Brain excitability

Affects mood and possibly causes neuronal or brain excitability, causing euphoria, anxiety, depression, psychosis, and an increase in motor activity in some individuals... 

Our first studies with compounds that alter Glu neurotransmission were not targeted at decreasing brain excitability. Rather, as noted above, we used the limbic hypermetabolism induced by non-competitive NMDA receptor antagonists to test whether an increase in the metabolic rate of these limbic structures... 

Hence an mGluR agonist and antagonist can both suppress REM sleep. This might seem incompatible with the opposing actions of these compounds on brain excitation that we have proposed. However, this apparent discrepancy can be explained by the one-stimulus model of NREM-REM sleep alternation described above. According to this model, REM sleep is a brain state of excitation or arousal that is intermediate between that of wakefulness and NREM... 

Epilepsy is an example of excessive neural signaling in the central nervous system. Relative cellular and extracellular space (ECS) volume has been demonstrated to play an important role in the propensity for epileptic seizures. For example, reducing ECS volume by exposure to hypotonic medium produces hyperexcitability and enhanced epileptiform activity, whereas hyperosmolar medium reduces excitability. The hypothesis that AQP4-dependent water transport in astrocytes might modulate intrinsic brain excitability was tested by seizure susceptibility in response to the GABAa antagonist convulsant pentylenetetrazol... 

Sleep lab recordings reveal that in the first three days following alcohol withdrawal, the REM sleep rebound becomes so intense as to practically displace the NREM sleep that alcohol had initially enhanced at the expense of REM. This is REM debt payback with a vengeance. As the subject becomes more and more tremulous, more and more delirious, and more and more seizure prone, REM sleep levels go to 100 percent of sleep, indicating a marked shift in brain excitability that we assume is related to a desperate attempt of the system to restore neuromodulatory equilibrium. 

Central nervous system effects adrenergic transmitter agent at synapses no brain excitation... 

Enkephalins Pain suppression pathways in spinal cord and brain Excitation... 

Schauwecker, RE. 2002. Complications associated with genetic background effects in models of experimental epilepsy. Prog Brain Res 135 139-148 Schwartzkroin, P.A., Baraban, S.C., and Hochman, D.W. 1998. Osmolarity, ionic flux, and changes in brain excitability. Epilepsy Res 32(l-2) 275-285... 

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