No abstract available.
Gerbillinae

No abstract available.
Gerbillinae* ; Vestibular Nuclei*

No abstract available.
Gerbillinae* ; Vestibular Nerve*

In the present study, we examined change of ionized calcium-binding adapter molecule 1 (Iba-1) in the adult and aged gerbil spinal cords. Significant change of morphological feature and neuronal cell loss were not observed in both adult and aged spinal cords of gerbil after NeuN immunohistochemistry and Fluoro-Jade B histofluoresce staining. Iba-1–immunoreactive microglia broadly distributed in the spinal cord. Most of Iba-1–immunoreactive microglia showed ramified forms in the adult gerbil cervical and lumbar spinal cords. However, morphological changes of Iba-1–immunoreactive microglia were observed in the cervical and lumbar regions of the aged gerbil spinal cord. These microglia were showed a hypertrophied body with shortened swollen processes which was characteristic of activated microglia. In addition, Iba-1 protein level significantly higher in aged cervical and lumbar spinal cords than those in the adult gerbil. The present study showed an increase of activated forms of Iba-1–immunoreactive microglia and its protein level without marked changes in morphological features and neuronal loss in the aged spinal cord compared to those in the adult gerbil spinal cord. This result suggests that the increase of Iba-1 expression in the aged spinal cord may be closely associated with age-related changes in aged gerbil spinal cord.
Adult* ; Gerbillinae* ; Humans ; Immunohistochemistry ; Lumbosacral Region ; Microglia ; Neurons ; Spinal Cord*

BACKGROUND: The present study was performed in order to evaluate the duration-dependent neuroprotective effect of post-ischemic mild hypothermia against delayed neuronal damage following transient global ischemia and to estimate the optimal duration of brief post-ischemic mild hypothermia. METHODS: Post-ischemic mild hypothermia of different duration(1 hour, 3 hours, and 6 hours) was performed immediately after 10-minute global ischemia in gerbils, and the hippocampal CA1 cell loss after 3 days was evaluated. The duration-dependent neuroprotective effect of post-ischemic mild(33-34degrees C) hypothermia of each duration was compared to the normothermic control by using histopathological methods. RESULTS: 1, 3 and 6 hours of mild hypothermia immediately following reperfusion resulted in progressively increased protection from ischemic damage, 10.0+/-8.2%, 33.7+/-21.9%, and 75.9+/-13.4%, respectively. The 3-hour and the 6-hour post-ischemic mild hypothermia groups revealed significant decreases in hippocampal CA1 area cell loss compared to the normothermic control group(9.0+/-7.7%, p<0.05), and the 6-hour group had a greater preservation than the 3-hour group(p<0.05). CONCLUSION: The results suggest that post-ischemic mild hypothermia protects against delayed neuronal damage in the hippocampal CA1 area following 10-minute transient global ischemia: 3-hour post-ischemic mild hypothermia provides a potential reduction of neuronal damage, but a 6-hour treatment is more effective in preventing neuronal damage than a 3-hour one.
Brain Ischemia ; Gerbillinae* ; Hypothermia* ; Ischemia ; Neurons ; Neuroprotective Agents* ; Reperfusion

BACKGROUND: Transient global ischemia causes delayed neuronal death (DND) in the CA1 area, of which the mecha-nism is controversial. Induction of apoptosis-regulating proteins during the process of DND has been reported, howev-er ,the exact role of Bcl-2/Bax is not well understood. We tried to reveal the pattern of the Bax/Bcl-2 expression modi-fied by the duration of ischemia and hypothermia. METHODS: Global ischemia was induced in Mongolian gerbils for 2, 5, and 10 minutes under the temperature of 36 degrees C and 32 degrees C. Hippocampal sections were evaluated 48 hours after ischemia with H&E and immunohistochemical staining to Bcl-2/Bax. Viable neuronal density and semi-quantitative grading were compared. RESULTS: In the CA1 area, neurons were intact in 2 min ischemia, while partial or significant ischemic changes were observed in 5-10 min ischemia of 36 degrees C setting, which were less severe in 32 degrees C . Bcl-2 was posi-tive in 2 min ischemia, while negative in 5~10 min ischemia of 36 degrees C . Bax was negative in 2 and 10 min ischemia, while positive in 5 min ischemia. In 32 degrees C setting, Bcl-2 was also positive in 2 min ischemia and partially positive in 5- 10 min ischemia, although Bax expression was not different from 36 degrees C. CONCLUSIONS: The complex mechanism of DND, which is in the spectrum of apoptosis and necrosis, seems to be determined by the severity of ischemia. The bal-ance between Bcl-2 and Bax may determine the survival of neurons in mild to moderate ischemia. Further evidence remains to be determined by morphological and molecular biological methods.
Apoptosis ; Body Temperature* ; Gerbillinae ; Hypothermia ; Ischemia* ; Necrosis ; Neurons

