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Synapses
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
Chemical synapses can be excitatory or inhibitory. The basic distinction between the two is that activation of an excitatory synapse enhances the likelihood of generation of an AP in the postsynaptic cell, whereas the activation of an inhibitory synapse reduces this likelihood. If the threshold for the generation of an AP in the postsynaptic cell is Vthr > Vm0, then the synapse is excitatory if: ES>Vthr>Vm0
Artificial Neural Networks (ANN)
Published in Phil Mars, J.R. Chen, Raghu Nambiar, Learning Algorithms, 1996
Phil Mars, J.R. Chen, Raghu Nambiar
A highly simplified sketch of a neuron is shown in Figure (3.1). Although it is simplified, it captures some of the most important features of neurons. The cell body of a neuron is called the soma. The spine-like extensions of the cell body are dendrites. They usually branch repeatedly and form a bushy tree around the cell body and provide connections to receive incoming signals from other neurons. The axon extends away from the cell body to provide a pathway for outgoing signals. Signals are transferred from one neuron to another through a contact point called a synapse. Although the synaptic junctions can be formed between axon and axon, between dendrite and dendrite, and between axon and cell body, the most common synaptic junction is between the axon of one neuron and the dendrite of another. There are two classes of synapses. The excitatory synapse tends to promote the activation of neurons, while the inhibitory synapse plays an opposite role. When a neuron is activated, or firing, (this could be caused by an external stimulus), an impulse signal travels down along the axon, until it reaches a synapse. At this point some kind of chemical transmitter is released to promote or inhibit the firing of the receptor neuron.
Lattice-Based Biomimetic Neural Networks
Published in Gerhard X. Ritter, Gonzalo Urcid, Introduction to Lattice Algebra, 2021
Gerhard X. Ritter, Gonzalo Urcid
The axon, which usually arises from the opposite pole of the cell at a point called the axon hillock, consists of a long fiber whose branches form the axonal arborization or axonal tree. For some neurons the axon may have branches at intervals along its length in addition to its terminal arborization. The tips of the branches of the axon are called nerve terminals or boutons or synaptic knobs. The axon is the principal fiber branch of the neuron for the transmission of signals to other neurons. Figure 8.1 shows an image and a typical schematic representation of a biological neuron with its branching processes. An impulse traveling along an axon from the axon hillock propagates through the axonal tree all the way to the nerve terminals. The terminals of the branches make contact with the soma and the many dendrites of other neurons. The sites of contact are the synaptic sites where the synapses take place. The synapse is a specialized structure whereby neurons communicate, but there is no actual structural union of the two neurons at the synaptic site. The synaptic knob is separated from the surface of the dendrite or soma by an extremely narrow space called the synaptic cleft. The exact mechanism of synaptic structures is fairly well-understood and there exist two kinds of synapses; excitatory synapses, which tend to depolarize the postsynaptic membrane and consequently excite the postsynaptic cell to fire impulses, and inhibitory synapses that try to prevent the neuron from firing impulses in response to excitatory synapses. In brief, it is at the synaptic cleft where the presynaptic neuron communicates with the postsynaptic neuron. This communication takes place via neurotransmitters. Neurotransmitters are small molecules that are released by the axon terminal of the presynaptic neuron after an action potential reaches the synapse. There exist various different types of neurotransmitters that have been identified [198, 301]. These transmitter molecules can bind with the dendritic receptors and create an excitatory electrical potential that is then transmitted down the cell membrane or it may block (inhibit) the signal from being carried to the soma.
Neurophysiological and molecular approaches to understanding the mechanisms of learning and memory
Published in Journal of the Royal Society of New Zealand, 2021
Shruthi Sateesh, Wickliffe C. Abraham
Induction of LTP at excitatory synapses typically necessitates repetitive synaptic activation to release the neurotransmitter glutamate, along with simultaneous depolarisation of the postsynaptic cell (Malinow and Miller 1986; Gustafsson et al. 1987). The combination of depolarisation and binding of glutamate to synaptic NMDA receptors leads to removal of their magnesium ion block and thus the opening of these ion channels that are permeable to calcium (Ca2+) ions. This makes the NMDA receptor/channel a ‘coincidence detector’ which explains the LTP properties of cooperativity, input specificity and associativity (Bliss and Collingridge 1993). The resulting rise in Ca2+, amplified in some cases by simultaneous activation of mGluRs and voltage-dependent calcium channels, is crucially important to the induction of both LTP and LTD (Lisman 1989). The direction of synaptic change is precisely controlled by the extent of the rise in Ca2+ and the associated activation of vital protein kinases and phosphatases (Figure 3). Generally, LTP is associated with protein kinase activation to enhance synaptic transmission processes, whereas LTD is more associated with protein phosphatase activation (Lisman 1989).
Inhibition of oxidative stress by testosterone improves synaptic plasticity in senescence accelerated mice
Published in Journal of Toxicology and Environmental Health, Part A, 2019
Lu Wang, Juan-Hui Pei, Jian-Xin Jia, Jing Wang, Wei Song, Xin Fang, Zhi-Ping Cai, Dong-Sheng Huo, He Wang, Zhan-Jun Yang
Glutamate is the predominant excitatory neurotransmitter involved in numerous CNS functions especially in cortical and hippocampal regions (Perez-Otano and Ehlers 2005). Approximately 70% of all excitatory synapses in the CNS of mammalian brains utilize glutamate as a neurotransmitter. Glutamate receptors, in particular, N-methyl D-aspartate receptors (NMDARs) are excitatory glutamate ionotropic receptors involved in various physiological and pathological processes (Lau and Zukin 2007; Perez-Otano and Ehlers 2005) and play important roles in CNS excitability synaptic transmission, synaptic plasticity and cognitive processes. It is of interest that in AD there is reduction in number of glutamatergic neurotransmitters and synaptic plasticity, which subsequently led to abnormal activation of NMDARs (De Felice et al. 2007; Lacor et al. 2007), attributed to result in Ca2+-dependent signaling pathway disorder (Parameshwaran, Dhanasekaran, and Suppiramaniam 2008). Previously Jia et al. (2015) noted that T significantly increased protein expression levels of synaptic NMDAR, promoting Ca2+ entry into hippocampal cells and phosphorylation of mouse cAMP response element-binding protein. Similarly, treatment of castrated SAMP8 mice with T was found in our study to enhance the protein expression levels of NMDAR. It is worthwhile noted that T significantly elevated the protein expression levels of p-CaMK II suggesting that Ca2+ flux may be associated with the effectiveness of this male hormone in ameliorating AD symptoms. Indeed, Berridge and Irvine (1989) reported that elevated levels of intracellular Ca2+ enhanced the activity of CaMK which increased neuronal synaptic plasticity. Evidence thus indicates that T inhibits neurotoxicity by promoting neuronal survival and synaptic plasticity.