Animals ; Hippocampus ; pathology ; physiopathology ; Male ; Motor Activity ; Rats ; Rats, Wistar

BACKGROUNDThe hippocampus and amygdala exhibit structural and functional alterations in patients with depression. The objective of this study was to investigate the structural and functional relationships between these core regions.

METHODSBased on the severity of their condition, 60 patients and 20 healthy controls were equally divided into four groups (mild group, moderate group, major group and health controls group), scanned by T1-MR, functional magnetic resonance imaging (fMRI), and susceptibility weighted imaging (SWI). Structural image, BOLD image, and SWI image were collected for processing and analysis. The characteristics of the depression and controls were checked by analysis of variance test, and the difference between groups was checked by Dunnett's test.

RESULTSThe volume of hippocampus and amygdala varied with the severity of the condition. The signal obtained under the stimulation of negative events was linearly decreased in the mild, moderate and major groups revealed by fMRI. The length and diameter of the lateral ventricle vein was reduced in the mild group, whereas the number of branches increased. In the moderate and major groups, the reduction in the length, diameter and increase in the number of branches of the lateral ventricle vein were greater.

CONCLUSIONThe alterations of the volume, fMRI, and cerebral veins in these core regions may account for the causal relationship between structure and function.

Adult ; Amygdala ; pathology ; Depression ; pathology ; Female ; Hippocampus ; pathology ; Humans ; Magnetic Resonance Spectroscopy ; Male

In order to explore the MRI volume of the amygdala and hippocampus in patients with major depression, quantitative MRI of the amygdala and hippocampus were studied in 22 patients with major depression and compared with 13 age-matched controls. The results showed that both groups exhibited similar significant hippocampal asymmetry (left smaller than right). The volume of the bilateral hippocampus was significantly smaller in the major depression group than that in control group. The patients had significant asymmetry of the amygdalar volumes (right smaller than left). No correlation was found between hippocampal volume abnormalities and ill duration. It was concluded that the hippocampus and amygdala within limbic-cortical networks may play a crucial role in the pathogenesis of major depression.
Amygdala/*pathology ; Anthropometry ; Depressive Disorder, Major/*pathology ; Hippocampus/*pathology ; Magnetic Resonance Imaging

In order to explore the MRI volume of the amygdala and hippocampus in patients with major depression, quantitative MRI of the amygdala and hippocampus were studied in 22 patients with major depression and compared with 13 age-matched controls. The results showed that both groups exhibited similar significant hippocampal asymmetry (left smaller than right). The volume of the bilateral hippocampus was significantly smaller in the major depression group than that in control group. The patients had significant asymmetry of the amygdalar volumes (right smaller than left). No correlation was found between hippocampal volume abnormalities and ill duration. It was concluded that the hippocampus and amygdala within limbic-cortical networks may play a crucial role in the pathogenesis of major depression.
Adult ; Amygdala ; pathology ; Anthropometry ; Depressive Disorder, Major ; pathology ; Female ; Hippocampus ; pathology ; Humans ; Magnetic Resonance Imaging ; Male

OBJECTIVEThe relationship between selenium deficiency and the changes of synaptic structure in the CA3 area of hippocampus were studied in the third generation rats.

METHODSA selenium deficiency model was established by feeding rats with selenium-deficient food. The rats were divided into 4 groups: control (Se+I+), selenium deficiency (Se-I+), iodine deficiency (Se+I-), and both deficient group (Se-I-). The hippocampuses were dissected from the third generation rats on the 21st gestational day and the ultrastructural features of hippocampal synapses were observed with electron microscope. The length of active zone, synaptic curvatures, post-synaptic density (PSD) and synaptic cleft were quantitatively described.

RESULTSCompared with the control, the length of active zone and the thickness of PSD were significantly decreased in Se-I+, Se+I- and Se-I- groups [(261.7 +/- 50.1) nm, (286.7 +/- 41.6) nm and (220.8 +/- 61.6) nm contrast to (312.4 +/- 47.7) nm, P < 0.01], so were the synaptic curvatures in Se-I+, Se+I- and Se-I- groups [(22.9 +/- 6.3) nm, (27.5 +/- 8.6) nm and (25.2 +/- 6.5) nm contrast to (48.1 +/- 12.3) nm, P < 0.01]; the width of synaptic cleft were also decreased significantly in Se-I- [(11.1 +/- 3.3) nm contrast to (16.1 +/- 4.0) nm, P < 0.01].

CONCLUSIONSelenium deficiency might cause changes of neuronal functions at the synaptic level, and furthermore, affect learning and memory.

Animals ; Female ; Hippocampus ; pathology ; Iodine ; deficiency ; Male ; Rats ; Rats, Sprague-Dawley ; Selenium ; deficiency ; Synapses ; pathology ; ultrastructure

Adolescent ; Adult ; Child ; Child, Preschool ; Electroencephalography ; Epilepsy ; pathology ; physiopathology ; Female ; Hippocampus ; pathology ; Humans ; Male

To explore the relationship between beta-amyloid (A beta) and the pathogenesis of Alzheimer disease (AD), after injection of beta-amyloid into the rat brain, the apoptosis of nerve cells and acetylcholine (Ach) content in rat hippocampus were examined by employing TUNEL technique and base hydroxylamine colorimetry respectively. The influence of age and glucocorticoid on the neurotoxic effect of A beta was also analyzed. A beta peptide could strongly induce the apoptosis of neurons in hippocampus, cortex and striate body (P < 0.05 or P < 0.01). In addition, the senility and glucocorticoid pre-treatment could enhance the toxic effect of A beta (P < 0.05 or P < 0.01). It is concluded that A beta may play an important role in the pathogenesis of Alzheimer disease via its induction of apoptosis of neurons and by decreasing the content of the Ach.
Acetylcholine/metabolism ; Aging ; Alzheimer Disease/etiology ; Amyloid beta-Protein/*toxicity ; Apoptosis/*drug effects ; Dexamethasone/*pharmacology ; Drug Synergism ; Hippocampus/metabolism ; Hippocampus/*pathology ; Injections, Intraventricular ; Neurons/pathology ; Rats, Wistar

