Nerve terminus

The cr.j receptor is a regulatory receptor, which acts by inhibition of adenylate cyclase and subsequent decrease in cAMP. a2-receptors are located primarily on the membrane of the adrenergic nerve terminus, where they act to decrease norepinephrine release from the neuronal ending. a2-receptors are also located on the nucleus tractus solitarius (NTS) of the hypothalamus, which regulates systemic sympathetic outflow. 

Norepinephrine (NE) is taken up into the nerve terminus of the adrenergic neuron by neuronal reuptake mechanisms ( pumps ). It is then degraded intracellularly, by monoamine oxidase (MAO) (primarily MAOa, a mitochondrial enzyme) to form dihydroxymandelic acid. This is further inactivated by the tissue enzyme catechol-O-methyl transferase (COMT). Transmitter remaining in the synaptic cleft is rapidly degraded, first by COMT, located on postsynaptic membranes, to form normetanephrine. This in turn is taken into the neuron and converted to 3-methoxy, 4-hydroxy mandelic acid (VMA) through the actions of MAO (see Figure, top of next page). 

Yes. Epinephrine may also be taken into the adrenergic nerve terminus and degraded by MAOa. It is also degraded by tissue COMT. The end product of the degradation of both epinephrine and norepinephrine is VMA. 

Clonidine has a high affinity for the regulatory a2 receptor. Thus, as an c -receptor agonist, it mediates a decrease in sympathetic outflow both from the noradrenergic nerve terminus, and through the central a, receptor located on the nucleus tractus solitarius of the hypothalamus. 

Methyldopa is taken up into the adrenergic nerve terminus and enters the norepinephrine synthesis pathway. It is converted, by dopa decarboxylase, into a-methylnorepinephrine, a potent a2 agonist. a-Methyldopa is generally considered to be a pro-drug. 

This drug depletes neuronal stores of norepinephrine. The drug enters the adrenergic nerve terminus through the synaptic reuptake mechanism, and is transported into the adrenergic vesicle. Once in the vesicle, it displaces norepinephrine from the vesicle to the cytoplasm, where it is degraded by monoamine oxidase (MAO). 

Drugs used for hypertension that have markedly delayed effects are those that have effects at the nerve terminus level. This drug could be guanethidine or reserpine, but, because effects are not seen before the trace is truncated, it is likely to be a-methyldopa, because the drug requires time for the enzymatic conversion to a-methylnorepinephrine before antihypertensive effects are seen. 

NPY Neuropeptide Y NRS Normal rabbit serum NSAID Non-steroidal antiinflammatory drug NSE Nerve-specific enolase NT Neurotensin N terminus Amino terminus of peptide... 

Heterozygous carriers of functionally relevant mutations usually present with HDL cholesterol levels that are frequently below the fifth percentile. As would be expected, apoA-I levels are also frequently below the fifth percentile (i.e., < 1.05 g/1 and < 1.1 g/1 in Caucasian men and women, respectively). In most cases, heterozygous carriers of apoA-I variants do not present with specific clinical symptoms. An important exception are some structural apoA-I variants with amino acid substitutions in the amino terminus, which have been detected in patients with familial amyloidosis of the liver, the intestine, the kidney, the heart, peripheral nerves, and in the skin. In addition, some apoA-I variants like apoA-I L178P or L159P have been associated with increased risk of premature coronary heart disease or enhanced progression of carotid intima media thickness, whereas others did not show this association, or were even claimed to have reduced cardiovascular risk and advocated as possible agents for the treatment or prevention of atherosclerosis (notably apoA-I R173CMiiano) [22,43,53]. 

Subsequent to the molecular cloning and cDNA sequence analysis of the delta opioid receptor, antireceptor antibodies were raised against synthetic peptides based on the deduced amino acid sequence of this receptor. To date, there have been a limited number of studies using antibodies directed toward the amino terminus of the cloned murine receptor to assess the distribution of delta opioid receptorlike immunoreactivity in the gastrointestinal tract, and these have been confined so far to the porcine small intestine. They have shown the presence of delta opioid receptor-immuno-reactive neurons and fibers in both the myenteric and submucosal plexuses and as well as in myenteric neurons maintained in primary culture [22, 23]. Receptor-like immunoreactivity in neuronal cell bodies appears to be localized in the cytoplasm and is likely to be trafficked to nerve terminals. These neurons are coimmunoreactive for the acetylcholine-synthesizing... 

Nerve cells (neurons) are specialized so that at one end there is a flared stracture termed the dendrite. At the dendrite, the neuron is able to process chemical signals from other neurons and endocrine hormones. H the signals received at the dendrite end of the neuron are of a sufficient strength, and priperly timed, they are transformed into action potentials that sweep down the neural cell body (axon) frc n the dendrite end to the other end of the neuron, the presynaptic portion of the axon that ends at the next synapse (the extra cellular gap between neurons)in the neural pathway. The arrival of the action potential at the pre aptic terminus causes the release of ions and chemicals (neurotrananitters) that travel... 

The tachykinins are a family of small peptides (fewer than 50 residues), each of which has the same amino acid sequence, Phe-X-Gly-Leu-Met-NH2, at the amidated carboxy terminus (Fig. 7.1). Although three primary mammahan tachykinins - substance P, neurokinin A (NkA) and neurokinin B (NkB) - have been recognized, only substance P and NkA have been identified in the lungs and airways. Tachykinins are synthesized in nerve cell bodies, appropriately processed, and then transported by axoplasmic flow to the terminal ramifications of axon dendrites, where they serve their neurotransmitter functions. Both substance P and NkA are derived from transcription and translation of the preprotachykinin I (PPT-I) gene (Nawa et al., 1984 Krause etal., 1987). NkB is derived from a separate gene. 

Alzheimer s disease A progressive disease where nerve cells in the brain degenerate. A common cause of dementia, amenorrhoea Stopping or absence of menstrual periods, aminopeptidases A group of enzymes that remove the amino-terminal amino acid residues from peptides or proteins, often leading to inactivation, amino terminus (IV-terminus) The end of a protein or peptide chain that bears the free a-amino group. 

In this section, we first Introduce some of the key properties of neurons and action potentials, which move down the axon very rapidly. We then describe how the voltagegated channels responsible for propagating action potentials In neurons operate. In the following section, we examine how arrival of an action potential at the axon terminus causes secretion of chemicals called neurotransmitters. These chemicals, in turn, bind to receptors on adjacent cells and cause changes in the membrane potential of these cells. Thus electric signals carry Information within a nerve cell, while chemical signals transmit Information from one neuron to another or from a neuron to a muscle or other target cell. 

Figure 1. The beginningof a nerve impulse. An exchange of charged atoms (ions) across the nerve cell membrane sends a wave of depolarisation towards the nerve cell terminus. The neurotransmitter, acetyl choline is held in vesicles ready for release.

Figure 2. When the wave of depolarisation arrives at the nerve cell terminus, acetylcholine is released into the space (synapse) between the two nerves. It moves across the synapse to the postsynaptic receptors.

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