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Electron shell

In atoms with a single electron (hydrogen-like atoms), the energy of an orbital (and, consequently, of any electrons in the orbital) is determined exclusively by. The orbital has the lowest possible energy in the atom. Each successively higher value of has a higher level of energy, but the difference decreases as   increases. For high , the level of energy becomes so high that the electron can easily escape from the atom. In single electron atoms, all levels with different   within a given  are (to a good approximation) degenerate, and have the same energy. This approximation is broken to a slight extent by the effect of the magnetic field of the nucleus, and by quantum electrodynamics effects. The latter induce tiny binding energy differences especially for s  electrons that go nearer the nucleus, since these feel a very slightly different nuclear charge, even in one-electron atoms; see  Lamb shift.

In atoms with multiple electrons, the energy of an electron depends not only on the intrinsic properties of its orbital but also on its interactions with the other electrons. These interactions depend on the detail of its spatial probability distribution, and so the energy levels of orbitals depend not only on but also on. Higher values of are associated with higher values of energy; for instance, the 2p state is higher than the 2s state. When the increase in energy of the orbital becomes so large as to push the energy of orbital above the energy of the s-orbital in the next higher shell; when the energy is pushed into the shell two steps higher. The filling of the 3d orbitals does not occur until the 4s orbitals have been filled.

The increase in energy for subshells of increasing angular momentum in larger atoms is due to electron-electron interaction effects, and it is specifically related to the ability of low angular momentum electrons to penetrate more effectively toward the nucleus, where they are subject to less screening from the charge of intervening electrons. Thus, in atoms of the higher atomic number of electrons become more and more of a determining factor in their energy, and the principal quantum numbers of electrons become less and less important in their energy placement.

The energy sequence of the first 24  subshells (e.g., 1s, 2p, 3d, etc.) is given in the following table. Each cell represents a subshell with and given by its row and column indices, respectively. The number in the cell is the subshell's position in the sequence. For a linear listing of the subshells in terms of increasing energies in multielectron atoms, see the section below.

 

References

Calcium, iron and neuronal function.

Hidalgo C1,  Núñez MT.

Author information

Abstract

Calcium and iron play dual roles in neuronal function: they are both essential but when present in excess they cause neuronal damage and may even induce neuronal death. Calcium signals are required for synaptic plasticity, a neuronal process that entails gene expression and which is presumably the cellular counterpart of cognitive brain functions such as learning and memory. Neuronal activity generates cytoplasmic and nuclear calcium signals that in turn stimulate pathways that promote the transcription of genes known to participate in synaptic plasticity. In addition, evidence discussed in this article shows that iron deficiency causes learning and memory impairments that persist following iron repletion, indicating that iron is necessary for normal development of cognitive functions. Recent results from our group indicate that iron is required for long-term potentiation in hippocampal CA1 neurons and that iron stimulates ryanodine receptor-mediated calcium release through ROS produced via the Fenton reaction leading to stimulation of the ERK signaling pathway. These combined results support a coordinated action between iron and calcium in synaptic plasticity and raise the possibility that elevated iron levels may contribute to neuronal degeneration through excessive intracellular calcium increase caused by iron-induced oxidative stress.





Antioxid Redox Signal.  2007 Feb;9(2):245-55.

A role for reactive oxygen/nitrogen species and iron on neuronal synaptic plasticity.

Hidalgo C1,  Carrasco MAMuñoz PNúñez MT.

Author information

Abstract

A great body of experimental evidence collected over many years indicates that calcium has a central role in a variety of neuronal functions. In particular, calcium participates in synaptic plasticity, a neuronal process presumably correlated with cognitive brain functions such as learning and memory. In contrast, only recently, evidence has begun to emerge supporting a physiological role of reactive oxygen (ROS) and nitrogen (RNS) species in synaptic plasticity. This subject will be the central topic of this review. The authors also present recent results showing that, in hippocampal neurons, ROS/RNS, including ROS generated by iron through the Fenton reaction, stimulate ryanodine receptor-mediated calcium release, and how the resulting calcium signals activate the signaling cascades that lead to the transcription of genes known to participate in synaptic plasticity. They discuss the possible participation of ryanodine receptors jointly stimulated by calcium and ROS/RNS in the normal signaling cascades needed for synaptic plasticity, and how too much ROS production may contribute to neurodegeneration via excessive calcium release. In addition, the dual role of iron as a necessary, but potentially toxic, element for normal neuronal function is discussed.



Ageing Res Rev.  2004 Nov;3(4):431-43.

Reactive oxygen species and synaptic plasticity in the aging hippocampus.

Serrano F1,  Klann E.

