ABSTRACT
Calbindin D-28k (CB), a calcium-binding protein, containing neurons in the hippocampus plays an important role in hippocampal excitability in epilepsy. In the present study, we investigated changes of CB immunoreactivity after adrenalectomy (ADX) in the hippocampus and dentate gyrus of the seizure sensitive gerbil, which is susceptible to seizure to identify roles of CB in epileptogenesis. The changes of the CB immunoreactivity after ADX were significant in the hippocampal CA1 region. By 24 h after ADX, CB-immunoreactive CA1 pyramidal cells and CB immunoreactivity increased. At this time, well-stained dendrites projected to the stratum radiatum. Thereafter, the CB immunoreactivity decreased time dependently by 96 h after ADX. In the dentate gyrus, the changes of CB-immunoreactive neurons were mainly observed in the granule cell layer. The number and immunoreactivity of CB-immunoreactive neurons was high at 24 h after ADX, thereafter, those decreased by 96 h after ADX. These results suggest that glucocorticoid has an important role in modulating the seizure activity and CB serves an inhibitory function, which regulates the seizure activity and output signals from the hippocampus.
Subject(s)
Dentate Gyrus/metabolism , Hippocampus/metabolism , S100 Calcium Binding Protein G/metabolism , Seizures/metabolism , Adrenalectomy , Animals , Calbindins , Dentate Gyrus/anatomy & histology , Gerbillinae , Hippocampus/anatomy & histology , Immunohistochemistry , Male , S100 Calcium Binding Protein G/immunologyABSTRACT
In the present study, we investigated the ischaemia-related neurodegeneration in the main and accessory olfactory bulb (AOB) after 5 min transient forebrain ischaemia in the Mongolian gerbil using the acid fuchsin staining method. Between 5 and 15 days after ischaemia, acid fuchsin positive cells markedly increased in the external plexiform layer (EPL), mitral cell layer (ML) and glomerular layer (GL) of the main olfactory bulb (MOB), and in the mixed cell layer (MCL) and GL of the AOB. By 30 days after ischaemia reperfusion, acid fuchsin positive neurons were shrunken and showed low acidophilia in somata. Many necrotic vacuoles were found in the EPL and GL of the MOB 30 days after ischaemia. At this time, necrotic vacuoles were very few in the AOB. Therefore, our results suggest that the GL and EPL of the MOB are vulnerable to ischaemic damage at a later time after ischaemic insult, and that the AOB is more resistant to ischaemic damage as compared with the MOB.
Subject(s)
Gerbillinae , Ischemic Attack, Transient/veterinary , Neurodegenerative Diseases/veterinary , Olfactory Bulb/pathology , Rodent Diseases/pathology , Animals , Immunohistochemistry/veterinary , Ischemic Attack, Transient/complications , Ischemic Attack, Transient/pathology , Male , Neurodegenerative Diseases/etiology , Neurodegenerative Diseases/pathology , Olfactory Bulb/anatomy & histology , Prosencephalon/blood supply , Prosencephalon/pathologyABSTRACT
P2X receptors play a role in the transduction of sensory signals like pain. Few studies have been undertaken on altered P2X(3) receptor (P2X3) expression in sensory neurones after peripheral nerve injury. In the present study, we investigated chronological alterations in P2X3 immunoreactivity and its protein content in the trigeminal ganglion after ischaemic insult in the Mongolian gerbil. In the sham-operated group, P2X3-immunoreactive neurones were found abundantly in small- and medium-sized neurones. From 1 day after ischaemic insult, the number of P2X3-immunoreactive neurones decreased significantly. At 5 days after ischaemic insult, P2X3 immunoreactivity was observed in few neurones, but its immunoreactivity was weak. However, the number of cresyl violet-positive neurones was unchanged throughout this period in all groups. These results suggest that transient trigeminal ganglion ischaemia may provoke a decrease of P2X3 expression and its protein content, and that this down-regulation of P2X3 may be related to the altered pain and thermal sensation without being associated with a transient ischaemic insult.
