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The Emerging Role of Exosome Nanoparticles in Regenerative Medicine
Published in Harishkumar Madhyastha, Durgesh Nandini Chauhan, Nanopharmaceuticals in Regenerative Medicine, 2022
Zahra Sadat Hashemi, Mahlegha Ghavami, Saeed Khalili, Seyed Morteza Naghib
One of the popular super resolution fluorescence microscopy techniques is known as the stimulated emission depletion (STED) microscopy. It is developed to avoid the diffraction limit of light microscopy and create images by selectively deactivating fluorophores using stimulated emission. The distribution of fluorescently labelled antigens present at the surface of EVs and the size of EVs could be measured by STED (Tønnesen et al. 2011). Some studies have reported STED resolution limit as 50 nm (even 10 nm) (Hein et al. 2008). The STED microscopy images managed to show the size of synaptic vesicles. The synaptic vesicle contains neurotransmitters and is approximately 40 nm in diameter (Willig et al. 2006).
Toxic Responses of the Nervous System
Published in Stephen K. Hall, Joana Chakraborty, Randall J. Ruch, Chemical Exposure and Toxic Responses, 2020
Impulses are conducted from one neuron to another across a junction referred to as the synapse. At the synapse, the axonal terminals of presynaptic neurons terminate in bulb-like structures referred to as synaptic end bulbs. These end bulbs commonly synapse with the dendrites or cell bodies of one or several postsynaptic neurons. Whether an impulse is conducted across a synapse depends on the presence of chemical messengers which are collectively referred to as neurotransmitters. The neurotransmitters are synthesized by the neuron, transported to the synaptic end bulbs, and stored in small membrane bound sacs called synaptic vesicles. Upon stimulation of the end bulbs, neurotransmitter molecules are released into the synaptic cleft where they subsequently interact with receptors located on the postsynaptic plasma membrane. This interaction may result in initiation or inhibition of impulse conduction in the opposing neuron. The specific outcome depends on the chemical nature of the neurotransmitter and its interaction with the receptors of the postsynaptic neuron. In either case, impulse conduction occurs in only one direction, from the presynaptic neuron to the opposing postsynaptic neuron.
Subneuronal Processing of Information by Solitary Waves and Stochastic Processes
Published in Sergey Edward Lyshevski, Nano and Molecular Electronics Handbook, 2018
Danko D. Georgiev, James F. Glazebrook
The vesicle fusion sites are so specialized for creating a protein fusion pore (aligned by a circular array of 5 to 8 syntaxin molecules), thus allowing the lipid bilayers of synaptic vesicles and AZ plasma membrane to unite. In this way, the main purpose of the plasma membrane at the AZ during neurotransmitter release is to mediate fusion of synaptic vesicles as they interact with the depolarization-triggered presynaptic Ca2+ microdomains. Multidomain scaffold proteins constitute the large protein complexes at the pre-and postsynaptic sites, while pre-assembled dense-core transport vesicles deliver the necessary protein constituents of the CAZ. Although christened with musical names, Piccolo and Bassoon are two types of scaffold proteins underlying the PTV (Piccolo–Bassoon transport vesicle), which transport components of the CAZ. Their vesicular features imply an amount of 3 to 5 PTV’s adequate for forming the functional presynapse [72].
Learning, memory deficits, and impaired neuronal maturation attributed to acrylamide
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Seulah Lee, Hee Ra Park, Joo Yeon Lee, Jung-Hyun Cho, Hye Min Song, Ah Hyun Kim, Wonjong Lee, Yujeong Lee, Seung-Cheol Chang, Hyung Sik Kim, Jaewon Lee
GAP-43 is localized at presynaptic terminals and expressed in neurons during axonal development and during regeneration of neural connections. Synaptophysin, a synaptic vesicle protein is an integral membrane phosphoprotein that plays a key role during calcium-dependent synaptic transmission (Fernandes et al. 2017). Furthermore, the expression levels of GAP-43 and synaptophysin are critical for establishing neural circuitry and for regulating neurotransmitter release and synaptic plasticity (Chambers et al. 2005; Jahn et al. 1985; Snipes et al. 1987; Webster et al. 2001). β-III-Tubulin is the main structural protein present in microtubules and found in cells of the nervous system (Korzhevskii, Karpenko, and Kirik 2011). Therefore, it is postulated that 500 μM ACR impaired neuronal networking and synaptic plasticity of primary cortical neuron without producing neuronal lethality.
