The developmental expression of calcium-binding protein, calbindin D-28k (CB), during the first 6 months was studied in the canine hippocampus by immunohistochemistry. CB immunoreactivity appeared from on P0 in the dentate granule cells, mossy fibers in CA 3 area, CA 2 and CA 1 pyramidal cells, and interneurons in all regions. According to their morphology and location, these could represent the presumptive pyramidal cells and interneurons. From on P7, the CB immunoreactive pyramidal cells clearly distinguished and started to form two rows in CA 1 area as time progressed, while scattered multipolar neurons gradually decreased. CB immunoreactive cell processes increased in length up to P28. The adult-like distribution of CB immunoreactivity was established about P60. After P60, CB immunoreactivity appeared in dentate granule cells, mossy fibers in CA 3 area and pyramidal cells in CA 1 where formed two rows and CA 2 areas as well as in interneurons of the strata oriens and pyramidale. Taken together, developmental expression of CB in the canine hippocampus was summarized that CB imunoreactivity was observed in all regions on P0 and reached adult-like distribution about P60. These data also suggested the possibility of prenatal expression of CB on the basis of the staining pattern at P0.
Calbindins* ; Hippocampus* ; Immunohistochemistry ; Interneurons ; Neurons ; Pyramidal Cells

The influences of adrenal corticosteroid on the development and regression of neurons of dentate and hippocampus were studied by adrenalectomy and steroid overload in neonatal rats. The results obtained were as follows. 1. The cell death occurred naturally in numerous dentate granule cells and hippocampal pyramidal cells. 2. The number of dentate granule cells undergoing cell death decreased by injection of adrenal corticosteroid, but increased in adrenalectomized rat brains. The changes occurred prominently at postnatal day 6. 3. The number of hippocampal pyramidal cells undergoing cell death decreased in CA3 region by injection of adrenal corticosteroid, but was not changed in adrenalectomized rat brains. However, other regions exhibited no change by adrenal corticosteroid and adrenalectomy. 4. The cell death of pyramidal cells of CA3 region occurred in close relationship with the cell death of dentate granule cells, which was different from other CA regions. In summary, the cell death of dentate and hippocampal neurons occurred naturally but seemed to be influenced by other factors as well as adrenal corticosteroid.
Adrenalectomy ; Animals ; Brain ; Cell Death ; Hippocampus* ; Neurons* ; Pyramidal Cells ; Rats*

The family of voltage-gated potassium Kv2 channels consists of the Kv2.1 and Kv2.2 subtypes. Kv2.1 is constitutively highly phosphorylated in neurons and its function relies on its phosphorylation state. Whether the function of Kv2.2 is also dependent on its phosphorylation state remains unknown. Here, we investigated whether Kv2.2 channels can be phosphorylated by protein kinase C (PKC) and examined the effects of PKC-induced phosphorylation on their activity and function. Activation of PKC inhibited Kv2.2 currents and altered their steady-state activation in HEK293 cells. Point mutations and specific antibodies against phosphorylated S481 or S488 demonstrated the importance of these residues for the PKC-dependent modulation of Kv2.2. In layer II pyramidal neurons in cortical slices, activation of PKC similarly regulated native Kv2.2 channels and simultaneously reduced the frequency of action potentials. In conclusion, this study provides the first evidence to our knowledge that PKC-induced phosphorylation of the Kv2.2 channel controls the excitability of cortical pyramidal neurons.
Action Potentials ; HEK293 Cells ; Humans ; Protein Kinase C/metabolism* ; Pyramidal Cells/enzymology* ; Shab Potassium Channels/genetics*