Author information

Abstract

Aging is associated with a general decline in physiological functions including cognitive functions. Given that the hippocampus is known to be critical for certain forms of learning and memory, it is not surprising that a number of neuronal processes in this brain area appear to be particularly vulnerable to the aging process. Long-term potentiation (LTP), a form of synaptic plasticity that has been proposed as a biological substrate for learning and memory, has been used to examine age-related changes in hippocampal synaptic plasticity. A current hypothesis states that oxidative stress contributes to age-related impairment in learning and memory. This is supported by a correlation between age, memory impairment, and the accumulation of oxidative damage to cellular macromolecules. However, it also has been demonstrated that ROS are necessary components of signal transduction cascades during normal physiological processes. This review discusses the evidence supporting the dual role of reactive oxygen species (ROS) as cellular messenger molecules in normal LTP, as well their role as damaging toxic molecules in the age-related impairment of LTP. In addition, we will discuss parallel analyses of LTP and behavioral tests in mice that overexpress antioxidant enzymes and how the role of antioxidant enzymes and ROS in modulating these processes may vary over the lifespan of an animal.



IUBMB Life.  2005 Apr-May;57(4-5):315-22.

The ryanodine receptors Ca2+ release channels: cellular redox sensors?

Hidalgo C1,  Donoso PCarrasco MA.

Author information

Abstract

The release of Ca2+ from intracellular stores mediated by ryanodine receptors (RyR) Ca2+ release channels is essential for striated muscle contraction and contributes to diverse neuronal functions including synaptic plasticity. Through Ca2+-induced Ca2+-release, RyR can amplify and propagate Ca2+ signals initially generated by Ca2+ entry into cardiac muscle cells or neurons. In contrast, RyR activation in skeletal muscle is under membrane potential control and does not require Ca2+ entry. Non-physiological or endogenous redox molecules can change RyR function via modification of a few RyR cysteine residues. This critical review will address the functional effects of RyR redox modification on Ca2+ release in skeletal muscle and cardiac muscle as well as in the activation of signaling cascades and transcriptional regulators required for synaptic plasticity in neurons. Specifically, the effects of endogenous redox-active agents, which induce S-nitrosylation or S-glutathionylation of particular channel cysteine residues, on the properties of muscle RyRs will be discussed. The effects of endogenous redox RyR modifications on cardiac preconditioning will be analyzed as well. In the hippocampus, sequential activation of ERKs and CREB is a requisite for Ca2+-dependent gene expression associated with long lasting synaptic plasticity. Results showing that reactive oxygen/nitrogen species modify RyR channels from neurons and the RyR-mediated sequential activation of neuronal ERKs and CREB produced by hydrogen peroxide and other stimuli will be also discussed.



IUBMB Life.  2007 Apr-May;59(4-5):280-5.

Calcium, iron and neuronal function.

Hidalgo C1,  Núñez MT.

Author information

Abstract

Calcium and iron play dual roles in neuronal function: they are both essential but when present in excess they cause neuronal damage and may even induce neuronal death. Calcium signals are required for synaptic plasticity, a neuronal process that entails gene expression and which is presumably the cellular counterpart of cognitive brain functions such as learning and memory. Neuronal activity generates cytoplasmic and nuclear calcium signals that in turn stimulate pathways that promote the transcription of genes known to participate in synaptic plasticity. In addition, evidence discussed in this article shows that iron deficiency causes learning and memory impairments that persist following iron repletion, indicating that iron is necessary for normal development of cognitive functions. Recent results from our group indicate that iron is required for long-term potentiation in hippocampal CA1 neurons and that iron stimulates ryanodine receptor-mediated calcium release through ROS produced via the Fenton reaction leading to stimulation of the ERK signaling pathway. These combined results support a coordinated action between iron and calcium in synaptic plasticity and raise the possibility that elevated iron levels may contribute to neuronal degeneration through excessive intracellular calcium increase caused by iron-induced oxidative stress.



Antioxid Redox Signal.  2007 Feb;9(2):245-55.

A role for reactive oxygen/nitrogen species and iron on neuronal synaptic plasticity.

Hidalgo C1,  Carrasco MAMuñoz PNúñez MT.

Author information

Abstract

A great body of experimental evidence collected over many years indicates that calcium has a central role in a variety of neuronal functions. In particular, calcium participates in synaptic plasticity, a neuronal process presumably correlated with cognitive brain functions such as learning and memory. In contrast, only recently, evidence has begun to emerge supporting a physiological role of reactive oxygen (ROS) and nitrogen (RNS) species in synaptic plasticity. This subject will be the central topic of this review. The authors also present recent results showing that, in hippocampal neurons, ROS/RNS, including ROS generated by iron through the Fenton reaction, stimulate ryanodine receptor-mediated calcium release, and how the resulting calcium signals activate the signaling cascades that lead to the transcription of genes known to participate in synaptic plasticity. They discuss the possible participation of ryanodine receptors jointly stimulated by calcium and ROS/RNS in the normal signaling cascades needed for synaptic plasticity, and how too much ROS production may contribute to neurodegeneration via excessive calcium release. In addition, the dual role of iron as a necessary, but potentially toxic, element for normal neuronal function is discussed.



