Effects of Urtica dioica extract on CA3 hippocampal pyramidal cell loss in young diabetic rats

BACKGROUND： Urtica dioica extract has been shown to play a protective role in the neurodegeneration associated with diabetes mellitus. OBJECTIVE： To verify the neuroprotective efficacy of nettle extract on pyramidal cell density in the CA3 hippocampal subfield following administration of Urtica dioica extract to young diabetic rats. DESIGN, TIME AND SETTING： A randomized, controlled, neurobiological study was performed at the Department of Histology and Embryology at the Gorgan University of Medical Sciences in Iran from 2006 to 2007. MATERIALS： Urtica dioica leaves were collected from a cultivated plant in the suburb of Gorgan （northem Iran） and taxonomically identified by the Department of Pharmacognosy, Mazandaran University of Medical Sciences. METHODS： A total of 20 male, albino, Wistar rats, aged 6-7 postnatal weeks, were randomly assigned to four groups： normal control, diabetic model, preventive, and treatment, with five rats in each group. Diabetes was induced by intraperitoneal injection of streptozotocin （80 mg/kg） in the diabetic and treatment groups. Rats from the preventive group received a hydroalcoholic extract of Urtica dioica （100 mg/kg per day） during the first 5 days, and then streptozotocin （80 mg/kg） was administered on day 6. One week following the streptozotocin injection, rats in the treatment group were intraperitoneally administered hydroalcoholic extract of Urtica dioica （100 mg/kg per day） for 4 weeks. MAIN OUTCOME MEASURES： Following administration of Urtica dioica extract, the dorsal hippocampal formation of the right cerebral hemispheres was stained with cresyl violet. Area densities of CA3 pyramidal cells were measured. RESULTS： The diabetic, preventive, and treatment groups exhibited reduced cell densities compared with the control group （P 〈 0.05）. Moreover, densities of CA3 pyramidal cells in the treatment group were significantly reduced compared with the diabetic model group （P 〈 0.05）. CONCLUSION： The Urtica dioica extract exhibited no significant neuroprotectJve benefits in diabetes-induced loss of pyramidal cells in the CA3 hippocampal subfields of young diabetic rats.

Structural changes in pyramidal cell dendrites and synapses in the unaffected side of the sensorimotor cortex following transcranial magnetic stimulation and rehabilitation training in a rat model of focal cerebral infarct

Very little is known about the effects of transcranial magnetic stimulation and rehabilitation training on pyramidal cell dendrites and synapses of the contralateral, unaffected sensorimotor cortex in a rat model of focal cerebral infarct. The present study was designed to explore the mechanisms underlying improved motor function via transcranial magnetic stimulation and rehabilitation training following cerebral infarction. Results showed that rehabilitation training or transcranial magnetic stimulation alone reduced neurological impairment in rats following cerebral infarction, as well as significantly increased synaptic curvatures and post-synaptic density in the non-injured cerebral hemisphere sensorimotor cortex and narrowed the synapse cleft width. In addition, the percentage of perforated synapses increased. The combination of transcranial magnetic stimulation and rehabilitation resulted in significantly increased total dendritic length, dendritic branching points, and dendritic density in layer V pyramidal cells of the non-injured cerebral hemisphere motor cortex. These results demonstrated that transcranial magnetic stimulation and rehabilitation training altered structural parameters of pyramidal cell dendrites and synapses in the non-injured cerebral hemisphere sensorimotor cortex, thereby improving the ability to compensate for neurological functions in rats following cerebral infarction.

