A transient increase in the activity of CA3 neurons induces a long-lasting reduction in the excitability of schaffer collateral terminals in rat hippocampus

1985 ◽  
Vol 54 (1-3) ◽  
pp. 51-56 ◽  
Author(s):  
B SASTRY ◽  
P MURALIMOHAN ◽  
J GOH
Keyword(s):  
Transient Increase ◽  
Rat Hippocampus ◽  
Schaffer Collateral ◽  
Ca3 Neurons

Autoradiographic Localization of Opioid and Spirodecanone Receptors in the Gerbil Hippocampus as Compared with the Rat Hippocampus

1988 ◽  
Vol 8 (4) ◽  
pp. 568-574 ◽  
Author(s):  
Hiroshi Onodera ◽  
Kyuya Kogure
Keyword(s):  
Opioid Receptor ◽  
Binding Sites ◽  
Cellular Localization ◽  
Neuronal Damage ◽  
Pyramidal Cells ◽  
Rat Hippocampus ◽  
High Concentration ◽  
Receptor Sites ◽  
Ca3 Neurons

Opioid ([3H]naloxone) and spirodecanone ([3H]spiperone) binding sites in the hippocampus were visualized in the Mongolian gerbil and in the rat using in vitro autoradiography. In the hippocampus, marked differences were noted in the stratum (sr.) pyramidale of the CA1 subfield where opioid and spirodecanone (assayed in the presence of mianserin and sulpiride) binding activities were very low in gerbils, but high in rats. Gerbils exhibited a high concentration of [3H]naloxone binding sites in the sr. pyramidale of the CA3 subfield, as observed in the rat. In addition, the gerbil has a very high opioid receptor density in the hilar region and in the sr. moleculare of the dentate gyrus. The cellular localization of opioid and spirodecanone receptor sites was studied in the rat hippocampus using selective neuronal damage to CA1 and CA3 neurons by means of ischemia and kainic acid treatment, respectively. The results suggest that the gerbil differs from the rat with respect to the characteristic pyramidal cells (spirodecanone binding site) and interneurons (opioid receptor) in the CA1 subfield of the hippocampus. Distinct localization of opioid and spirodecanone receptors in the gerbil provides a good model with which to investigate the electrophysiological and biochemical roles of opioid peptides and butyrophenone spirodecanone drugs.

Post-ischemic potentiation of Schaffer collateral/CA1 pyramidal cell responses of the rat hippocampus in vivo: involvement of receptors

1993 ◽  
Vol 611 (1) ◽  
pp. 155-159 ◽  
Author(s):  
Shuhei Miyazaki ◽  
Yoichi Katayama ◽  
Makoto Furuichi ◽  
Kosaku Kinoshita ◽  
Tatsuro Kawamata ◽  
...  
Keyword(s):  
Pyramidal Cell ◽  
Rat Hippocampus ◽  
Schaffer Collateral ◽  
Cell Responses

scholarly journals Persistent decrease in synaptic efficacy induced by nicotine at Schaffer collateral-CA1 synapses in the immature rat hippocampus

2004 ◽  
Vol 559 (3) ◽  
pp. 863-874 ◽  
Author(s):  
Laura Maggi ◽  
Elisabetta Sola ◽  
Federico Minneci ◽  
Corentin Le Magueresse ◽  
Jean Pierre Changeux ◽  
...  
Keyword(s):  
Rat Hippocampus ◽  
Synaptic Efficacy ◽  
Schaffer Collateral ◽  
Immature Rat

scholarly journals Delayed Neuronal Recovery and Neuronal Death in Rat Hippocampus following Severe Cerebral Ischemia: Possible Relationship to Abnormalities in Neuronal Processes

1984 ◽  
Vol 4 (2) ◽  
pp. 194-205 ◽  
Author(s):  
C. K. Petito ◽  
W. A. Pulsinelli
Keyword(s):  
Endoplasmic Reticulum ◽  
Cerebral Ischemia ◽  
Hippocampal Neurons ◽  
Smooth Endoplasmic Reticulum ◽  
Light And Electron Microscopy ◽  
Rat Hippocampus ◽  
Cell Recovery ◽  
Ca1 Neurons ◽  
Neuronal Processes ◽  
Ca3 Neurons

Mechanisms involved in the postischemic delay in neuronal recovery or death in rat hippocampus were evaluated by light and electron microscopy at 3, 15, 30, and 120 min and 24, 36, 48, and 72 h following severe cerebral ischemia that was produced by permanent occlusion of the vertebral arteries and 30-min occlusion of the common carotid arteries. During the early postischemic period, neurons in the Ca1 and Ca3 regions both showed transient mitochondrial swelling followed by the disaggregation of polyribosomes, decrease in rough endoplasmic reticulum (RER), loss of Golgi apparatus (GA) cisterns, and decrease in GA vesicles. Recovery of these organelles in Ca3 neurons was first noted between 24 and 36 h and was accompanied by a marked proliferation of smooth endoplasmic reticulum (SER). Many Ca1 neurons initially recovered between 24 and 36 h, but subsequent cell death at 48–72 h was often preceded by peripheral chromatolysis, constriction and shrinkage of the proximal dendrites, and cytoplasmic dilatation that was continuous with focal expansion of RER cisterns. Because SER accumulates in resistant Ca3 neurons and proximal neuronal processes are damaged in vulnerable Ca1 neurons, we hypothesize that delayed cell recovery or death in vulnerable and resistant postischemic hippocampal neurons is related to abnormalities in neuronal processes.

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