Translational control of synaptic plasticity

2010 ◽  
Vol 38 (6) ◽  
pp. 1527-1530 ◽  
Author(s):  
Joel D. Richter
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Synaptic Plasticity ◽  
Synaptic Transmission ◽  
Learning And Memory ◽  
Translational Control ◽  
Synaptic Strength ◽  
Memory Formation ◽  
The Central Nervous System ◽  
Flow Of Information

Synapses, points of contact between axons and dendrites, are conduits for the flow of information in the circuitry of the central nervous system. The strength of synaptic transmission reflects the interconnectedness of the axons and dendrites at synapses; synaptic strength in turn is modified by the frequency with which the synapses are stimulated. This modulation of synaptic strength, or synaptic plasticity, probably forms the cellular basis for learning and memory. RNA metabolism, particularly translational control at or near the synapse, is one process that controls long-lasting synaptic plasticity and, by extension, memory formation and consolidation. In the present paper, I review some salient features of translational control of synaptic plasticity.

Tissue Plasminogen Activator in Central Nervous System Physiology and Pathology: From Synaptic Plasticity to Alzheimer's Disease

2021 ◽  
Author(s):  
Tamara K. Stevenson ◽  
Shannon J. Moore ◽  
Geoffrey G. Murphy ◽  
Daniel A. Lawrence
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Central Nervous System ◽  
Nervous System ◽  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Blood Brain Barrier ◽  
Brain Barrier Permeability ◽  
Tissue Plasminogen ◽  
The Central Nervous System

AbstractTissue plasminogen activator's (tPA) fibrinolytic function in the vasculature is well-established. This specific role for tPA in the vasculature, however, contrasts with its pleiotropic activities in the central nervous system. Numerous physiological and pathological functions have been attributed to tPA in the central nervous system, including neurite outgrowth and regeneration; synaptic and spine plasticity; neurovascular coupling; neurodegeneration; microglial activation; and blood–brain barrier permeability. In addition, multiple substrates, both plasminogen-dependent and -independent, have been proposed to be responsible for tPA's action(s) in the central nervous system. This review aims to dissect a subset of these different functions and the different molecular mechanisms attributed to tPA in the context of learning and memory. We start from the original research that identified tPA as an immediate-early gene with a putative role in synaptic plasticity to what is currently known about tPA's role in a learning and memory disorder, Alzheimer's disease. We specifically focus on studies demonstrating tPA's involvement in the clearance of amyloid-β and neurovascular coupling. In addition, given that tPA has been shown to regulate blood–brain barrier permeability, which is perturbed in Alzheimer's disease, this review also discusses tPA-mediated vascular dysfunction and possible alternative mechanisms of action for tPA in Alzheimer's disease pathology.

scholarly journals The Function of Selenium in Central Nervous System: Lessons from MsrB1 Knockout Mouse Models

Molecules ◽  
2021 ◽  
Vol 26 (5) ◽  
pp. 1372
Author(s):  
Tengrui Shi ◽  
Jianxi Song ◽  
Guanying You ◽  
Yujie Yang ◽  
Qiong Liu ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Synaptic Plasticity ◽  
Mouse Model ◽  
Mouse Models ◽  
Knockout Mouse ◽  
Methionine Sulfoxide ◽  
Methionine Sulfoxide Reductase ◽  
Knockout Mouse Model ◽  
The Central Nervous System

MsrB1 used to be named selenoprotein R, for it was first identified as a selenocysteine containing protein by searching for the selenocysteine insert sequence (SECIS) in the human genome. Later, it was found that MsrB1 is homologous to PilB in Neisseria gonorrhoeae, which is a methionine sulfoxide reductase (Msr), specifically reducing L-methionine sulfoxide (L-Met-O) in proteins. In humans and mice, four members constitute the Msr family, which are MsrA, MsrB1, MsrB2, and MsrB3. MsrA can reduce free or protein-containing L-Met-O (S), whereas MsrBs can only function on the L-Met-O (R) epimer in proteins. Though there are isomerases existent that could transfer L-Met-O (S) to L-Met-O (R) and vice-versa, the loss of Msr individually results in different phenotypes in mice models. These observations indicate that the function of one Msr cannot be totally complemented by another. Among the mammalian Msrs, MsrB1 is the only selenocysteine-containing protein, and we recently found that loss of MsrB1 perturbs the synaptic plasticity in mice, along with the astrogliosis in their brains. In this review, we summarized the effects resulting from Msr deficiency and the bioactivity of selenium in the central nervous system, especially those that we learned from the MsrB1 knockout mouse model. We hope it will be helpful in better understanding how the trace element selenium participates in the reduction of L-Met-O and becomes involved in neurobiology.

