Morphological alterations of hippocampal pyramidal neurons heterotopically transplanted into the somatosensory cortex of adult rats: a quantitative Golgi study

1995 ◽  
Vol 192 (4) ◽  
pp. 351-361 ◽  
Author(s):  
Martina Plaschke ◽  
Manivanh Souphanthong ◽  
J�rgen Wenzel
Keyword(s):  
Somatosensory Cortex ◽  
Pyramidal Neurons ◽  
Golgi Study ◽  
Adult Rats ◽  
Hippocampal Pyramidal Neurons ◽  
Morphological Alterations

scholarly journals Age- and location-dependent differences in store depletion-induced h-channel plasticity in hippocampal pyramidal neurons

2014 ◽  
Vol 111 (6) ◽  
pp. 1369-1382 ◽  
Author(s):  
Ann M. Clemens ◽  
Daniel Johnston
Keyword(s):  
Pyramidal Neurons ◽  
Cyclopiazonic Acid ◽  
Neural Basis ◽  
Adult Rats ◽  
Hippocampal Pyramidal Neurons ◽  
Store Depletion ◽  
Whole Cell Patch Clamp ◽  
Age Dependent ◽  
Adaptive Processes ◽  
Cellular Dysfunction

Disruptions of endoplasmic reticulum (ER) Ca2+ homeostasis are heavily linked to neuronal pathology. Depletion of ER Ca2+ stores can result in cellular dysfunction and potentially cell death, although adaptive processes exist to aid in survival. We examined the age and region dependence of one postulated, adaptive response to ER store-depletion (SD), hyperpolarization-activated cation-nonspecific ( h)-channel plasticity in neurons of the dorsal and ventral hippocampus (DHC and VHC, respectively) from adolescent and adult rats. With the use of whole-cell patch-clamp recordings from the soma and dendrites of CA1 pyramidal neurons, we observed a change in h-sensitive measurements in response to SD, induced by treatment with cyclopiazonic acid, a sarcoplasmic reticulum/ER Ca2+-ATPase blocker. We found that whereas DHC and VHC neurons in adolescent animals respond to SD with a perisomatic expression of SD h plasticity, adult animals express SD h plasticity with a dendritic and somatodendritic locus of plasticity in DHC and VHC neurons, respectively. Furthermore, SD h plasticity in adults was dependent on membrane potential and on the activation of L-type voltage-gated Ca2+ channels. These results suggest that cellular responses to the impairment of ER function, or ER stress, are dependent on brain region and age and that the differential expression of SD h plasticity could provide a neural basis for region- and age-dependent disease vulnerabilities.

scholarly journals Ultrastructural Signs of Regenerative-Degenerative Processes in Long-Term Dentate Fascia Grafts

1994 ◽  
Vol 5 (3) ◽  
pp. 183-197 ◽  
Author(s):  
Z. N. Zhuravleva
Keyword(s):  
Pyramidal Neurons ◽  
Degenerative Change ◽  
Pyramidal Cells ◽  
Afferent Input ◽  
Dynamic State ◽  
Adult Rats ◽  
Hippocampal Pyramidal Neurons ◽  
Dentate Fascia ◽  
Neuronal Processes ◽  
Continuous Dynamic

An ultrastructural investigation of embryonic (E20) dentate fascia grafts transplanted into an acute cavity in the somatosensory neocortex of adult rats revealed a continuous dynamic state of the tissue nine months postgrafting. The grafts consisted mainly of typical granular cells with some admixture of hippocampal pyramidal neurons and polymorph hilar cells with a normal, mature ultrastructure. Many features of the transplanted tissue suggested continuing development and growth. Dendritic branches with growth tips, axonal growth cones, synaptic boutons with growth vesicles, immature myelin sheaths and myelin-producing cells were observed. In contrast, ultrastructural signs of degeneration were present in some axons, and, less often, in dendrites. These processes, as well as some of the terminal synapses, contained various amounts of lysosomes and lipofuscine granules. In many such terminals the signs of degenerative change were combined with the presence of multiple mitochondria, polymorph vesicles and tubular reticulum, indicating simultaneous reparative processes. It is suggested that continuous recycling of neuronal processes occurs in longterm dentate grafts. This morphological instability nay depend on the paucity of synaptic targets within the dentate tissue transplanted with a minimal quantity of hippocampal pyramidal cells and on the limitation of the afferent input. However, the observed features of the grafted dentate tissue are not qualitatively different from those observed in normal dentate with its protracted development and active compensatory reorganization.

