolonged mean escape latency at only certain time periods (P<0.05) in the short term, but with swimming time in the platform quadrant and number of platform crossings similar to the control group (P>0.05). The short-term TE of GNCSE rats increased significantly (P<0.05), but in the long term, TE was similar to that in the control group (P>0.05). The expression of pCREB decreased significantly in SE group in comparison with the control group in the short term.

CONCLUSIONEpileptic seizures can lead to learning and memory function impairment in rats, and SE seems to cause greater impact than GNCSE on the learning and memory functions. pCREB might be involved in the pathophysiology of learning and memory deficit in epileptic rats.

Animals ; CREB-Binding Protein ; metabolism ; Hippocampus ; metabolism ; physiopathology ; Kindling, Neurologic ; Maze Learning ; Memory Disorders ; physiopathology ; Pentylenetetrazole ; Rats ; Rats, Sprague-Dawley ; Status Epilepticus ; chemically induced ; metabolism ; physiopathology

AIMTo study the expression and effect of TLR4 and NFkappaB protein in hippocampus neuron in rats exposed to chronic hypoxic hypercapnia.

METHODSThe disorder of learning-memory in pulmonary hypertension rat model was reproduced by chronic hypoxic hypercapnia. Thirty rats were randomly divided into three groups: normal control group, hypoxic hypercapnia 2-week and 4-week group. The number of apoptosis neurons in hippocampus CA1/3 was counted by TUNEL method. Activity of TLR4 and NFkappaB in hippocampus CA1/3 was detected by using SP immunocytochemical technique.

RESULTSThe expression of TLR4 protein in hippocampus CA1/3 in group 2HH( CA1: 0.1275 +/- 0.0242, CA3: 0.1156 +/- 0.0376) and 4HH (CA1: 0.1522 +/- 0.0187, CA3: 0.1427 +/- 0.0453) were significantly higher than those in the NC group (P < 0.05, P < 0.01). The positive expression of NFkappaB were showed in cell nucleus in group 2HH (CA1: 0.1326 +/- 0.0324, CA3: 0.1301 +/- 0.0112) and group 4HH (CA1: 0.1612 +/- 0.0428, CA3: 0.1578 +/- 0.0365), and significantly higher than those in the NC group (P < 0.05, P < 0.01). The apoptosis of neural cells in hippocampus CA1/3 gradually increased with the time of exposure, and reached peak at 4 weeks (P < 0.01 vs NC group).

CONCLUSIONThe activation of TLR4 and NFkappaB may play an important role in the apoptosis of hippocampus neural cells in rat exposed to chronic hypoxic hypercapnia.

Animals ; Apoptosis ; Hippocampus ; metabolism ; pathology ; physiopathology ; Hypercapnia ; metabolism ; physiopathology ; Hypertension, Pulmonary ; metabolism ; physiopathology ; Hypoxia ; metabolism ; physiopathology ; Male ; NF-kappa B ; metabolism ; Neurons ; metabolism ; physiology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Toll-Like Receptor 4 ; metabolism

OBJECTIVETo investigate whether intracerebral hemorrhage (ICH) can promote neurogenesis in the dentate gyrus (DG) of rat hippocampus.

METHODSWestern blot analysis, immunohistochemical staining, and immunofluorescent double labeling combined with confocal microscope were used to detect neurogenesis in the DG of the hippocampus in rats after ICH.

RESULTSThe expression of DCX protein in the ipsilateral DG of the hippocampus was enhanced in the rats 1 day after ICH (0.202∓0.062) as compared with that in normal rats (0.127∓0.088), reaching the peak level at 14 days (0.771∓0.108, P<0.01) and beginning to decrease at 28 days (0.582∓0.121, P<0.01). Meanwhile, DCX-positive cells and BrdU-positive cells, and DCX/BrdU double-labeled cells were detected in the DG of the hippocampus. Compared with those in the control group, BrdU/NeuN double-labeled cells were markedly increased in the granular cell layer of the DG at 28 days after ICH (1.808∓1.020 vs 5.654∓1.671, P<0.01).

CONCLUSIONICH can promote neurogenesis in the DG of rat hippocampus.

