Neurophysiology

Before discussing the excitotoxins, the neurophysiologic effects of excitatory amino acids will be reviewed since this provides a conceptual background for understanding the mechanism of action of these compounds. More than 70 a-amino acids have been shown to have excitatory effects in the vertebrate central nervous system (Table 1) with the recent 

Relative Excitatory Potencies of Acidic Amino Acids and Their Analogs  

Structure-Activity Relations at the Rat Cerebellar Receptor for [ H]Kainic Acid s 

Whereas L-glutamic acid exhibits a substantial affinity for the kainate site with a Ki of 700 nM, D-glutamic acid has a 60-fold lower affinity notably, l- and D-glutamic acid and dihydrokainic acid all exhibit shallow 

From the neurophysiologic and ligand-binding studies, it is apparent that there are a number of receptors that mediate the excitatory effects of acidic amino acids and their conformationally restricted or synthetic analogs. As noted by Watkins (1978), the flexibility of the linear acidic amino acids such as glutamic acid may allow them to assume a variety of conformations capable of binding to subpopulations of these receptors, some of which are selectively activated by the conformationally restricted analogs. While neuronal excitation appears to be a property common to all the acidic amino acids, specific receptors could also activate distinct sets 

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Institute of Neurophysiology, Heinrich-Heine University, Diisseldorf, Germany... 

Gawin FH Cocaine addiction psychology and neurophysiology. Science 251 1580-1586, 1991... 

Accurate diagnosis of patients with inhalant use disorders may require a variety of methods, including psychiatric history and mental status examination, physical examination and laboratory testing, neuropsychological testing, and neurophysiological testing. 

Some of the best evidence of links between effects at different organizational levels comes from studies with OPs, where levels of AChE inhibition have been compared with associated neurophysiological and behavioral effects. In adopting this approach, however, the picture is complicated by mounting evidence for these compounds acting on target sites other than AChE, as discussed in Section 16.3. Thus, behavioral disturbances caused by an OP may be the outcome of interaction with both AChE and one or more other sites of action. The following account, however, will be concerned with situations where effects of OPs are closely related to levels of AChE inhibition. More complex scenarios will be discussed in the next section. 

Misra, U.K. (1992). Neurophysiological monitors of anticholinesterase exposure. In B. Ballantyne and T.C. Marrs. (Eds.) Clinical and Experimental Toxicology of the Organophosphates and Carbamates 446-459. 

Vajda, A. Schmid, H., and Groll-Knapp, E. et al. (1974). EEC changes in evoked potentials caused by insecticides. Electroencephalography and Clinical Neurophysiology 37, 442. 

Caniatti EM, Tugnoli V et al (1996) Cryoglobulinemic neuropathy related to hepatitis C virus infection. Clinical, laboratory and neurophysiological study. J Peripher Nerv Syst 1(2) 131-138... 

Rocamora R, Kurthen M, Lickfett L, Von Oertzen J, Eiger CE. Cardiac asystole in epilepsy clinical and neurophysiologic features. Epilepsia 2003 44(2) 179-185. 

Wilmer JW, Albee RR, Nitschke KD, et al. 1992. Acute neurophysiological effects of trichloroethylene in rats. The Dow Chemical Company, Health and Environmental Sciences, Toxicology Research Laboratory, Midland, Ml. 

Figure 2.14 Relation between the EEG recorded from an epileptic focus on the surface of the cerebral cortex (EEG) and the activity of a single cortical neuron recorded extracellularly (e.c.) and intracellularly (i.c.) during an experimental epilepsy induced by topical application of penicillin. Note that the large EEG excursions correspond to the large (synchronised) depolarisations of the neuron, not to action potential discharges. (Adapted from Brain Res. 52 Ayala, GF et al. Genesis of Epileptic Interictal Spikes. New Knowledge of Cortical Feedback systems suggests a Neurophysiological Explanation of Brief Paroxysms, 1-17 (1973) with permission from Elsevier Science)...

Gottesmann, C (1999) Neurophysiological support of consciousness during waking and sleep. 

What are the effects on the developing nervous system after chronic in utero exposure Neurophysiological, neurophar-macol ogical, and neuroanatomi cal studies should be useful. 

Complicated processes govern wakefulness, sleep, and the transitions leading to sleep initiation and maintenance. Although the neurophysiology of sleep is complex, certain neurotransmitters promote sleep and wakefulness in different areas of the central nervous system (CNS). Serotonin is thought to control non-REM sleep, whereas cholinergic and adrenergic transmitters mediate REM sleep. Dopamine, norepinephrine, hypocretin, substance P, and histamine all play a role in wakefulness. Perturbations of various neurotransmitters are responsible for some sleep disorders and explain why various treatment modalities are beneficial. 

Belyavin, A., and Wright, N. A., Changes in electrical activity of the brain with vigilance. Electroencephalography and Clinical Neurophysiology 66(2), 137-144, 1987. 

Kilbum KH, Warshaw RH. 1995. Hydrogen sulfide and reduced-sulfur gases adversely affect neurophysiological functions. Toxicol Ind Health 11 185-197. 

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