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.
Adult ; Amygdala ; pathology ; Anthropometry ; Depressive Disorder, Major ; pathology ; Female ; Hippocampus ; pathology ; Humans ; Magnetic Resonance Imaging ; 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

OBJECTIVE: To investigate the effects of central nucleus of amygdala (CeA) lesion on the initiation and expression of sodium appetite in sodium-deficient rats. METHODS: Three groups of SD rats (n=6 in each group) were treated with bilateral CeA lesion, sham lesion or no lesion. After the recovery, the rats were fed with low-sodium diets for 14 days to establish a sodium-deficient rat model. The double-bottle selection in single cage test was used to observe the intake of 0.3 mol/L NaCl and DW in 5 timepoint with 24 hours in sodium-deficient rats. Immunofluorescence staining of aldosterone-sensitive neurons in the nucleus tractus solitarii (NTS)was used to investigate the effect of CeA lesion or not on the activity of aldosterone-sensitive neurons in rats with or without sodium deficiency. RESULTS: After fed with low-sodium diet for14 days, the volume and preference rate of 0.3 mol/L NaCl intake of the rats within 24 h were significantly increased compared with those before low-sodium diet (P＜0.01). The intake volume and the preference rate of 0.3 mol/L NaCl in CeA lesion rats were significantly decreased than those in CeA sham lesion rats and normal rats in the sodium-deficient condition (P＜0.01). The CeA lesion had no effects on the activity of aldosterone-sensitive neurons in NTS in rats with low-sodium diet. CONCLUSION Low-sodium diet induces an increase in the expression of sodium appetite in rats. CeA lesions inhibit the behavioral expression of sodium appetite in sodium-deficient rats but have no effects on the initiation of sodium appetite in rats with sodium-deficient rats.
Amygdala ; pathology ; Animals ; Appetite ; Diet, Sodium-Restricted ; Neurons ; Rats ; Rats, Sprague-Dawley ; Sodium ; Sodium, Dietary ; pharmacology

Objective: To explore the topological properties of the degree and strength of nodes in the binary and weighted brain white matter networks of the patients with psychogenic erectile dysfunction (pED) and analyze the changes of myelin integrity, number and length of the white matter fibers in the topological space. METHODS: Diffusion tensor imaging data were obtained from 21 patients with pED and 24 healthy controls matched in sex, age, and years of education and subjected to preprocessing. The whole cerebral cortex was divided into 90 regions, followed by fiber tracking, construction of the binary and weighted white matter networks, and calculation of the node degrees and connectivity strengths in different brain regions. The property values were compared between the two groups using the two-sample t-test, the results were corrected by multiple testing correction, and the correlation of the property values with the erectile function of the patients was subjected to Pearson's correlation analysis. RESULTS: Compared with the healthy controls, the pED patients showed significantly decreased node degree of the left triangular part of inferior frontal gyrus (IFG) (7.54±1.44 vs 5.95±1.28, t = －3.88, corrected P = 0.02), medial orbital part of superior frontal gyrus (SFG) (10.08±3.60 vs 6.29±3.30, t = －3.67, corrected P = 0.02), and amygdala (6.50±2.11 vs 4.29±1.31, t = －4.16, corrected P = 0.01) in the binary networks, as well as the connectivity strength of the left triangular part of IFG (2.50±0.68 vs 1.72±0.50, t = －4.35, corrected P = 0.01), medial orbital part of SFG (3.17±0.97 vs 2.08±1.10, t = －3.53, corrected P = 0.03), and amygdala (1.80±0.69 vs 1.11±0.39, t = －4.03, corrected P = 0.01) in the fractional anisotropy (FA) weighted networks. The node degree of the left amygdala was negatively correlated with the total score (r = －0.47,P = 0.04), second item score (r = －0.46, P = 0.03), and third item score of IIEF-5 (r = －0.45, P = 0.04) in the pED patients. CONCLUSIONS The myelin integrity of the white matter fibers in the left frontal lobe and amygdale is impaired in pED patients, which leads to the aberrant generation, processing and regulation of their emotions. The decreased pivotal role and importance of the white matter fibers connecting the left amygdale may be associated with pED.
Amygdala ; diagnostic imaging ; Anisotropy ; Case-Control Studies ; Diffusion Tensor Imaging ; Erectile Dysfunction ; etiology ; psychology ; Frontal Lobe ; diagnostic imaging ; Humans ; Male ; Myelin Sheath ; pathology ; White Matter ; diagnostic imaging

