Maintenance neurons

Nicotine and the neurotransmitter acetylcholine, which acts on maintenance neurons, have similar structures, as Figure 14.28 illustrates. Nicotine molecules are therefore able to bind to acetylcholine receptor sites and trigger many of acetylcholines effects, including relaxation and increased digestion, which... 

What are some of the things going on in the body when maintenance neurons are more active than stress neurons ... 

A common strategy for treating chronic opiate addiction iavolves the substitution of methadone which can either be provided as maintenance therapy or tapered until abstinence is achieved. Naltrexone and buprenorphine [52485-79-7] have also been used ia this manner. The a2 adrenergic agonist clonidine [4205-90-7] provides some rehef from the symptoms of opiate withdrawal, probably the result of its mimicking the inhibitory effect of opiates on the activity of locus coerukus neurons. 

Maintenance of electrical potential between the cell membrane exterior and interior is a necessity for the proper functioning of excitable neuronal and muscle cells. Chemical compounds can disturb ion fluxes that are essential for the maintenance of the membrane potentials. Fluxes of ions into the cells or out of the cells can be blocked by ion channel blockers (for example, some marine tox-... 

Neurotrophins are peptides or protein molecules that regulate both cell survival and cell death of specific neuronal phenotypes and thus serve to influence development, maintenance, function, and plasticity of the nervous system. 

Fig. 4.1 Hypothetical model of pathogenesis of pain in DSP. (1) Injury of peripheral nerve fibers due to multifocal inflammation and secreted macrophage activation products results in abnormal spontaneous activity of neighboring uninjured nociceptive fibers ( peripheral sensitization ). (2) Furthermore, the aberrant inflammatory response in DRG leads to alterations in neuronal sodium and calcium channel expression and ectopic impulse generation. (3) This results in central remodeling within the dorsal horn due to A-fiber sprouting and synaptic formation with pain fibers in lamina 11, and maintenance of neuropathic pain ( central sensitization ). Reproduced with permission from (Keswani et al. 2002)...

MCP1/CCR2 by DRG neurons occurs some days following the initial injury, it is also likely that excitation produced in this fashion may be more important for the maintenance of chronic pain rather than its initiation. Thus, according to this view the major site of action of MCP-1 is within the DRG rather than in the SC. 

To achieve their different effects NTs are not only released from different neurons to act on different receptors but their biochemistry is different. While the mechanism of their release may be similar (Chapter 4) their turnover varies. Most NTs are synthesised from precursors in the axon terminals, stored in vesicles and released by arriving action potentials. Some are subsequently broken down extracellularly, e.g. acetylcholine by cholinesterase, but many, like the amino acids, are taken back into the nerve where they are incorporated into biochemical pathways that may modify their structure initially but ultimately ensure a maintained NT level. Such processes are ideally suited to the fast transmission effected by the amino acids and acetylcholine in some cases (nicotinic), and complements the anatomical features of their neurons and the recepter mechanisms they activate. Further, to ensure the maintenance of function in vital pathways, glutamate and GABA are stored in very high concentrations (10 pmol/mg) just as ACh is at the neuromuscular junction. 

Maintenance of these frequencies relies on the degree of depolarisation of the thalamic neurons (Jahnsen and Elinas 1985) and this, in turn, depends on the nature and intensity of their afferent inputs. The NspRTN and other thalamic nuclei receive reciprocal inputs from the cortex and it is possible that it is the ensuing oscillations in neuronal activity in this circuit between the cortex and thalamus that give rise to the sleep spindle waves in stages 2-4. In fact, it has been suggested that the stronger and clearer these oscillations become, the more likely it is that there will be loss of consciousness. 

Embedded within the brain are four ventricles or chambers that form a continuous fluid-filled system. In the roof of each of these ventricles is a network of capillaries referred to as the choroid plexus. It is from the choroid plexuses of the two lateral ventricles (one in each cerebral hemisphere) that cerebrospinal fluid (CSF) is primarily derived. Due to the presence of the blood-brain barrier, the selective transport processes of the choroid plexus determine the composition of the CSF. Therefore, the composition of the CSF is markedly different from the composition of the plasma. However, the CSF is in equilibrium with the interstitial fluid of the brain and contributes to the maintenance of a consistent chemical environment for neurons, which serves to optimize their function. 

Forebrain neurons would not be necessary for PS onset and maintenance. However, hypocretin and MCH hypothalamic neurons would participate in the homeostasis of PS through reciprocal connections and their respective excitatory and inhibitory projections on the brainstem monoaminergic and GABAergic PS-off neurons. 

Boissard, R., Gervasoni, D., Fort, P. et al. (2000). Neuronal networks responsible for paradoxical sleep onset and maintenance in rats a new hypothesis. Sleep 23 (suppl.), 107. 

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