Neurotoxic and Neuroprotective Actions of Catecholamines in Cortical Neurons

The Activation of Dopamine D4 Receptors Inhibits Oxidative Stress-Induced Nerve Cell Death

“…Because there have been suggestions in the literature that catecholamines can protect nerve cells from oxidative stress (Noh et al, 1999;Grünblatt et al, 1999), it was asked whether this phenomenon could be reproduced in a well characterized form of programmed cell death that is initiated by oxidative stress. HT22 cells, which lack ionotropic glutamate receptors, were exposed to increasing concentrations of several catecholamines followed by 2.5 mM glutamate.…”

“…In addition, dopamine may have a neuroprotective role. Catecholamines, such as dopamine, norepinephrine, and epinephrine, are thought to protect nerve cells at low doses by virtue of their antioxidant activities, but are neurotoxic at high doses, acting as pro-oxidants (Noh et al, 1999). It has also been reported that dopamine receptor agonists have neuroprotective effects that are caused by nonreceptor-mediated mechanisms.…”

Controversial Issues Concerning Norepinephrine and Intensive Care Following Severe Traumatic Brain Injury

“…Agerelated reduction in cortical noradrenergic neurotransmission affects spatial learning and memory performance [119]. Norepinephrine exerts anti-and prooxidative functions on various isolated neurons [120][121][122]. As all transmitters, norepinephrine not only influences neuronal and glial function but is also subject to site-dependent regulatory influences by other transmitters: norepinephrine stimulates glial release of ATP which regulates postsynaptic efficacy of glutamatergic neurons [123]; activation of presynaptic cholinergic receptors facilitates noradrenergic transmission [124] [125]; noradrenergic stimulation of basal ganglia and cortical glutamatergic neurons can be inhibitory (a 2 ) [126,127] or excitatory (b 1 ) [126]; activation of a 1 receptors inhibits dopamine release in midbrain neurons [128] but induces dopamine release in the medial prefrontal cortex [129]; hippo-campal and cortical norepinephrine release are under glutamatergic and dopaminergic influence [129,130]; a 2 -adrenergic presynaptic activation diminishes norepinephrine release and reduces the inhibitory action of GABAergic inputs in brainstem neurons, thereby disinhibiting histaminergic neurons [131]; glial glutamate uptake is mediated by a 1 -adrenergic stimulation and inhibited by b-adrenergic activation [132].…”

Effects of diclofenac sodium on the hippocampus of rats with acute subdural hematoma: histological, stereological, and molecular approach

“…Although there were mostly positive opinions, negative results were reported for high catecholamine levels. In a previous study, it was suggested that high adrenaline levels might have induced the apoptotic pathways in neonatal rats exposed to hypoxia [31]. Also, some researchers stated that high noradrenaline levels have potential for deleterious effects and the ability to induce apoptosis in PC12 cells, neuronal cells, and cardiac myocytes [6,51].…”