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Using the in vitro Hippocampal Slice as a Model to Teach Methods in Neurophysiology
Published in Avital Schurr, Benjamin M. Rigor, BRAIN SLICES in BASIC and CLINICAL RESEARCH, 2020
In this laboratory, the Schaffer collateral input to the CA1 pyramidal cell layer was used as the substrate for studying the principles of electrical stimulation of neuronal tissue. During the laboratory exercise, the students investigated the stimulus artifact and how it is influenced by electrode position and the mode of stimulation (i.e., bipolar vs. monopolar). They also experimented with cathodal vs. anodal stimulation, anode block, and antidromic vs. orthodromic stimulation. In addition, they investigated the strength-duration relationship and generated a strength-duration curve. The slice preparation consistently worked well for all the manipulations described above, except for anode block.
Brain Metabolism During Aging
Published in Alvaro Macieira-Coelho, Molecular Basis of Aging, 2017
Under normal conditions, glucose carbon is rapidly transferred into amino acids via the tricarboxylic acid cycle (TCAC) and the gamma-aminobutyric acid (GABA) shunt.57,58 Glutamate, glutamine, aspartate, and GABA are formed most abundantly.59–61 At least two compartments of these acidic amino acids are assumed in the brain, one of which is a storage compartment. These glucoplastic amino acids may serve in part as a fuel reserve under emergency conditions when glucose is lacking. Additionally, glutamate and aspartate function as excitatory neurotransmitters active in nearly the whole brain but particularly in the entorhinal afferents and the Schaffer collaterals, both ending in the CA1 subfield of the hippocampus and also in its mossy fibers.62 Cholinergic neurons receive glutamatergic afferents.63–65 Upon K+-evoked depolarization, aspartate, glutamate, and GABA were preferentially released from neocortical tissue, the efflux of glutamate being calcium dependent.66 After its release from nerve endings, glutamate binds with high affinity to postsynaptic dendritic membranes.67 Furthermore, glutamate induced release of GABA from cerebral cortex interneurons68 and enhanced GABA-activated conductances in hippocampal pyramidal neurons at concentrations below that required for excitation.69
Neurophysiology of Old Neurons and Synapses
Published in David R. Riddle, Brain Aging, 2007
A number of researchers have suggested that changes in synaptic function provide a principal physiological correlate of brain aging and memory decline [88–91]. Within the aging hippocampus, a decrease in transmission can be observed for Schaffer collateral synapses connecting region CA3 to region CA1 [92–96] and for perforant path synapses from the entorhinal cortex to granule cells of the dentate gyrus [86, 97–99].
The impact of different dark chocolate dietary patterns on synaptic potency and plasticity in the hippocampal CA1 area of the rats under chronic isolation stress
Published in Nutritional Neuroscience, 2023
Elham Kalantarzadeh, Maryam Radahmadi, Parham Reisi
Recordings from the hippocampal CA1 area were prepared as has been described previously [18,19]. In brief, two small holes were drilled at the positions of stimulating and recording electrodes. A Teflon-coated stainless steel bipolar stimulation electrode (Advent, UK; diameter: 0.125 mm) was implanted in the right hippocampal Schaffer collateral pathway (AP = −4.2 mm, ML = 3.8 mm, DV = −2.7 to −3.8 mm); also, a Teflon-coated stainless steel unipolar recording electrode was moved from the upper left towards the right CA1 area (AP = −3.4 mm; ML = 1.5 mm, DV = −4.4 to −5.1 mm; at an angle of 52.5°) until the maximal response was recorded. The extracellular field potentials were recorded from the CA1 pyramidal cells while the right Schaffer collateral pathway was under electrical stimulation. To mitigate brain tissue trauma, these electrodes were inserted (2 mm/min). Correct implantation of these electrodes in their proper position was confirmed by physiological and stereotaxic indicators. The electrophysiological experiments were performed a day after the exposure to the last stress session (Day 15).
Combination of tea polyphenols and proanthocyanidins prevents menopause-related memory decline in rats via increased hippocampal synaptic plasticity by inhibiting p38 MAPK and TNF-α pathway
Published in Nutritional Neuroscience, 2022
Qian Yang, Yusen Zhang, Luping Zhang, Xuemin Li, Ruirui Dong, Chenmeng Song, Le Cheng, Mengqian Shi, Haifeng Zhao
Memory function declines with age, and is believed to deteriorate because of changes in synaptic function rather than loss of neurons [16]. It is thought that memories are formed and stored by long-term changes in the strength of synaptic connections between neurons, a process known as synaptic plasticity that can be defined as structural and functional adaptations of neuronal circuits to changes due to learning and memory. Structural plasticity refers to changes in synaptic morphology and quantity caused by repetitive synaptic activity. Long-term potentiation (LTP) is one of the important manifestations of the functional plasticity [17,18]. LTP is a long lasting enhancement of synaptic transmission induced by high frequency stimulation of presynaptic afferents into fibers, mainly for the high frequency stimulation of postsynaptic population spike (PS) the increase of the amplitude and shortened the latency of group, excitatory postsynaptic potential (fEPSP) the amplitude and slope increase the phenomenon of enhanced synaptic transmission efficiency [19]. LTP of Schaffer collateral to CA1 pyramidal neuron synapse of the hippocampus is thought to play a key role in episodic memory formation [17]. Strong antioxidant vitamin E and 17-beta estradiol (E2) treatment in different rat models prevents the LTP impairment and neuronal apoptosis as well as increases synapse density and enhances the magnitude of LTP [20,21]. In this study, we want to know if the TP and PC combination can improve memory by improving synaptic plasticity and try to explore the mechanism.
Comparison of ELF-EMFs stimulation with current stimulation on the regulation of LTP of SC-CA1 synapses in young rat hippocampus
Published in International Journal of Radiation Biology, 2021
Yu Zheng, Wenjun Zhao, Xiaoxu Ma, Lei Dong, Lei Tian, Mei Zhou
The number of brain slices selected was 10 due to the difference in the shape and placement of the Schaffer’s collaterals during the conductivity measurement. The location of the Schaffer collaterals ran through the hippocampus CA1 and CA3. Then, the Schaffer collaterals of each brain slice were approximately evenly divided into four segments in order to obtain a more accurate Schaffer collateral conductivity value of the whole pathway, and a current stimulation point and two adjacent voltage recording points were selected in each segment. Thus, each brain slice had four stimulation points, corresponding to eight voltage recording points. Three current stimulations from small to large were applied to each current stimulation point. The current values were selected according to the 20%, 40%, and 60% of the induced maximum fEPSP. The specific process is shown in Figure 2①–⑩. The orange points in Figure 2 represent the four stimulation points in each brain slice. The detailed measurement data are shown in Table S1. The calculated results of the conductivity at 80 points were homogenized at the end of the measurement of ten brain slices. The average conductivity was 0.310711583 S/m, which was close to the conductivity of 0.33 S/m of the brain gray matter previously published (Coba et al. 2012). The gray matter is a major component of the central nervous system formed by the aggregation of a large number of neuron cell bodies and dendrites, while the Schaffer collaterals are composed of a bunch of axons. However, the cell structure properties of the two are similar. Therefore, the Schaffer collateral conductivity value measured was 0.3107711583 S/m, which was similar to the conductivity of the gray matter, thus, it might be considered as a certain reference value for the Schaffer collateral.