Biological Basis of Behavior
Mohamed Ahmed Abd El-Hay in 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.
Synapses
Nassir H. Sabah in Neuromuscular Fundamentals, 2020
This is because the activation of the GS–ES branch depolarizes the membrane and moves vm toward ES, closer to Vthr, as illustrated by the vertical arrow and the dashed line in Figure 6.4a, where it is assumed that Vm0 = –60 mV, Vthr = –50 mV, and ES = ES1 = –45 mV. Inequality 6.4 implies that iS < 0 in Equation 6.1. This means that cations will move inward, or anions outward, thereby depolarizing the membrane. The synapse is excitatory since depolarization brings the membrane voltage closer to threshold (Figure 6.4a), which enhances the likelihood of generating an AP by other psps. The psp is termed in this case the excitatory post-synaptic potential (epsp).
Imaging of Intracellular Calcium in Hippocampal Slices: Methods, Limitations, and Achievements
Avital Schurr, Benjamin M. Rigor in BRAIN SLICES in BASIC and CLINICAL RESEARCH, 2020
One way to isolate the role of NMDA channels is to inactivate the voltage-gated channels by depolarizing the cell and demonstrate an influx through the remaining NMDA channels.17 This, of course, does not preclude that in the normal case there is no activation of the voltage-gated channel. In fact, a recent study suggests that most, if not all, of the calcium influx during synaptic activation of cortical neurons comes from NMDA-independent channels.15 While the two channel types can coexist, it is still not clear what the contribution of either of them is in the normal synaptic potential as well as in conditions that promote synaptic plasticity. It is clear that voltage-gated calcium channels provide a major contribution to the integration of calcium signals on dendrites,27 but what is less clear is which channel species is most relevant to this function. While recording of whole-cell currents can provide a tentative estimate of the channel types residing on the cell in study, only recording of channel activity in specific patches of membrane on dendrites can provide a decisive answer as to the nature of the dendritic calcium channels. Alternately, measurements of [Ca2+]i in dendrites, provided they are restricted and do not spread to adjacent regions of dendrites and soma, can provide this information. Preliminary information on these issues is beginning to emerge.
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].
Targeting glucose-dependent insulinotropic polypeptide receptor for neurodegenerative disorders
Published in Expert Opinion on Therapeutic Targets, 2018
Mahip K. Verma, Rajan Goel, Nandakumar Krishnadas, Kumar V. S. Nemmani
Incretin hormones, GLP-1 and GIP, display neuroprotective properties, improving synaptic plasticity, reducing the toxic effects of amyloid beta (Aβ), and also reversing the damage in vitro [89]. Stable and brain penetrating incretin analogs, like liraglutide and Val(8)GLP-1 (GLP-1 analogs), D-Ala2GIP (GIP analog), prevented the Aβ-induced impairments in memory in mouse models of AD [33,40]. Treatment with the incretin analogs was associated with both per se increase in synaptic plasticity and reversal of deficits induced by Aβ. Specifically, the hippocampus-dependent synaptic plasticity was demonstrated to be enhanced in a dose-dependent manner in normal mice [33]. Treatment with D-Ala2GIP (2.5–250 nmol/kg, i.p.) was not associated with effects on locomotion and any aversive symptoms, whereas significant improvement in the episodic memory-based tasks (novel object recognition task, 25 nmol/kg, i.p.) and on spatial memory (morris water maze, 25 nmol/kg, i.p.) was observed [33]. These effects were further correlated with the enhancement of the excitatory post-synaptic potential (EPSP), as a marker of LTP, in the CA1 regions of mice chronically treated with D-Ala2GIP and (Pro3)GIP [33]. Apart from the wild-type mice, subchronic (21 days) administration of GIP analog, D-Ala2GIP, prevented the deterioration of the synaptic function in 12 month old APP/PS1 mice, bearing Swedish mutation of amyloid precursor protein (APP) and L166P mutation in the presenilin 1 (PSEN1) [28]. APP/PS1 mice at the age of 12 months displayed impaired recognition memory and spatial reference memory in the object recognition task and morris water maze, which were rescued with D-Ala2GIP treatment [28]. Further, D-Ala2GIP reduced synaptic deterioration, increased synaptogenesis, increased post-synaptic LTP induction, reduced cortical Aβ plaques, enhanced neuronal progenitor cells proliferation, and reduced microglia neuroinflammation in APP/PS1 mice [28]. Therefore, stable GIP analogs, like D-Ala2GIP, acting as agonist of GIPR, have demonstrated to ameliorate the sequelae of AD in the mouse models by correcting the metabolic abnormalities and also restoring the neuropathology associated with the disorder.
Related Knowledge Centers
- Action Potential
- Excitatory Postsynaptic Potential
- Inhibitory Postsynaptic Potential
- Synaptic Plasticity
- Summation
- Long-Term Potentiation
- Long-Term Depression
- Graded Potential