Toxicol Lett.  2015 Apr 16. pii: S0378-4274(15)00137-X. doi: 10.1016/j.toxlet.2015.04.008. [Epub ahead of print]

Endogenous  hydrogen peroxide  in the hypothalamic paraventricular nucleus regulates neurohormonal excitation in high salt-induced hypertension.

Zhang M1,  Qin DN2,  Suo YP3,  Su Q1,  Li HB1,  Miao YW1,  Guo J1,  Feng ZP1,  Qi J1,  Gao HL1,  Mu JJ4,  Zhu GQ5,  Kang YM6.

Author information

Abstract

Reactive oxygen species (ROS) in the  brain  plays an important role in the progression of hypertension and  hydrogen peroxide  (H2O2) is a major component of ROS. The aim of this study is to explore whether endogenous H2O2  changed by polyethylene glycol-catalase (PEG-CAT) and aminotriazole (ATZ) in the hypothalamic paraventricular nucleus (PVN) regulates neurotransmitters, renin-angiotensin system (RAS), and cytokines, and whether subsequently affects the renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) in high salt-induced hypertension. Male Sprague-Dawley rats received a high-salt diet (HS, 8% NaCl) or a normal-salt diet (NS, 0.3% NaCl) for 10 weeks. Then rats were treated with bilateral PVN microinjection of PEG-CAT (0.2 i.u./50nl), an analog of endogenous catalase, the catalase inhibitor ATZ (10nmol/50nl) or vehicle. High salt-fed rats had significantly increased MAP, RSNA, plasma norepinephrine (NE) and pro-inflammatory cytokines (PICs). In addition, rats with high-salt diet had higher levels of NOX-2, NOX-4 (subunits of NAD(P)H oxidase), angiotensin-converting enzyme (ACE), interleukin-1beta (IL-1β), glutamate and NE, and lower levels of gamma-aminobutyric acid (GABA) and interleukin-10 (IL-10) in the PVN than normal diet rats. Bilateral PVN microinjection of PEG-CAT attenuated the levels of RAS and restored the balance of neurotransmitters and cytokines, while microinjection of ATZ into the PVN augmented those changes occurring in hypertensive rats. Our findings demonstrate that ROS component H2O2  in the PVN regulating MAP and RSNA are partly due to modulate neurotransmitters, renin-angiotensin system, and cytokines within the PVN in salt-induced hypertension.



Exp Physiol.  2011 Dec;96(12):1282-92. doi: 10.1113/expphysiol.2011.059733. Epub 2011 Sep 2.

Endogenous  hydrogen peroxide  in paraventricular nucleus mediates sympathetic activation and enhanced cardiac sympathetic afferent reflex in renovascular hypertensive rats.

Xu Y1,  Gao QGan XBChen LZhang LZhu GQGao XY.

Author information

Abstract

An enhancement of the cardiac sympathetic afferent reflex (CSAR) contributes to sympathetic activation in renovascular hypertension. Angiotensin II in the paraventricular nucleus (PVN) augments the CSAR and increases sympathetic outflow and blood pressure. The present study aimed to determine whether endogenous  hydrogen peroxide  in the PVN mediated the enhanced CSAR, sympathetic activity and the effects of angiotensin II in the PVN in renovascular hypertension induced by the two-kidney, one-clip method (2K1C) in rats. At the end of the fourth week, the rats underwent sino-aortic and vagal denervation under general anaesthesia with urethane and α-chloralose. Renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) were recorded. The CSAR was evaluated by the RSNA response to epicardial application of bradykinin. Microinjection of polyethylene glycol-catalase (PEG-CAT), an analogue of endogenous catalase, into the PVN decreased the RSNA and MAP and abolished the CSAR in both sham-operated and 2K1C rats. Microinjection into the PVN of the catalase inhibitor, aminotriazole, increased the RSNA and MAP and enhanced the CSAR. The effects of PEG-CAT or aminotriazole were greater in 2K1C rats than in sham-operated animals. The effects of angiotensin II in the PVN were abolished by pretreatment with PEG-CAT in both sham-operated and 2K1C rats; however, aminotriazole failed to potentiate the effects of angiotensin II. The catalase activity was decreased but the H(2)O(2) levels were increased in the PVN of 2K1C rats. These results indicate that endogenous H(2)O(2) in the PVN not only mediates the enhanced sympathetic activity and CSAR, but also the effects of angiotensin II in the PVN in renovascular hypertensive rats.