Pyramidal motor evoked potential (PMEP) was recored in rat using the specially designed stimulating electrode for preferential activation of a pyramidal cell layer of the motor cortex. The PMEPs, recorded in the upper levels of a neural axis (medulla and C7), were composed of short latency complex waves and a long latency positive wave with a large amplitude and prolonged duration. However, the PMEP recorded at the lower level of a neural axis (T8) only showed the long latency a large positive wave. Conduction velocity of the short latency wave was approximately 11.1m/sec. Judging by the conduction velocities of these waves, it appeared that the short latency-wave complex originated from direct activation of pyramidal cells in the motor cortex (D-wave). The long latency-wave seemed to be evoked by indirect activation of the pyramidal cells (I-wave). This view was further supported by the serial depth recordings of PMEPs in the medulla as well as by the field mapping of PMEPs in the T4 spinal cord. PMEPs completely disappeared following the acute lesion of an internal capsule, indicating that these waves originated from the motor cortex rather than the brain stem nuclei such as the reticular nuclei.
Animals ; Axis, Cervical Vertebra ; Brain Stem ; Electrodes ; Evoked Potentials, Motor* ; Internal Capsule ; Motor Cortex ; Pyramidal Cells ; Pyramidal Tracts ; Rats* ; Spinal Cord

Numerous studies have implicated the hippocampus in the encoding and storage of declarative and spatial memories. Several models have considered the hippocampus and its distinct subfields to contain homogeneous pyramidal cell populations. Yet, recent studies have led to a consensus that the dorso-ventral and proximo-distal axes have different connectivities and physiologies. The remaining deep-superficial axis of the pyramidal layer, however, remains relatively unexplored due to a lack of techniques that can record from neurons simultaneously at different depths. Recent advances in transgenic mice, two-photon imaging and dense multisite recording have revealed extensive disparities between the pyramidal cells located in the deep and the superficial layers. Here, we summarize differences between the two populations in terms of gene expression and connectivity with other intra-hippocampal subregions and local interneurons that underlie distinct learning processes and spatial representations. A unified picture will emerge to describe how such local segregations can increase the capacity of the hippocampus to compute and process numerous tasks in parallel.
Animals ; Consensus ; Gene Expression ; Hippocampus ; Interneurons ; Learning ; Memory ; Mice ; Mice, Transgenic ; Neurons ; Pyramidal Cells ; Spatial Memory

OBJECTIVE: A previous study indicated that acute treatment of clozapine increased the neural activity of prefrontal cortical neurons of anesthetized rats. This study was to investigate the effect of clozapine on prefrontal cortical neurons in behaving rats. METHODS: Neural activities of prefrontal cortical neurons of behaving rats were measured before and after clozapine administration using single unit recording. RESULTS: Sixty nine single units (N=69) in the medial prefrontal cortex were isolated in forty three Sprague-Dawley rats. Although clozapine did not change the overall average firing rate of prefrontal cortical neurons, there was a tendency to increase in the neural activity of neurons with low firing rate that were considered to be putative pyramidal cells (N=40). In contrast, neurons with high firing rate assumed to be putative interneurons (N=29) tended to decrease in neural activity by clozapine treatment. CONCLUSION: This result suggests that clozapine treatment enhances the neural activity of pyramidal cells and to inhibit interneurons in the prefrontal cortex. It is speculated that the enhancement of neural activity of pyramidal cells in the prefrontal cortex by clozapine treatment may contribute to its therapeutic effect.
Animals ; Clozapine* ; Fires ; Interneurons ; Neurons* ; Prefrontal Cortex ; Pyramidal Cells ; Rats* ; Rats, Sprague-Dawley ; Schizophrenia

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

Hippocalcin participates in the maintenance of neuronal calcium homeostasis. In the present study, we examined the time-course changes of neuronal degeneration and hippocalcin protein level in the mouse hippocampus following pilocarpine-induced status epilepticus (SE). Marked neuronal degeneration was observed in the hippocampus after SE in a time-dependent manner, although neuronal degeneration differed according to the hippocampal subregions. Almost no hippocalcin immunoreactivity was detected in the pyramidal neurons of the cornu ammonis 1 (CA1) region from 6 h after SE. However, many pyramidal neurons in the CA2 region showed hippocalcin immunoreactivity until 24 h after SE. In the CA3 region, only a few hippocalcin immunoreactive cells were observed at 12 h after SE, and almost no hippocalcin immunoreactivity was observed in the pyramidal neurons from 24 h after SE. Hippocalcin immunoreactivity in the polymorphic cells of the dentate gyrus was markedly decreased from 6 h after SE. In addition, hippocalcin protein level in the hippocampus began to decrease from 6 h after SE, and was significantly decreased at 24 h and 48 h after pilocarpine-induced SE. These results indicate that marked reduction of hippocalcin level may be closely related to neuronal degeneration in the hippocampus following pilocarpine-induced SE.
Animals ; Calcium ; Dentate Gyrus ; Hippocalcin* ; Hippocampus* ; Homeostasis ; Mice* ; Neurons ; Pyramidal Cells ; Status Epilepticus*

