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Modulation of Long-Term Synaptic Depression in Visual Cortex by Acetylcholine and Norepinephrine

It is proposed that paired-pulse stimulation is a mechanism by which cholinergic and noradrenergic inputs to the neocortex modulate naturally occurring receptive field plasticity.
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Developmental Inhibitory Gate Controls the Relay of Activity to the Superficial Layers of the Visual Cortex

Results from paired-pulse stimulation are consistent with the idea that the maturation of intracortical inhibition reduces the capability of the cortex to relay incoming high-frequency patterns of activity to the supragranular layers.
SFN (opens in a new tab)

Spatiotemporal profile of synaptic activation produced by the electrical and visual stimulation of retinal inputs to the optic tectum: a current source density analysis in the pigeon (Columba livia)

It is concluded that electrical stimulation activates most of the populations of ganglion cells as well as their primary tectal synapses, but is unable to elicit a significant activation of secondary tectAL synapses.
Wiley (opens in a new tab)

MDMA ("ecstasy") impairs learning in the Morris Water Maze and reduces hippocampal LTP in young rats.

It is concluded that low, nontoxic doses of MDMA, applied during several days, slow learning by impairing postsynaptic plasticity.
PubMed (opens in a new tab)

Zinc enhances long‐term potentiation through P2X receptor modulation in the hippocampal CA1 region

Zn2+ at low concentrations enhances LTP by modulating P2X receptors and leads to an increase in the affinity of P2x receptors for ATP, which confirms the previous results from heterologous expression systems.
Wiley (opens in a new tab)

Methylphenidate amplifies long-term potentiation in rat hippocampus CA1 area involving the insertion of AMPA receptors by activation of β-adrenergic and D1/D5 receptors.

It is proposed that MPH increases TBS-dependent LTP in CA3-CA1 synapses through a polysynaptic mechanism involving activation of β-adrenergic and D1/D5 dopaminergic receptors and promoting the trafficking and insertion of functional AMPA receptors to the plasma membrane.
PubMed (opens in a new tab)

MAP1B‐dependent Rac activation is required for AMPA receptor endocytosis during long‐term depression

Results indicate that the MAP1B‐Tiam1‐Rac1 relay is essential for spine structural plasticity and removal of AMPA receptors from synapses during LTD, highlighting the importance of MAPs as signalling hubs controlling the actin cytoskeleton and receptor trafficking during plasticity in mature neurons.
Wiley (opens in a new tab)

Oxidative Damage in Lymphocytes of Copper Smelter Workers Correlated to Higher Levels of Excreted Arsenic

It is demonstrated that in human beings exposed to high arsenic concentrations, lymphocyte MDA and arsenic urinary levels showed a positive correlation with SOD activity, and a negative correlation with vitamin E serum levels, which suggest that chronic human exposure to arsenic induces oxidative damage in lymphocytes.
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Mutation in protein disulfide isomerase A3 causes neurodevelopmental defects by disturbing endoplasmic reticulum proteostasis

Proteomic and functional analyses reveal that PDIA3C57Y expression leads to dysregulation of cell adhesion and actin cytoskeleton dynamics, associated with altered integrin biogenesis and reduced neuritogenesis, and can provide insight into how perturbations of neuronal proteostasis can affect the function of the nervous system.
Springer Nature (opens in a new tab)

Atomoxetine Reestablishes Long Term Potentiation in a Mouse Model of Attention Deficit/Hyperactivity Disorder.

Results indicate that administration of ATX in a PNE model of ADHD reestablishes TBS-dependent LTP in CA3-CA1 synapses and suggest postsynaptic changes in synaptic plasticity as part of the mechanisms that underlie improvement of ADHD symptoms induced by ATX.
PubMed (opens in a new tab)
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