Extracellular diffusion is fast and isotropic in the stratum radiatum of hippocampal CA1 region in rat brain slices

Hippocampus ◽  
2005 ◽  
Vol 15 (4) ◽  
pp. 441-450 ◽  
Author(s):  
Sabina Hrabětová
Keyword(s):  
Rat Brain ◽  
Brain Slices ◽  
Stratum Radiatum ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Hippocampal Ca1

Changes in the Calcium Dependence of Glutamate Transmission in the Hippocampal CA1 Region After Brief Hypoxia-Hypoglycemia

1999 ◽  
Vol 82 (3) ◽  
pp. 1147-1155 ◽  
Author(s):  
A. Ouanonou ◽  
Y. Zhang ◽  
L. Zhang
Keyword(s):  
Calcium Influx ◽  
Brain Slices ◽  
Ca1 Neurons ◽  
Synaptic Potentials ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Hippocampal Ca1 ◽  
Glutamate Transmission ◽  
Intracellular Ca ◽  
Dependent Processes

Using the model of hypoxia-hypoglycemia (HH) in rat brain slices, we asked whether glutamate transmission is altered following a brief HH episode. The HH challenge was conducted by exposing slices to a glucose-free medium aerated with 95% N2-5% CO2, for ∼4 min, and glutamate transmission in the hippocampal CA1 region was monitored at different post HH times. In slices examined ≤8 h post HH, CA1 synaptic field potentials are comparable in amplitude to controls, but are less sensitive to experimental manipulations designed to attenuate intracellular Ca2+ signals, as compared with controls. Reducing calcium influx, by applying a nonspecific calcium channel blocker Co2+ or lowering external Ca2+, attenuated CA1 synaptic potentials much less in challenged slices than in controls. Buffering intracellular Ca2+ by bis-( o-aminophenoxy)- N,N,N′,N′-tetraacetic acid-AM (BAPTA-AM) attenuated CA1 synaptic potentials in control but not in slices post HH. Furthermore, minimally evoked excitatory postsynaptic currents displayed a lower failure rate in post-hypoxic CA1 neurons compared with controls. Based on these convergent observations, we suggest that evoked CA1 glutamate transmission is altered in the first several hours after brief hypoxia, likely resulting from alterations in intracellular Ca2+homeostasis and/or Ca2+-dependent processes governing transmitter release.

Hyperexcitability of hippocampal CA1 region in brain slices after GABA withdrawal

1992 ◽  
Vol 147 (2) ◽  
pp. 229-232 ◽  
Author(s):  
G. García-Ugalde ◽  
E. Galarraga ◽  
J. Bargas ◽  
S. Brailowsky
Keyword(s):  
Brain Slices ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Hippocampal Ca1

scholarly journals Calretinin expression in hippocampus of mouse offspring from dams treated with β-hydroxy-β-methylbutyrate

2016 ◽  
Vol 72 (7) ◽  
pp. 423-429 ◽  
Author(s):  
Aleksandra Krawczyk ◽  
Karol Rycerz ◽  
Jadwiga Jaworska-Adamu ◽  
Ewa Tomaszewska ◽  
Piotr Dobrowolski
Keyword(s):  
Dentate Gyrus ◽  
Cognitive Processes ◽  
Specific Antibody ◽  
Light Microscope ◽  
Brain Slices ◽  
Male Mice ◽  
Expression Intensity ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Hippocampal Ca1

The aim of the study was the immunohistochemical evaluation of calretinin (CR) expression in the hippocam-pus of neonatal (P0) and 21-day-old (P21) male mice from dams that received 0.2 g/kg b.w./day of β-hydroxy-β-methylbutyrate between the 26th and 39th day of pregnancy. The immunohistochemical peroxidase-antiperoxidase reaction was conducted on brain slices of offspring from control (C) and experimental (HMB) groups, using the specific antibody against CR. CR-immunopositive neurons of the hippocampal CA1 region and the dentate gyrus with the hilus were qualitatively and quantitatively assessed by means of an Olympus BX51 light microscope and the ImageJ 1.48v program. To demonstrate statistically significant differences, the Kruskal-Wallis test was used. The results of our studies revealed a decrease in CR expression intensity and the number of neurons only in the hilus of the dentate gyrus in both groups of mice (P0 and P21). The results indi-cate that HMB administration to pregnant dams may lead to damage or even loss of CR-immunopositive neu-rons in their offspring. This phenomenon may be related to calcium excess. Cells with CR expression inhibit the activity of other interneurons, causing a reverse of inhibition in principal neurons. The loss of cells with CR ex-pression may interfere with the control and synchronisation of neuron excitability. In consequence, this may affect cognitive processes, memory and animal behaviour.

scholarly journals High levels of 27-hydroxycholesterol results in synaptic plasticity alterations in the hippocampus

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Raul Loera-Valencia ◽  
Erika Vazquez-Juarez ◽  
Alberto Muñoz ◽  
Gorka Gerenu ◽  
Marta Gómez-Galán ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Memory Function ◽  
Long Term Potentiation ◽  
Synaptic Function ◽  
Cholesterol Homeostasis ◽  
Stratum Radiatum ◽  
Actin Binding ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Term Potentiation

AbstractAlterations in brain cholesterol homeostasis in midlife are correlated with a higher risk of developing Alzheimer’s disease (AD). However, global cholesterol-lowering therapies have yielded mixed results when it comes to slowing down or preventing cognitive decline in AD. We used the transgenic mouse model Cyp27Tg, with systemically high levels of 27-hydroxycholesterol (27-OH) to examine long-term potentiation (LTP) in the hippocampal CA1 region, combined with dendritic spine reconstruction of CA1 pyramidal neurons to detect morphological and functional synaptic alterations induced by 27-OH high levels. Our results show that elevated 27-OH levels lead to enhanced LTP in the Schaffer collateral-CA1 synapses. This increase is correlated with abnormally large dendritic spines in the stratum radiatum. Using immunohistochemistry for synaptopodin (actin-binding protein involved in the recruitment of the spine apparatus), we found a significantly higher density of synaptopodin-positive puncta in CA1 in Cyp27Tg mice. We hypothesize that high 27-OH levels alter synaptic potentiation and could lead to dysfunction of fine-tuned processing of information in hippocampal circuits resulting in cognitive impairment. We suggest that these alterations could be detrimental for synaptic function and cognition later in life, representing a potential mechanism by which hypercholesterolemia could lead to alterations in memory function in neurodegenerative diseases.

Ultrastructure of stratum lacunosum moleculare interneurons of hippocampal CA1 region

Synapse ◽  
1988 ◽  
Vol 2 (4) ◽  
pp. 382-394 ◽  
Author(s):  
Dennis D. Kunkel ◽  
Jean-Claude Lacaille ◽  
Philip A. Schwartzkroin
Keyword(s):  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Hippocampal Ca1 ◽  
Stratum Lacunosum Moleculare

Chronic Effects of Pyridoxine in the Gerbil Hippocampal CA1 Region after Transient Forebrain Ischemia

2012 ◽  
Vol 37 (5) ◽  
pp. 1011-1018 ◽  
Author(s):  
Dae Young Yoo ◽  
Woosuk Kim ◽  
Sung Min Nam ◽  
Jin Young Chung ◽  
Jung Hoon Choi ◽  
...  
Keyword(s):  
Forebrain Ischemia ◽  
Transient Forebrain Ischemia ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Chronic Effects ◽  
Hippocampal Ca1
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