To understand the changes in expression of calcium binding proteins(CaBP) during the experimental focal ischemia, expression of two kinds of CaBP, paralvumin(PV) and calbindin D-28K(Calbindin), immunocytochemically, and activities of cytochrome oxidase(CO) and acetylcholinesterase(AchE), histochemically, in focal ischemic brain of the rat were investigated. Two groups of focal ischemic infarction were produced in Sprague Dawley rats(200-350 mg):Group I, Clip compression of left middle cerebral artery(MCA) for 5-10 mins and release;Group II, Electric coagulation of left MCA for 2-24 hrs. In the group I, CO activity and PV- and Calbindin-immunoreactivity(IR) were decreased in the left MCA territory, and decreased in number of PV- and Calbindin-IR neurons and degree of IR, but AchE activity was nearly same as that of control cortex. In the group II, decrease of CO and AchE activities, and marked increase of PV- and Calbindin IRs were noted on neuropil in the layers I through VI of ischemic region. Characteristically pyramidal cells, which did not express the both CaBPs in the control cortex, of layer V of ischemic cortex showed PV- and Calbindin Irs in the cell body and apical dendrite. These findings suggest that 1) PV- and Calbindin-IR neurons, mainly non-pyramidal cells, are more vulnerable than pyramidal cell to ischemic injury, 2) CaBP may have some roles in hypoxic neuronal injury, and 3) PV and Calbindin-immunocytochemistry can be used as useful technique in evaluation of experimental ischemia.
Animals ; Brain ; Calbindins ; Calcium ; Cytochromes ; Dendrites ; Infarction ; Ischemia* ; Neocortex* ; Neurons* ; Neuropil ; Pyramidal Cells ; Rats*

The excitotoxic effect of kainic acid on dendrites and neuronal cell bodies of hippocampus and dentate gyrus was studied with time (1, 4, 8, 16 hours, 2, 7, 14 days) light and electron microscopically by intraperitonial injection into rat. The results obtained were as follows. 1) The acute dendrotoxic effect was observed as laminar pattern of swelling along pyramidal cell body layer and dendritic fields and was most prominently at 2-4 hours after kainic acid injection. In ultractructural study, the acute change occurred in dendrites of pyramidal cells in hipocampus because the synapses between nerve terminals and swollen components were not destroyed and remained intact and, identified the swollen structures as dendrites. So, it was obvious from the results that the acute change by kainic acid was osmolysis and was continued till initial 4 hours but was finally faded out. 2) The distribution of kainic acid receptor within hippocampus was different because the prominent dendritic swelling occurred in proximal basilar dendritic field of CA 3 and 4 and the proximal and distal basilar dendritic fields of CA 1 and 2, and no change was observable in dentate granule cell. The sensitivity of hippocampal dendritic fields to kainic acid could be put in decreasing order as CA3, CA4, CA1, CA2 and dentate granule cell 3) With the elapse of time, the acute change disappeared and pyramidal cells began to degenerate by the chronic reaction about 7 days after kainic acid injury, and the pyramidal cell density in CA regions greatly decreased. Almost all pyramidal cells degenerated the dentate granule cells were not affected to kainic acid throughout the time. In conclusions, hippocampal neurons were postulated to be very sensitive to kainic acid, and in contrast to the gradual disappearance of acute change within several hours, the degeneration of pyramidal neurons by chronic change was developed within several days regardless of acute change.
Animals ; Brain* ; Dendrites ; Dentate Gyrus ; Hippocampus ; Kainic Acid* ; Neurons* ; Pyramidal Cells ; Rats* ; Receptors, Kainic Acid ; Synapses