Nogo-A Represses Anatomical and Synaptic Plasticity in the Central Nervous System

Physiology ◽  
2013 ◽  
Vol 28 (3) ◽  
pp. 151-163 ◽  
Author(s):  
Anissa Kempf ◽  
Martin E. Schwab
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Synaptic Plasticity ◽  
Axonal Regeneration ◽  
Current Knowledge ◽  
Cns Injury ◽  
Inhibitory Protein ◽  
Growth Inhibitory ◽  
The Central Nervous System ◽  
Regulation Of Growth

Nogo-A was initially discovered as a myelin-associated growth inhibitory protein limiting axonal regeneration after central nervous system (CNS) injury. This review summarizes current knowledge on how myelin and neuronal Nogo-A and its receptors exert physiological functions ranging from the regulation of growth suppression to synaptic plasticity in the developing and adult intact CNS.

scholarly journals Effect of Barbiturates on Synaptic Currents

1976 ◽  
Vol 4 (3) ◽  
pp. 199-202 ◽  
Author(s):  
T. A. Torda ◽  
P. W. Gage
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neuromuscular Junction ◽  
Synaptic Transmission ◽  
Time Constant ◽  
Mode Of Action ◽  
Synaptic Currents ◽  
End Plate ◽  
The Central Nervous System ◽  
Central Synapses

Thiopentone and pentobarbitone reduce the time constant of decay of miniature end-plate currents when applied in anaesthetic concentrations to the neuromuscular junction. Such an effect at central synapses would lead to failure of synaptic transmission in the central nervous system and may reflect a common mode of action of many anaesthetic drugs.

Effect of Nicotine on the Synapse of the Central Nervous System

1958 ◽  
Vol 192 (3) ◽  
pp. 447-452 ◽  
Author(s):  
Sadayuki F. Takagi ◽  
Yutaka Oomura
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Synaptic Transmission ◽  
Reflex Activity ◽  
Synaptic Delay ◽  
Synaptic Potential ◽  
Before And After ◽  
The Central Nervous System ◽  
High Concentrations

The effect of nicotine on synaptic transmission in the frog and cat spinal cord was studied. Both a regular wick electrode and a microelectrode of the Ling-Gerard type were used. The reflex activity of the bullfrog spinal cord is facilitated by 0.01% nicotine solution, but is depressed and abolished by 0.1% solution. In the cat, intravenous administration of 150 mg/kg fails to block reflex activity, but topical application does block. The intracellular potential, of both frog and cat motoneurones, shows no change in the synaptic potential after application of the drug, but the spike appears after a shorter synaptic delay and one or more additional spikes appear. When the synaptic delay becomes sufficiently short, however, all spikes suddenly disappear, leaving the still unchanged synaptic potential. Occasionally the synaptic delay is again increased just before the spike potentials disappear. The excitability of a frog motoneurone was measured, by a recording microelectrode, before and after nicotine application. The drug first increased and then decreases excitability. Epinephrine can restore a reflex discharge depressed or abolished by nicotine. It is concluded that high concentrations of nicotine block synaptic transmission in the central nervous system, acting on the cell body but not on the synaptic potential.

Afferent and Efferent Synaptic Transmissions in Hair Cells

Physiology ◽  
1996 ◽  
Vol 11 (4) ◽  
pp. 161-166
Author(s):  
H Ohmori
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Synaptic Transmission ◽  
Nerve Terminal ◽  
Hair Cells ◽  
Electrical Signal ◽  
Membrane Hyperpolarization ◽  
K Channels ◽  
The Central Nervous System ◽  
Mechanical Information

Hair cells transduce mechanical information into electrical signal and, via afferent synapse, transmit it to the central nervous system (CNS). Hair cells receive cholinergic efferent innervation from the CNS, and a long-lasting membrane hyperpolarization is produced by activation of Ca2+-activated K+ channels. Acetylcholine may facilitate afferent synaptic transmission by suppressing K+ channels on the afferent nerve terminal.

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