Corticotrophin-releasing factor (CRF), a key regulator of the hypothalamic-pituitary axis, is expressed in the central nucleus of the amygdala (CeA) and its expression is upregulated in stress-related disorders. We investigated here the effect of noxious colorectal distension (CRD) on the expression of CRF in the CeA of conscious and unconscious rats. Adult male rats with or without general anesthesia were exposed to visceral pain induced by CRD for 5 min; this procedure was repeated 3 times with 1 min resting after each distension. The rats were sacrificed and sections of the CeA were immunostained for CRF as an indicator for anxiety response, and for phosphorylated extracellular signal-regulated kinase (p-ERK) as a marker for pain-specific activation of neurons; sections of lumbosacral spinal cord were immunostained for c-Fos as a marker for activation of spinal neurons. CRD elicited a significant increase in the expression of CRF and p-ERK in the CeA and of c-Fos in the spinal cord. General anesthesia attenuated the increase in CRF and p-ERK in the CeA, but did not affect the expression of spinal c-Fos. These results suggest that conscious recognition of pain at higher brain centers is an important determinant of CRF expression in the CeA.
Amygdala/*metabolism/pathology ; *Anesthesia, General ; Animals ; Colon ; Corticotropin-Releasing Hormone/*metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Immunohistochemistry ; Male ; Neurons/metabolism ; Pain/prevention & control ; Phosphorylation ; Proto-Oncogene Proteins c-fos/metabolism ; Rats ; Rats, Sprague-Dawley ; Rectum

Here we present an autopsy case of chronic traumatic encephalopathy (CTE) in a 36-year-old man. He had a history of febrile seizures at the age of four and was severely demented at age 10 when he was admitted to a mental hospital. He had suffered repetitive self-harm, such as frequent banging of the head on the wall in his hospital record, but he had no clear history between the ages of four and ten. Autopsy revealed global cerebral atrophy, including the basal ganglia, thalamus, hippocampus, amygdala, mammilary bodies and lateral geniculate bodies. This case showed typical pathological features of CTE. Phosphorylated tau (p-tau)-positive neurofibrillary tangles (NFTs) and neuropil threads (NT) we are widely distributed in the brain, especially in the depth of the cerebral sulci. NFT and NT were also found in the basal ganglia, thalamus, amygdala and brainstem. Scanty β-amyloid deposits were found in the motor and sensory cortices, but α-synuclein was completely negative in the brain. This example showed that CTE can occur in young ages and that even children can experience CTE dementia.
Adult ; Amygdala ; Atrophy ; Autopsy* ; Basal Ganglia ; Brain ; Brain Injuries ; Brain Injury, Chronic* ; Brain Stem ; Child* ; Dementia ; Geniculate Bodies ; Head ; Hippocampus ; Hospital Records ; Hospitals, Psychiatric ; Humans ; Neurofibrillary Tangles ; Neuropil Threads ; Pathology ; Seizures, Febrile ; Thalamus

In the present study, extracellular recording was used to examine the neuronal activity of the basolateral nucleus (BL) of the amygdala and the effects of systemic administration of the selective 5-HT(1A) receptor antagonist WAY-100635 on the neuronal activity in the normal rats and rats with 6-hydroxydopamine (6-OHDA)-produced lesions in the substantia nigra pars compacta (SNc). The results showed that the firing rates of BL projection neurons and interneurons were (0.39±0.04) Hz and (0.83±0.16) Hz in the normal rats, and (0.32±0.04) Hz and (0.53±0.12) Hz in 6-OHDA-lesioned rats. There was no significant difference in the firing rates of BL projection neurons and interneurons between the normal and 6-OHDA-lesioned rats. In the normal rats, all BL projection neurons fired in burst; 94% of BL interneurons fired in burst and 6% fired irregularly. In 6-OHDA-lesioned rats, 85% of BL projection neurons displayed a burst firing pattern and 15% fired irregularly; 86% of BL interneurons had a burst firing pattern and 14% fired irregularly. The distribution of firing patterns of projection neurons and interneurons in the BL in 6-OHDA-lesioned rats did not differ from that in the normal rats. Systemic administration of WAY-100635 at 0.1 mg/kg body weight did not change the mean firing rates of projection neurons and interneurons in the BL in both normal and 6-OHDA-lesioned rats. However, a higher dose of WAY-100635 at 0.5 mg/kg body weight significantly decreased the mean firing rate of BL projection neurons from (0.43±0.07) to (0.15±0.02) Hz in the normal rats (P<0.01), but significantly increased the activity of BL projection neurons in 6-OHDA-lesioned rats from (0.37±0.08) to (0.69±0.18) Hz (P<0.004). The mean firing rates of BL interneurons in the normal and 6-OHDA-lesioned rats did not change after administration of a higher dose of WAY-100635 at 0.5 mg/kg body weight. These results demonstrate that the activity of BL neurons after substantia nigra dopaminergic lesion in the SNc is regulated by activation of intrinsic and extrinsic inputs, and that 5-HT(1A) receptors significantly contribute to the regulation of the activity of BL projection neurons in both normal and 6-OHDA-lesioned rats. Furthermore, WAY-100635 induced an increase in the mean firing rate of projection neurons in the BL in 6-OHDA-lesioned rats, suggesting that 5-HT(1A) receptor is likely to play a role in generating affective symptoms in Parkinson's disease.
Action Potentials ; Amygdala ; drug effects ; Animals ; Neurons ; drug effects ; Oxidopamine ; adverse effects ; Piperazines ; pharmacology ; Pyridines ; pharmacology ; Rats ; Receptor, Serotonin, 5-HT1A ; Serotonin 5-HT1 Receptor Antagonists ; pharmacology ; Substantia Nigra ; pathology