The present study involves a chronological and comparative analysis of both microtubule-associated protein 1A (MAP1A) and microtubule-associated protein 2 (MAP2) immunoreactivities in the striatum of both seizure resistant (SR) and seizure sensitive (SS) gerbil. The MAP1A immunoreactivity is weakly detected in perikarya of SR gerbils. However, MAP1A immunoreactivity is more accumulated in perikarya and dendrites in the pre-seizure group. At 30 min postictal, MAP1A immunoreactivity in the perikarya is decreased. At 3 hr postictal, MAP1A immunoreactivity in perikarya and dendrites is similarly decreased to the level of SR gerbils. The MAP2 immunoreactivity is weakly detected in the perikarya and dendrites of SR gerbils. However, MAP2 immunoreactivity is more accumulated in perikarya and dendrites. In particular, the neuropil between unstained fiber tracts obviously contains strong MAP2 immunoreactivity. At 30 min postictal, MAP2 immunoreactivity isn't almost observed in striatum. At 3 hr postictal, the MAP2 immunoreactivity is not different in the 30 min post -seizure groups but is only observed in the neuropil. However, at 12 hr postictal, the decrease of both MAP1A and MAP2 immunoreactivities had recovered to the pre -seizure level of SS gerbils. These results suggest that MAPs immunoreactivity in the striatum is different in SR and SS gerbils, and that this difference may be the results of seizure activity in this animal.
Animals ; Dendrites ; Epilepsy ; Gerbillinae* ; Microtubule-Associated Proteins* ; Microtubules* ; Neuropil ; Seizures*

BACKGROUND AND OBJECTIVES: Bone resorption of adjacent structures in aural cholesteatoma is mostly responsible for serious complication of the disease. Recent researches have been aimed at preventing bone resorption with tools of non-surgical therapy. The effect of pam-idronate disodium on systemic bone resorption is mainly attributed by its function against osteoclast recruitment and activation. In this study, we investigated the effect of systemic pam-idronate disodium on localized osteoclastic bone resorption in experimental cholesteatoma. MATERIAL AND METHODS: Experimental cholesteatomas were induced in 40 mongolian gerbils. pam-idronate disodium (Aredia(R), Ciba-Geigy Limited)were injected subcutaneously once a week in 20 gerbils (treated group)and none were injected in the other 20 gerbils (untreated group). pam-idronate disodium were injected with a dose of 2 mg/kg in 10 of the treated group (low dose group) and with a dose of 4 mg/kg in the remainder (high dose group). Gerbils were sacrificed at 12 weeks (3 month group) or 17 weeks (4 month group) after the injection. Harvested temporal bones were examined by light microscope and transmission electron microscope. RESULTS: The clinical stage of cholesteatoma tended to be more advanced in the untreated group than in the treated group although it was not statistically significant. Scores of osteoclast number per total bone length in millimeter were lower in the treated group than in the untreated, although the percentage of surface occupied by osteoclasts per total bone surface were not different between the groups. CONCLUSION: These results will provide fundamental data for further studies on the prevention and treatment of osteoclastic bone resorption in aural cholesteatoma.
Bone Resorption ; Cholesteatoma* ; Cholesteatoma, Middle Ear ; Gerbillinae ; Osteoclasts ; Temporal Bone

Rat mite dermatitis caused by Ornithonysus bacoti, commonly referred to as the tropical rat mite, is characterized by pruritic papules in patients exposed to tropical rat mite. Histopathologic sections from the lesions of infected patients show moderate perivascular lymphohistiocytic infiltration intermingled with some eosinophils. Causative female mites, Ornithonyssus bacoti, can be collected from around the skin lesions. The conclusive diagnosis of tropical rat mite dermatitis is based on the identification of the arthropod O. bacoti at the home of the patient (husbandry of gerbils, etc.). Moreover, the diagnosis of rat mite dermatitis requires the detection of the parasite, which is more likely to be found in the host's environment rather than on the host's skin. We report a case of rat mite dermatitis in a 22-year-old female who presented with pruritic, multiple, erythematous papules on the abdomen, back and axilla.
Abdomen ; Animals ; Arthropods ; Axilla ; Dermatitis* ; Diagnosis ; Eosinophils ; Female ; Gerbillinae ; Humans ; Mites* ; Parasites ; Rats* ; Skin ; Young Adult

Stress has long been known to be a causative factor of various disease states. In this study, we investigated the effects of repeated restraint stress on platelet endothelial cell adhesion molecule-1 (PECAM-1), a very important mediator in inflammation, immunoreactivity and protein levels as well as neuronal damage, in the gerbil hippocampus after 5 minutes of transient cerebral ischemia. Transient ischemia-induced neuronal death was shown in CA1 pyramidal cells 4 days after ischemia/reperfusion. However, repeated restraint stress protected neuronal death induced by ischemic damage. In the ischemia-group, PECAM-1 immunoreactivity and its protein levels were significantly increased in all the hippocampal subregions 4 days after ischemia/reperfusion. However, PECAM-1 immunoreactivity and its protein levels did not change significantly in the hippocampus of the stress-ischemia-group compared to the sham-groups. These results indicate that repeated restraint stress protects neuronal damage induced by transient cerebral ischemia, and this may be associated with maintenance of PECAM-1levels.
Antigens, CD31 ; Blood Platelets ; Brain Ischemia ; Gerbillinae ; Hippocampus ; Inflammation ; Ischemic Attack, Transient ; Neurons ; Pyramidal Cells