Animals ; Antigens, Nuclear ; metabolism ; Bromodeoxyuridine ; metabolism ; Cerebral Hemorrhage ; metabolism ; pathology ; physiopathology ; Dentate Gyrus ; metabolism ; physiopathology ; Hippocampus ; metabolism ; physiopathology ; Microtubule-Associated Proteins ; metabolism ; Nerve Tissue Proteins ; metabolism ; Neurogenesis ; physiology ; Neurons ; metabolism ; physiology ; Neuropeptides ; metabolism ; Rats ; Rats, Sprague-Dawley

Animals ; Dementia, Vascular ; metabolism ; physiopathology ; Extracellular Signal-Regulated MAP Kinases ; metabolism ; Hippocampus ; cytology ; metabolism ; physiopathology ; Male ; Mice ; Neurons ; metabolism ; physiology ; Random Allocation

Animals ; Antidepressive Agents ; pharmacology ; Brain-Derived Neurotrophic Factor ; metabolism ; Cyclic AMP Response Element-Binding Protein ; metabolism ; Depression ; metabolism ; pathology ; physiopathology ; Hippocampus ; metabolism ; pathology ; physiopathology ; Humans ; Nerve Degeneration ; physiopathology ; Nerve Regeneration ; drug effects ; Neurons ; pathology ; Stress, Psychological ; metabolism ; pathology ; physiopathology

Type 1 diabetes is a common metabolic disorder accompanied by increased blood glucose levels along with glucocorticoid and cognitive deficits. The disease is also thought to be associated with environmental changes in brain and constantly induces oxidative stress in patients. Therefore, glucocorticoid-mediated negative feedback mechanisms involving the glucocorticoid receptor (GR) binding site are very important to understand the development of this disease. Many researchers have used streptozotocin (STZ)-treated diabetic animals to study changes in GR expression in the brain. However, few scientists have evaluated the hyperglycemic period following STZ exposure. In the present study, we found GR expression in the hippocampus varied based on the period after STZ administration for up to 4 weeks. We performed immunohistochemistry and Western blotting to validate the sequential alterations of GR expression in the hippocampus of STZ-treated type 1 diabetic rats. GR protein expression increased significantly until week 3 but decreased at week 4 following STZ administration. GR expression after 70 mg/kg STZ administration was highest at 3 weeks post-treatment and decreased thereafter. Although STZ-induced increase in GR expression in diabetic animals has been described, our data indicate that researchers should consider the sequential GR expression changes during the hyperglycemic period following STZ exposure.
Animals ; Diabetes Mellitus, Experimental/chemically induced/*metabolism/*physiopathology ; Disease Models, Animal ; *Gene Expression Regulation ; Hippocampus/metabolism/*physiopathology ; Humans ; Male ; Rats ; Rats, Wistar ; Receptors, Glucocorticoid/*genetics/*metabolism ; Time Factors

AIMTo investigate whether formalin inflammatory pain can induce hippocampal neuronal apoptosis of rats or not.

METHODSRats were subcutaneously injected with 0.2 ml 0.5% formalin into the ventral surface of right hind paw to induce periphery inflammatory pain. The flinches of rats were counted to observe their painful reaction. Flow cytometry was used to assay the ratio of apoptosis of hippocampal neurons. The immunohistochemistry was used to observe the expression of p53 protein in hippocampal subregions.

RESULTSCompared with control group, the apoptotic ratio of hippocampal neurons was significantly increased in rats with inflammatory pain, and formalin inflammatory pain induced upregulation of p53 protein expression in all hippocampal subregions. Both the apoptotic ratio and the p53 protein expression peaked on the third day after the formalin injection. The twice injection of formalin into the hind paws of rats resulted in an enhancement of painful reaction and increase in apoptotic ratio of hippocampal neurons compared with the rats of injection formalin once group.

CONCLUSIONFormalin inflammatory pain can induce the hippocampal neuronal apoptosis in rats with a certain time course. Neuronal apoptosis is relevant to the intensity of pain. The up-regulation of p53 protein expression may implicate in the induction of hippocampal neuronal apoptosis in rats with inflammatory pain.

Animals ; Apoptosis ; Formaldehyde ; Hippocampus ; pathology ; physiopathology ; Inflammation ; chemically induced ; physiopathology ; Male ; Neurons ; pathology ; Pain ; chemically induced ; physiopathology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Tumor Suppressor Protein p53 ; metabolism