The role of NMDA receptors in the pathophysiology and treatment of mood disorders

A case report of anti-N-methyl-d-aspartate receptor autoimmune encephalitis with sensory attack. Is limbic encephalitis only “limbic”?

“…It is known that, although NMDARs are more concentrated in the hippocampal area, they also can be found in many other areas of the brain, including sensory and association cortex and subcortical regions. [7] The widespread distribution of the receptor in cortical regions could explain the diffuse slow waves on the EEGs and the persistent sensory symptoms seen in our patient. Oral-facial dyskinesias indicated basal ganglion involvement.…”

Alcohol use in bipolar disorder: A neurobiological model to help predict susceptibility, select treatments and attenuate cortical insult

“…There does not appear to be a specific site on the receptor where ethanol exerts this action but rather a number of various residues arising from a combination of transmembrane domains predominantly located within GluN1 and GluN2 subunits. The NMDA receptor is implicated in the pathophysiology of BD (Ghasemi et al, 2014). B: Oxidative stress is implicated in the pathophysiology of BD ) C: BD is a neuroprogressive illness and oxidative stress is believed to contribute to the gradual worsening of the disorder over time (Post, 2007;Berk et al, 2011).…”

“…The role of NMDA receptors in the pathophysiology of BD is receiving increased attention and has been described in depth previously (Ghasemi et al, 2014;Sanacora et al, 2008). There have been several investigations that have revealed abnormalities in NMDA receptor expression, binding and functioning in BD.…”

“…The first of these was the NMDA receptor. The NMDA receptor has been implicated in the pathophysiology of BD (for review see: (Ghasemi et al, 2014)), is a well-known recipient of the neural effects of alcohol, including tolerance (for review see: Krystal et al, 2003c) and it is an established treatment target for mood (Sanacora et al, 2008) and alcohol use (Krystal et al, 2003c) disorders with genetic links to both BD and alcohol dependence (Schuckit et al, 2003). The second BDalcohol neurobiological 'intersection' we selected for enquiry was neural oxidative stress.…”

Novel mechanisms for DHEA action

“…The NMDA receptor is a PM receptor composed of a large family of glutamate receptors, which are large heterotetrameric complexes that bind neurotransmitters and allosteric effectors to regulate transmembrane ion channels involved in learning and memory (Regan et al 2015). Mutation and altered activity of NMDA receptors have been associated with autism and epilepsy (Burnashev & Szepetowski 2015) and with major depressive and bipolar disorders (Ghasemi et al 2014). The GABA A receptors (GABA A Rs) are heteropentameric ligand-gated chloride and bicarbonate channels that promote hyperpolarizing postsynaptic responses, that is, the inhibitory postsynaptic potential when activated (Braat & Kooy 2015, Farrant & Nusser 2005.…”