Discharge of Neurons

L-Dihydroxyphenylalanine 4-Dihydroxyphenylethylamine Dimeric Transcription Factors Dioxins Dipeptidase Dipeptidylpeptidase Dipeptidylpeptidase IV Direct Thrombin Inhibitors Discharge of Neurons... 

Both systems are tonically active. In other words, they provide some degree of nervous input to a given tissue at all times. Therefore, the frequency of discharge of neurons in both systems can increase or decrease and, as a result, tissue activity may be enhanced or inhibited. This characteristic of the ANS improves its ability to regulate a tissue s function more precisely. Without tonic activity, nervous input to a tissue could only increase. 

Sleep-waking discharge of neurons in the posterior lateral hypothalamus of the albino rat. Brain Res. 840, 138-47. 

Epilepsy is a chronic often progressive disorder of the central nervous system (CNS). Periodic and unpredictable epileptic seizures caused by the abnormal electrical discharge of neurones in various anatomic structures of the CNS is the characteristic feature. This is an approximate definition based on international classifications of seizures and syndromes which take into account the extremely variable clinical and electroencephalographic expression of the disease. The annual incidence of epilepsy is an estimated 20-70 cases per 100,000 inhabitants with a prevalence of 0.4-0.8%. Globally, incidence is higher during childhood, remaining rather stable... 

In the CNS there are many forms of neuronal organisation. One neuron can have many synaptic inputs and a multiplicity of NTs and NT effects are utilised within a complex interrelationship of neurons. There are also positive and negative feedback circuits as well as presynaptic influences all designed to effect changes in excitability and frequency of neuronal firing, i.e. patterns of neuronal discharge. 

That an episode arises and spreads from the synchronous as well as excessive discharge of a group of neurons (focus) means that not only must those neurons be in some way predisposed to so discharging but they can also recruit neurons that are otherwise normal. How that discharge manifests itself, i.e. which type of epilepsy occurs, will depend not only on where the abnormal focal neurons are located but also to what extent the activity they initiate can and does spread through the brain. There are consequently a number of different forms of epilepsy, i.e. the epilepsies. 

It is equally well known that if a neuron dies, or is destroyed, then any other neuron, which had been innervated by it, gradually becomes supersensitive to the NT it released. In the case of degenerating pyramidal cells this would be glutamate, the excitatory NT. Not surprisingly, undercutting the cortex in animals to produce a deafferentation of some of its neurons not only renders them more likely to show epileptic-like discharges but neurons in hippocampal slices from kindled rats and human focal cortex show supersensitivity to the excitatory amino acids. Such supersensitivity could make some neurons so easily activated that they become epileptic . 

The dendrites of neurons adjacent to those which degenerate also show extensive growth and sprouting which could facilitate abnormal and disorganised synaptic transmission and cause hyperactivity. It is also known that the dendrites of cells around an alumina focus in monkeys, as well as in human epileptic brain, lose their spinous processes, which might contribute to the paroxysmal discharge by facilitating the spread of depolarisation to the neuron soma. Certainly an increase in the number of Na+ channels on the dendrites of spinal motoneurons, which would facilitate the occurrence of reactive dendritic Na+ spikes, has been seen after axotomy. 

Regardless of the underlying etiology, all seizures involve a sudden electrical disturbance of the cerebral cortex. A population of neurons fires rapidly and repetitively for seconds to minutes. Cortical electrical discharges become excessively rapid, rhythmic, and synchronous. This phenomenon is presumably related to an excess of excitatory neurotransmitter action, a failure of inhibitory neurotransmitter action, or a combination of the two. In the individual patient, however, it is usually impossible to identify which neurochemical factors are responsible. 

Studies of sleep-active neuronal discharge across the sleep-wake cycle in freely moving animals provide important information about the hypnogenic process (see below) but, because of sampling limitations, are not suitable for systematic mapping of the exact locations of putative hypnogenic neurons. The application of the c-Fos immunoreactivity (IR) method to map sleep-active neurons has stimulated several advances. C-Fos IR is a marker of neuronal activation in most brain sites immunohistochemically labeled neurons can be mapped systematically. The localization of c-Fos IR following sustained sleep, but not... 

Figure 1.7 Effects of local POA warming on discharges of a DRN, wake-active, REM-off, putative serotonin-containing neuron. POA warming suppressed DRN neuronal discharge, without any change in behavioral state, as shown by EEG spectral analysis. Thus activation of POA WSNs can suppress DRN discharge. The DRN receives direct projections from the POA. From Guzman-Marin el al (2000).

Figure 1.8 Effects of local POA warming on a PLH wake-active, REM-off, putative hypocretin/orexin-containing neuron. POA warming suppressed the waking-related discharge of PLH neurons, in the absence of any state change. The PLH receives strong projections from all subregions of the POA, including GABAergic projections. From Methippara et al. (2003).

Alam, Md. N., McGinty, D., Szymusiak, R. (1995a). Neuronal discharge of... 

Alam, Md. N., Gong, H., Alam, T., Jaganath, R., McGinty, D., Szymusiak, R. (2002). Sleep-waking discharge patterns of neurons recorded in the rat perifornical lateral hypothalamic area. J. Physiol. 538, 619-31. 

Lee, M. G., Hassani, O. K. 8r Jones, B. E. (2005). Discharge of identified orexin/ hypocretin neurons across the sleep-waking cycle. J. Neurosci. 25, 6716-20. 

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