Carob extract attenuates brain and lung injury in rats exposed to waterpipe smoke
Published in Egyptian Journal of Basic and Applied Sciences, 2018
Mona Abdel-Rahman, Amira A. Bauomy, Fatma Elzahraa H. Salem, Mona Ahmed Khalifa
Wyss et al. [27] reported that amiodarone pass into the brain and it has an anticonvulsant and hypnotic effects. Moreover, amiodarone prolonged the sleeping time and behaved as central nervous system depressant drug in pentobarbital-induced sleeping in rat model [28]. Many reports attributed the anticonvulsant activity of amiodarone to its activity as a multiple ion-channel blocker drug which inhibit Na+, Ca2+ inward and K+ outward currents [28,29] . It well known that when action potentials depolarize the plasma membrane of the axon terminal, voltage-gated Ca2+ channels is open. This permits Ca2+ to diffuse down its concentration gradient into the cytoplasm, where it stimulates the release of neurotransmitters which stored in synaptic vesicles by exocytosis [30]. Because of the amiodarone is a calcium ion-channel blocker [29]; so the neurotransmitters release is inhibited and as the result their content is increased in brain which may explain the increment in neurotransmitters content in some time intervals in the present study.
Biological function simulation in neuromorphic devices: from synapse and neuron to behavior
Published in Science and Technology of Advanced Materials, 2023
Hui Chen, Huilin Li, Ting Ma, Shuangshuang Han, Qiuping Zhao
Electrical synapse is the gap junction, a special way of cell-to-cell linkage, which makes the action potential direct transmission between cells (Figure 1(c-i)). For this synapse, the synaptic cleft is very small, only several nanometers. In the presynaptic and postsynaptic membrane, there are some connexons that are made up of connexins. Two connexons form a gap junction channel, a non-gate control channel, which allows some small molecules of water-soluble substances and ions to pass through. When the action potential is generated in a neuron, the local current based on ionic current can be directly stimulated and transmitted to another neuron through the gap junction channel. By this way, the action potential is propagated from neuron to neuron. From this, the electrical synapse has lots of outstanding features, such as low resistive, rapid and bidirectional propagation. Different from electrical synapse, chemical synapse depends on the neurotransmitters to accomplish the information transfer from neuron to neuron (Figure 1(c-ii)). In chemical synapse, there are more mitochondria and a large number of vesicles, in which the latter is also called synaptic vesicle with 20–80 nm diameter and high contains concentrations of neurotransmitters such as acetylcholine or amino acid transmitters, catecholamine transmitters and neuropeptide transmitters. When the action potential is transmitted to the presynaptic terminal of a neuron, the presynaptic membrane depolarizes. After the depolarization exceeds the threshold value, Ca2+ channel is activated and Ca2+ enters into the axoplasm of the terminal from the outside of the cell. The increase of Ca2+ can trigger the efflux of synaptic vesicles and cause the quantized release of neurotransmitters. Meanwhile, excess Ca2+ in the axoplasm is transported outside through Na+-Ca2+ reverse transporter in order to its normal concentration in the presynaptic terminal. Once the neurotransmitters are released, they can enter into the synaptic cleft and reach the postsynaptic membrane by diffusion. Ultimately, these neurotransmitters can act on the ionotropic receptor and control the permeability of certain ions. When certain ions enter the postsynaptic terminal, if the terminal occurs depolarization, the signal is called excitatory postsynaptic potential (EPSP). In this process, the excitatory neurotransmitters act on the ionotropic receptors in the postsynaptic terminal to open the specific ion channels (Na+ and K+). The net inward current is generated because Na+ influx of is greater than K+ outflow, in turn, lead to the depolarization of the postsynaptic terminal. On the contrary, inhibitory neurotransmitters are released from the presynaptic terminal to act on the ionotropic receptors, and then open the Cl- channel to generate the outward current that hyperpolarizes the postsynaptic membrane. In this case, it is called inhibitory postsynaptic potential (IPSP). By this way, the information is transmitted to the next neuron by releasing neurotransmitters. The distinguishing between electrical and chemical synapses is listed in Table 1. However, the chemical synapse is the majority of synapses in the human brain.