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Integrative Synchronization Mechanisms and Models in the Cognitive Neurosciences
Published in Harald Maurer, Cognitive Science, 2021
In summary, according to Singer et al.322 neuronal information processing is characterized by two complementary coding mechanisms (or coding strategies) that solve the binding problem. On the one hand, elementary object features are analyzed using the classical coding strategy, according to which the average frequency of the action potentials of the active neurons increases. This increased neuronal activity makes it more likely that the information in question will be selected for subsequent joint processing by more effective summation of the synaptic potentials in the downstream neuronal structures. This leads to the formation of neurons with increasingly specific feature preferences (e.g. neurons in V1) via the class of ascending, excitatory pathways (e.g. the retinofugal projection), on the basis of repeated recombination and the selective convergence of input signals. On the other hand, there is a second and far more important class of connections, the cortico-cortical connections of the neocortex. By reciprocal coupling of the feature-sensitive neurons (and using the dynamic grouping mechanism of population coding), these connections are responsible for the flexible association of these spatially distributed neurons to functionally coherent and synchronously active assemblies. Very different complex constellations or configurations of percept components, e.g. in visual scenes, can then be analyzed and represented in succession within the same network.
The Use of Brain Slices in the Study of Free Radical Actions
Published in Avital Schurr, Benjamin M. Rigor, BRAIN SLICES in BASIC and CLINICAL RESEARCH, 2020
Synaptic potentials can be reduced by changes in postsynaptic receptor sensitivity or by decreased release of neurotransmitter. Using intracellular electrophysiological techniques in hippocampal pyramidal cells of field CA1, the effects of free radicals on postsynaptic sensitivity to neurotransmitter were evaluated.41 Both inhibitory and excitatory postsynaptic potentials are decreased by peroxide. The inhibitory neurotransmitter, GABA (γ-amino butyric acid), elicits a hyperpolarizing response (reversal potential around −70 mV) when applied to the cell bodies. At the dendrites, the response to GABA is depolarizing, with a reversal potential near −40 mV. Application of glutamate, the amino acid considered to be the excitatory neurotransmitter, produces a strong depolarizing response in pyramidal cells. Peroxide, at concentrations that strongly reduce synaptic potentials, did not alter the responses to these iontophoretically applied neurotransmitters41 (Figure 3). These results suggest that the postsynaptic receptors for GABA and for glutamate (primarily the kainate/AMPA subtype) are not sensitive to free radicals. Receptor changes cannot account for the decreased synaptic potentials seen with free radical generating systems; rather, a change in the release of neurotransmitter is indicated.
Biological Basis of Behavior
Published in Mohamed Ahmed Abd El-Hay, Understanding Psychology for Medicine and Nursing, 2019
Operation of the nervous system is achieved through electrochemical processes. Within each neuron, when a signal is received by the dendrites, it is transmitted to the soma in the form of an electrical signal, and, if the signal is strong enough, it may then be passed on to the axon and then to the terminal buttons. If the signal reaches the terminal buttons, it triggers the release of chemical substances called “neurotransmitters” into the synapse. The binding of the neurotransmitter to the receptor molecules on the membrane of the postsynaptic cell gives rise, in turn, to a new class of signals called synaptic potentials. Thus, whereas the action potential is a purely electrical signal, the synaptic potential is an electrical signal initiated by a chemical one. The neurotransmitters fit into receptors on the receiving dendrites in a lock and key manner. More than 100 chemical substances produced in the body have been identified as neurotransmitters, and these substances have a wide and profound effect on emotion, cognition, behavior, appetite, memory, as well as muscle action and movement. Neurotransmitters range from small molecules such as acetylcholine, noradrenaline, and serotonin to much larger molecules such as peptides.