The characteristic features of Alzheimer's disease (AD) are the appearance of extracellular amyloid-beta (Aβ) plaques and neurofibrillary tangles in the intracellular environment, neuronal death and the loss of synapses, all of which contribute to cognitive decline in a progressive manner. A number of hypotheses have been advanced to explain AD. Abnormal tau phosphorylation may contribute to the formation of abnormal neurofibrillary structures. Many different structures are susceptible to AD, including the reticular formation, the nuclei in the brain stem (e.g., raphe nucleus), thalamus, hypothalamus, locus ceruleus, amygdala, substantia nigra, striatum, and claustrum. Excitotoxicity results from continuous, low-level activation of N-methyl-D-aspartate (NMDA) receptors. Premature synaptotoxicity, changes in neurotransmitter expression, neurophils loss, accumulation of amyloid β-protein deposits (amyloid/senile plaques), and neuronal loss and brain atrophy are all associated with stages of AD progression. Several recent studies have examined the relationship between Aβ and NMDA receptors. Aβ-induced spine loss is associated with a decrease in glutamate receptors and is dependent upon the calcium-dependent phosphatase calcineurin, which has also been linked to long-term depression.
Alzheimer Disease* ; Amygdala ; Amyloid ; Animals, Genetically Modified ; Atrophy ; Basal Ganglia ; Brain Stem ; Brain* ; Calcineurin ; Depression ; Hypothalamus ; Locus Coeruleus ; N-Methylaspartate* ; Neurofibrillary Tangles ; Neurons ; Neurotransmitter Agents ; Pathology* ; Phosphorylation ; Receptors, Glutamate ; Receptors, N-Methyl-D-Aspartate* ; Reticular Formation ; Risk Factors* ; Spine ; Substantia Nigra ; Synapses ; tau Proteins* ; Thalamus

Synaptic vesicle protein 2A (SV2A) involvement has been reported in the animal models of epilepsy and in human intractable epilepsy. The difference between pharmacosensitive epilepsy and pharmacoresistant epilepsy remains poorly understood. The present study aimed to observe the hippocampus SV2A protein expression in amygdale-kindling pharmacoresistant epileptic rats. The pharmacosensitive epileptic rats served as control. Amygdaloid-kindling model of epilepsy was established in 100 healthy adult male Sprague-Dawley rats. The kindled rat model of epilepsy was used to select pharmacoresistance by testing their seizure response to phenytoin and phenobarbital. The selected pharmacoresistant rats were assigned to a pharmacoresistant epileptic group (PRE group). Another 12 pharmacosensitive epileptic rats (PSE group) served as control. Immunohistochemistry, real-time PCR and Western blotting were used to determine SV2A expression in the hippocampus tissue samples from both the PRE and the PSE rats. Immunohistochemistry staining showed that SV2A was mainly accumulated in the cytoplasm of the neurons, as well as along their dendrites throughout all subfields of the hippocampus. Immunoreactive staining level of SV2A-positive cells was 0.483 ± 0.304 in the PRE group and 0.866 ± 0.090 in the PSE group (P < 0.05). Real-time PCR analysis demonstrated that 2(-ΔΔCt) value of SV2A mRNA was 0.30 ± 0.43 in the PRE group and 0.76 ± 0.18 in the PSE group (P < 0.05). Western blotting analysis obtained the similar findings (0.27 ± 0.21 versus 1.12 ± 0.21, P < 0.05). PRE rats displayed a significant decrease of SV2A in the brain. SV2A may be associated with the pathogenesis of intractable epilepsy of the amygdaloid-kindling rats.
Amygdala ; drug effects ; metabolism ; physiopathology ; Animals ; Anticonvulsants ; pharmacology ; Disease Models, Animal ; Drug Resistance ; Electric Stimulation ; Epilepsy ; drug therapy ; genetics ; metabolism ; pathology ; Gene Expression Regulation ; Hippocampus ; drug effects ; metabolism ; physiopathology ; Kindling, Neurologic ; drug effects ; genetics ; metabolism ; pathology ; Male ; Membrane Glycoproteins ; genetics ; metabolism ; Nerve Tissue Proteins ; genetics ; metabolism ; Phenobarbital ; pharmacology ; Phenytoin ; pharmacology ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Synaptic Transmission ; Synaptic Vesicles ; drug effects ; metabolism ; pathology