The participation of activated leukocytes and subsequent production of chemical mediators has been well accepted in the pathophysiology of hypoxic-ischemic injury. This study was performed to see the effects of leukocytes on hippocampal neuronal damage in transient global ischemia induced by 10-min occlusion of bilateral common carotid arteries (CCAs) with reperfusion for various times, and in complete unilateral ischemia induced by 24-hr ligation of left CCA. Leukopenia was induced by intraperitoneal injection of cyclophosphamide for 4 days. The results showed that hippocampal neuronal damages were worse at 6-hr reperfusion in leukopenic experimental group than in the control group. In comparison, 24-hr and 3-day reperfusion leukopenic groups showed less numbers of damaged neurons and milder changes. The 5-day reperfusion group showed inconsistent changes. Unilateral CCA occlusion showed extensive infarction in 83.3% of gerbils in the control group, compared to 25% of gerbils in the experimental group (p<0.05). These results strongly suggest that the number of peripheral leukocytes were closely related to the development of delayed neuronal damage of hippocampus in transient global ischemia and the incidence of infarction induced by 24-hr unilateral CCA ligation.
Animal ; Cerebral Infarction/pathology* ; Female ; Gerbillinae ; Hippocampus/pathology* ; Leukocyte Count ; Leukocytes/physiology* ; Male ; Neurons/pathology* ; Reperfusion Injury

OBJECTIVETo elucidate the long-term effect of repeated febrile convulsions (FC) on seizure susceptibility in immature rats.

METHODSWarm-water-immersion rat FC model was developed with SD rats 22 days of age, 15 attacks of seizures were induced in the rats every other day, and some of the rats were left un-stimulated for 3 months, then were re-stimulated. Seizure phenomenon was observed, including the latency and the duration of seizures and the temperature of rats. Hippocampal neuron loss and mossy fiber sprouting were detected by thionine staining and Timm staining.

RESULTSAfter the 15th bath, the latency, the duration of seizures, and the temperature of rats were respectively (4.3 +/- 0.8) min, (5.5 +/- 2.9) min, (42.2 +/- 0.7) degrees C. Three months later, on re-stimulation, in 14 of 19 rats with previous FC experience seizures occurred while in only one of 13 non-FC rats seizure occurred and lasted for 8.5 min. Three months later, the latency, the duration of seizures, and the temperature of rats were respectively (5.4 +/- 0.6) min, (19.3 +/- 5.1) min, and (42.4 +/- 0.4) degrees C (4 rats with status epileptics were not included). The incidence of seizures on re-stimulation in rats of FC group (74%) was significantly higher than that in non-FC group (8%) (chi(2) = 13.50, P < 0.01), and the duration of seizures [(19.3 +/- 5.1) min] was significantly longer than those induced in early life [(5.5 +/- 2.9) min] (t = 10.49, P < 0.01). After the 15th bath, no significant change was demonstrated in rats of different groups. While 3 months later, prominent neuron loss was observed in hippocampal CA(3) region in rats with previous FC experience (P < 0.01). Significant mossy fiber sprouting phenomenon was detected after the 15th bath and 3 months later (P < 0.05).

CONCLUSIONRepeated FC in early life enhances long term susceptibility of rats to seizure.

Animals ; Disease Models, Animal ; Disease Susceptibility ; Hippocampus ; pathology ; Rats ; Rats, Sprague-Dawley ; Seizures ; pathology ; Seizures, Febrile ; pathology ; Time Factors

AIMTo make approach to the relationship between the changes of free zinc and ischemic neuronal damage in hippocampus after forebrain ischemia/reperfusion.

METHODSThe models of forebrain ischemia/reperfusion were established in rats. The contents of free Zn2+ were measured by TSQ fluorescence method. The Zn2+ chelator (CaEDTA) was injected into lateral ventricles in order to evaluate the effect of free Zn2+ on ischemic neuronal damage.

RESULTS(1) Zn2+ fluorescence in the hilus of dentate gyrus, CA3 region and the stratum radiatum and stratum oriens of CA1 decreased slightly at forty-eight hours after reperfusion. From seventy-two hours to ninety-six hour after reperfusion, the decreased fluorescence gradually returned to the normal level, but some fluorescence dots were found in pyramidal neurons of CA1 and the hilus of dentate gyrus. Seven days after reperfusion, all the changes of the fluorescence almost recovered. (2) The cell membrane-impermeable Zn2+ chelator CaEDTA could reduce the intracellular concentration of free Zn2+ and reduced neuronal damage after forebrain ischemia/reperfusion.

CONCLUSION(1) The synaptic vesicle Zn2+ released and then translocated into postsynaptic neurons after forebrain ischemia/reperfusion and played a role in ischemic neuronal damage. (2) The cell membrane-impermeable chelator CaEDTA could provide neuroprotection.

Animals ; Brain Ischemia ; metabolism ; pathology ; Hippocampus ; pathology ; Male ; Neurons ; metabolism ; Rats ; Rats, Wistar ; Reperfusion Injury ; metabolism ; pathology ; Zinc ; metabolism