Syntaphilin mediates axonal growth and synaptic changes through regulation of mitochondrial transport: a potential pharmacological target for neurodegenerative diseases
Published in Journal of Drug Targeting, 2023
Qing-Yun Wu, Hui-Lin Liu, Hai-Yan Wang, Kai-Bin Hu, Ping Liao, Sen Li, Zai-Yun Long, Xiu-Min Lu, Yong-Tang Wang
Physiological activities such as the generation of nerve impulses, the formation of synapses, and the transmission of nerve signalling are all heavily energy-consuming processes. Mitochondria, the organelles found in eukaryotic cells, are responsible for converting stored energy from organic matter into adenosine triphosphate (ATP). They play a critical role in cellular energy metabolism and produce 90% of the ATP required for cellular metabolism [1]. The brain relies heavily on mitochondria to produce most of the ATP needed for its functions and energy metabolism [2], and synapses are the main site of energy expenditure [3]. As the primary energy source for neurons, mitochondria are crucial for maintaining synaptic activities, including synaptic assembly, action potential and synaptic potential production, and synaptic vesicle (SV) transport and recycling [4]. Axonal mitochondrial deficiency affects synaptic transmission, and defective mitochondrial transport and energy deficiency are associated with the failure of axonal regeneration after injury and the pathogenesis of multiple neurological diseases [5–7]. Mitochondrial motility is also affected by stress or damage to its integrity. Consequently, ensuring mitochondrial health and motor function is essential for axonal growth, maintenance of synaptic energy balance, and synaptic function.
Repetitive transcranial magnetic stimulation (rTMS) fails to improve cognition in patients with parkinson’s disease: a Meta-analysis of randomized controlled trials
Published in International Journal of Neuroscience, 2022
Pei Kun He, Li Min Wang, Jia Ning Chen, Yu Hu Zhang, Yu Yuan Gao, Qi Huan Xu, Yi Hui Qiu, Hui Min Cai, You Li, Zhi Heng Huang, Shu Jun Feng, Jie Hao Zhao, Gui Xian Ma, Kun Nie, Li Juan Wang
Repetitive transcranial magnetic stimulation (rTMS), a neuromodulation technique, has emerged as a therapeutic for numerous brain diseases. This procedure is non-invasive and painless, and it does not require pharmacological substances. rTMS induces a current in brain tissues by generating a magnetic field, which further results in an excitatory or inhibitory effect [5]. The cognitive symptoms in PD are related to aberrant neural activity in the cortex and higher cognitive regions [6], which indicates that rTMS may be an effective treatment for cognitive function. Applying high-frequency rTMS on the task-related cortex has been shown to transiently enhance response inhibition [7], mental rotation [8], and confrontation naming [9]. Luber and Lisanby suggest that rTMS can enhance post-synaptic potential, drive oscillatory activity, and change synaptic plasticity to form long term potential (LTP) [5]. It was recently demonstrated that rTMS can improve cognitive behavior in a mouse model of PD [10], and two clinical trials suggest that rTMS elicits a cognitive-enhancing effect in PD patients [11,12]. However, several studies did not see this effect following rTMS treatment [13–15].
The effect of serotonin on penicillin-induced epileptiform activity
Published in International Journal of Neuroscience, 2019
Mehmet Taskiran, Abdulkadir Tasdemir, Nusret Ayyildiz, Mustafa Ayyildiz, Erdal Agar
In the mammalian central nervous system, there are seven families of 5-HT receptors which are structurally and pharmacologically distinct [16]. The 5-HT2 receptor is a member of the serotonin receptor family. It is known that 5-HT2 receptors potentiate GABAergic inhibition and activation of these receptors increases the frequency and amplitude of spontaneous inhibitory post-synaptic potentials (sIPSCs) recorded from the cerebral cortex [17]. 5-HT2C receptor mutant mice have lower thresholds and higher excitability [18]. 5-HT2 agonists suppressed seizure activity in both PTZ, an antagonist of GABAA receptor, and electrically-induced epilepsy [19]. It is also suggested that selective 5-HT2A antagonists increased the duration of convulsions when injected in GAERs rats [20]. Orban et al. demonstrated that the 5-HT2C agonists mCPP and lorcaserin, but not RO60-0175 (an agonist of 5-HT2B and 5-HT2C), have anti-epileptic activity in limbic seizures in rats [21]. According to the literature, serotonin agonists and antagonists may have different effects in various experimental epilepsy models.