Glucose metabolism and neurogenesis in the gerbil hippocampus after transient forebrain ischemia

Recent evidence exists that glucose transporter 3（GLUT3） plays an important role in the energy metabolism in the brain.Most previous studies have been conducted using focal or hypoxic ischemia models and have focused on changes in GLUT3 expression based on protein and m RNA levels rather than tissue levels.In the present study,we observed change in GLUT3 immunoreactivity in the adult gerbil hippocampus at various time points after 5 minutes of transient forebrain ischemia.In the sham-operated group,GLUT3 immunoreactivity in the hippocampal CA1 region was weak,in the pyramidal cells of the CA1 region increased in a time-dependent fashion 24 hours after ischemia,and in the hippocampal CA1 region decreased significantly between 2 and 5 days after ischemia,with high level of GLUT3 immunoreactivity observed in the CA1 region 10 days after ischemia.In a double immunofluorescence study using GLUT3 and glial-fibrillary acidic protein（GFAP）,we observed strong GLUT3 immunoreactivity in the astrocytes.GLUT3 immunoreactivity increased after ischemia and peaked 7 days in the dentate gyrus after ischemia/reperfusion.In a double immunofluorescence study using GLUT3 and doublecortin（DCX）,we observed low level of GLUT3 immunoreactivity in the differentiated neuroblasts of the subgranular zone of the dentate gyrus after ischemia.GLUT3 immunoreactivity in the sham-operated group was mainly detected in the subgranular zone of the dentate gyrus.These results suggest that the increase in GLUT3 immunoreactivity may be a compensatory mechanism to modulate glucose level in the hippocampal CA1 region and to promote adult neurogenesis in the dentate gyrus.

Age-dependent loss of cholinergic neurons in learning and memory-related brain regions and impaired learning in SAMP8 mice with trigeminal nerve damage

The tooth belongs to the trigeminal sensory pathway. Dental damage has been associated with impairments in the central nervous system that may be mediated by injury to the trigeminal nerve. In the present study, we investigated the effects of damage to the inferior alveolar nerve, an important peripheral nerve in the trigeminal sensory pathway, on learning and memory be-haviors and structural changes in related brain regions, in a mouse model of Alzheimer’s disease. Inferior alveolar nerve transection or sham surgery was performed in middle-aged （4-month-old） or elderly （7-month-old） senescence-accelerated mouse prone 8 （SAMP8） mice. When the middle-aged mice reached 8 months （middle-aged group 1） or 11 months （middle-aged group 2）, and the elderly group reached 11 months, step-down passive avoidance and Y-maze tests of learn-ing and memory were performed, and the cholinergic system was examined in the hippocampus （Nissl staining and acetylcholinesterase histochemistry） and basal forebrain （choline acetyltrans-ferase immunohistochemistry）. In the elderly group, animals that underwent nerve transection had fewer pyramidal neurons in the hippocampal CA1 and CA3 regions, fewer cholinergic ifbers in the CA1 and dentate gyrus, and fewer cholinergic neurons in the medial septal nucleus and vertical limb of the diagonal band, compared with sham-operated animals, as well as showing impairments in learning and memory. Conversely, no signiifcant differences in histology or be-havior were observed between middle-aged group 1 or group 2 transected mice and age-matched sham-operated mice. The present ifndings suggest that trigeminal nerve damage in old age, but not middle age, can induce degeneration of the septal-hippocampal cholinergic system and loss of hippocampal pyramidal neurons, and ultimately impair learning ability. Our results highlight the importance of active treatment of trigeminal nerve damage in elderly patients and those with Alzheimer’s disease, and indicate that tooth extraction should be avoided in these populations.

Profiles of hippocampal neuron activity during auditory discrimination cognition in guinea pigs

Objective: To clarify the firing characteristics of the hippocampal pyramidal cells and in-terneurons in the auditory discrimination cognition. Methods: Thirteen guinea pigs were studied by the paired (active cognition group. n=10) or unpaired (passive cognition group. n = 3) training with 1 kHz (CS+)and 500 Hz tones (CS- ) and the air puff (US) applied 250 ms after the CS+ onset. Results: In active group. 32 pyramidal cells showed exciting response to the CS+ tone. 16 cells inhibited response and 4 cells revealed no response to the high frequency tone and 18 interneurons almost unchanged. In passive group, the pyramidal cells responded to the tone casually and 10 out of the 13 interneurons remained invariably. Conclusion: The result suggests that the pyramidal cells play a major role in coding auditory information by the networks, and the interneuons may modulate it via forward and feedback.