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Abstract
In 1959, E. G. Gray described two different types of synapses in the brain for the first time: symmetric and asymmetric. Later on, symmetric synapses were associated with inhibitory terminals, and asymmetric synapses to excitatory signaling. The balance between these two systems is critical to maintain a correct brain function. Likewise, the modulation of both types of synapses is also important to maintain a healthy equilibrium. Cerebral circuitry responds differently depending on the type of damage and the timeline of the injury. For example, promoting symmetric signaling following ischemic damage is beneficial only during the acute phase; afterwards, it further increases the initial damage. Synapses can be also altered by players not directly related to them; the chronic and long-term neurodegeneration mediated by tau proteins primarily targets asymmetric synapses by decreasing neuronal plasticity and functionality. Dopamine represents the main modulating system within the central nervous system. Indeed, the death of midbrain dopaminergic neurons impairs locomotion, underlying the devastating Parkinson’s disease. Herein, we will review studies on symmetric and asymmetric synapses plasticity after three different stressors: symmetric signaling under acute damage—ischemic stroke; asymmetric signaling under chronic and long-term neurodegeneration—Alzheimer’s disease; symmetric and asymmetric synapses without modulation—Parkinson’s disease.
Highlights
IntroductionTo postsynaptic density (PSD)-95, gephyrin plays an important role in the structure of the inhibitory PSD by clustering gamma-aminobutyric acid (GABA) receptors and acting as a scaffold protein [12,13]
NKCC1 in cortical and striatal neurons at 6 and 24 h after ischemic stroke in mice [65]. These findings suggest that blocking the activation of the WNK cascade offers a new therapeutic target to improve the outcome following stroke by targeting NKCC1 activation [62,69,70,71,72]
Likewise, increasing KCC2 levels displays a beneficial role at least during the acute phase, which raises the interesting question of what would happen if KCC2 was manipulated during the post-acute/chronic phase, since higher levels of KCC2 would induce gamma-aminobutyric acid (GABA)-mediated hyperpolarization leading to a tonic currents-like effect
Summary
To PSD-95, gephyrin plays an important role in the structure of the inhibitory PSD by clustering GABA receptors and acting as a scaffold protein [12,13] Both asymmetric and symmetric PSDs are not fixed but constantly changing, reflecting the high plasticity presents in this network. Through the activation of metabotropic receptors (D1-D5), DA can modify the excitability of neurons by regulating the voltage- or ligand-gated channels [15], as well as regulating the function and trafficking of GABA receptors, NMDARs, and AMPARs [22] In this way, DA is able to affect different synaptic dynamics [23]. DA is able to affect different synaptic dynamics [23] Both asymmetric and symmetric synapses have important roles in shaping the structural and functional outcomes of the brain.
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