A Golgi study of the superficial pyramidal cells in the somatosensory cortex of socially reared old adult rats

1982 ◽  
Vol 76 (1) ◽  
pp. 35-45 ◽  
Author(s):  
James R. Connor ◽  
Suzanne E. Beban ◽  
Patrick A. Hopper ◽  
Bente Hansen ◽  
Marian C. Diamond
Keyword(s):  
Somatosensory Cortex ◽  
Pyramidal Cells ◽  
Golgi Study ◽  
Adult Rats ◽  
Old Adult

scholarly journals DNA Fragmentation and HSP70 Protein Induction in Hippocampus and Cortex Occurs in Separate Neurons following Permanent Middle Cerebral Artery Occlusions

1996 ◽  
Vol 16 (6) ◽  
pp. 1165-1175 ◽  
Author(s):  
Bradley A. States ◽  
Jari Honkaniemi ◽  
Philip R. Weinstein ◽  
Frank R. Sharp
Keyword(s):  
Middle Cerebral Artery ◽  
Dna Fragmentation ◽  
Cerebral Artery ◽  
Cortical Neurons ◽  
Hippocampal Neurons ◽  
Pyramidal Neurons ◽  
Adult Rats ◽  
Hippocampal Pyramidal Neurons ◽  
Ca1 Neurons ◽  
Hsp70 Protein

DNA nick end-labeling (TUNEL) and heat shock protein (HSP)70 immunocytochemistry were performed on the same brain sections 1 (n = 6), 3 (n = 12), and 7 (n = 7) days following permanent middle cerebral artery (MCA) occlusions produced in adult rats using the endovascular carotid suture method. In the cortex at 1 and 3 days following MCA occlusions, HSP70 immunoreactive neurons were located outside areas of infarction and showed little evidence of DNA fragmentation. HSP70-stained cortical neurons were intermingled with TUNEL cells near the infarct, but extended for greater distances away from the infarct. DNA fragmentation occurred in CA1 hippocampal neurons in 39% of the animals at 1 and 3 days following ipsilateral MCA occlusion. Bilateral DNA fragmentation occurred in CA1 neurons in one subject. HSP70 protein was expressed in CA1 hippocampal neurons in nine of 18 (50%) animals at 1 and 3 days following MCA occlusions, including all animals that exhibited hippocampal DNA fragmentation. Three animals had bilateral expression of HSP70 in CA1 neurons. Cells that stained for either HSP70 protein or DNA fragmentation existed in close proximity to one another. Approximately 5–7% of HSP70-stained cells were TUNEL stained and 3% of TUNEL-positive cells also stained for HSP70. There was no HSP70 staining or DNA fragmentation in the brains of sham-operated controls (n = 4) or in the brains of animals 7 days following MCA occlusions. These data suggest that ischemic cells capable of translating HSP70 protein generally do not undergo DNA fragmentation. These data support the concept that most HSP70 protein-containing neurons in the cortical “penumbra” and hippocampus survive ischemic injury and are “reversibly injured.” It is shown that CA1 hippocampal pyramidal neurons die or are reversibly injured in ˜50% of animals following permanent MCA occlusions. Although the mechanism of this hippocampal injury is unknown, it could relate to transynaptic activation of N-methyl-d-aspartate (NMDA) receptors that mediate induction of early genes in hippocampus.

scholarly journals Prenatal treatment with rapamycin restores enhanced hippocampal mGluR-LTD and mushroom spine size in a Down’s syndrome mouse model

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Jesús David Urbano-Gámez ◽  
Juan José Casañas ◽  
Itziar Benito ◽  
María Luz Montesinos
Keyword(s):  
Intellectual Disability ◽  
Pyramidal Neurons ◽  
Metabotropic Glutamate Receptor ◽  
Therapeutic Potential ◽  
Mammalian Target Of Rapamycin ◽  
Memory Deficits ◽  
Prenatal Treatment ◽  
Hippocampal Pyramidal Neurons ◽  
Metabotropic Glutamate ◽  
Mushroom Spines

AbstractDown syndrome (DS) is the most frequent genetic cause of intellectual disability including hippocampal-dependent memory deficits. We have previously reported hippocampal mTOR (mammalian target of rapamycin) hyperactivation, and related plasticity as well as memory deficits in Ts1Cje mice, a DS experimental model. Here we characterize the proteome of hippocampal synaptoneurosomes (SNs) from these mice, and found a predicted alteration of synaptic plasticity pathways, including long term depression (LTD). Accordingly, mGluR-LTD (metabotropic Glutamate Receptor-LTD) is enhanced in the hippocampus of Ts1Cje mice and this is correlated with an increased proportion of a particular category of mushroom spines in hippocampal pyramidal neurons. Remarkably, prenatal treatment of these mice with rapamycin has a positive pharmacological effect on both phenotypes, supporting the therapeutic potential of rapamycin/rapalogs for DS intellectual disability.

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