Parasympathetic neurons

Peripheral Gl, vascular and bronchial smooth muscle, vascular endothelium, platelets Peripheral Smooth muscle of ileum, stomach fundus (rat), uterus, vasculature, endothelium Peripheral None identified Peripheral Post-ganglionic sympathetic neurons, sensory neurons Peripheral Cardiac muscle, post-ganglionic parasympathetic neurons (myenteric plexus), esophageal and vascular smooth muscle... 

Synthesis of noradrenaline (norepinephrine) is shown in Figure 4.7. This follows the same route as synthesis of adrenaline (epinephrine) but terminates at noradrenaline (norepinephrine) because parasympathetic neurones lack the phenylethanolamine-N-methyl transferase required to form adrenaline (epinephrine). Acetylcholine is synthesized from acetyl-Co A and choline by the enzyme choline acetyltransferase (CAT). Choline is made available for this reaction by uptake, via specific high-affinity transporters, within the axonal membrane. Following their synthesis, noradrenaline (norepinephrine) or acetylcholine are stored within vesicles. Release from the vesicle occurs when the incoming nerve impulse causes an influx of calcium ions resulting in exocytosis of the neurotransmitter. 

Atropine generally increases heart rate, but it may briefly and mildly decrease it initially, due to Ml receptors on postganglionic parasympathetic neurons. Larger doses of atropine produce greater tachycardia, due to M2 receptors on the sinoatrial node pacemaker cells. There are no changes in blood pressure, but arrhythmias may occur. Scopolamine produces more bradycardia and decreases arterial pressure, whereas atropine has little effect on blood pressure (Vesalainen et al. 1997 Brown and Taylor 1996). 

Target tissues of 2"" parasympathetic neurons ACh Muscarine Atropine Muscarinic (M) cholinoceptor G-protein-coupled-receptor protein with 7 transmembrane domains... 

A number of other substances are released by sympathetic and parasympathetic neurons, often the same neurons that release norepinephrine or acetylcholine. These substances include adenosine triphosphate (ATP), neuropeptide Y, and substance P. 

The heart is innervated by both sympathetic and parasympathetic neurons however, their distribution in the heart is quite different. Postganglionic noradrenergic fibers from the stellate and inferior cervical ganglia innervate the sinoatrial (S-A) node and myocardial tissues of the atria and ventricles. Activation of the sympathetic outflow to the heart results in an increase in rate (positive chronotropic effect), in force of contraction (positive inotropic effect), conduction tissue (positive dro-motropic effect). 

Figure. 2—4. The two major components of the ANS. The parasympathetic neurons release acetylcholine the sympathetic neurons release norepinephrine. These two systems provide a balance of control of the function of the organs and structures...

Except for skeletal muscle, virtually all tissues in the body are innervated in some way by the ANS.9 Table 18-1 summarizes the innervation and effects of the sympathetic and parasympathetic divisions on some of the major organs and tissues in the body. As indicated in Table 18-1, some organs, such as the heart, are innervated by both sympathetic and parasympathetic neurons. Other tissues, however, may only be supplied by the sympathetic division. The peripheral arterioles, for instance, are innervated by the sympathetic division but receive no parasympathetic innervation. 

Botulinum toxin inhibits release of acetylcholine (Ach) at me neuromuscular junction and in cholinergic sympathetic and parasympathetic neurons. 

Hypersecretion of Glands Supplied by Cholinergic Sympathetic or Parasympathetic Neurons... 

Inhibition of neurotransmitter release mediated by Ai adenosine receptors is a widespread phenomenon. As mentioned in Section 1, it was first described for cholinergic neurons. But presynaptic Ai receptors also inhibit the release of several other neurotransmitters both in CNS and PNS. Table 2 summarizes early relevant studies. As to postganglionic parasympathetic neurons, there is only one study to our knowledge. In that study, carried out in guinea pig atria, no A] receptor-mediated modulation of acetylcholine release was found (Nakatsuka et al. 1995). 

Parasympathetic neurons The parasympathetic preganglionic fibers arise from the cranial and sacral areas of the spinal cord and synapse in ganglia near or on the effector organs. In both the sympathetic and parasympathetic systems, postganglionic fibers extend from the ganglia to effector organs. 

The afferent neurons of the autonomic nervous system are important in the reflex regulation, for example, by sensing pressure in the carotid sinus and aortic arch and signaling the CNS to influence the efferent branch of the system to respond. Conditions such as trauma, fear, hypoglycemia, cold, or exercise activate the sympathetic neurons. Both sympathetic and parasympathetic neurons emerge from the brain stem or spinal cord. Blood pressure is regulated largely by sympathetic control of vascular tone. 

Q1 The iris contains pigment cells, blood vessels and two layers of smooth muscle fibres. The papillary constrictor muscles are arranged in concentric circles round the pupil when they contract, the size of the pupil decreases. The papillary dilator muscles are arranged radially away from the edge of the pupil. Contraction of these muscles widens, or dilates, the pupil. Both sympathetic and parasympathetic neurones supply and control the function of the muscles in the iris. 

Usually excitatory, except for some parasympathetic nerve endings where it is inhibitory (such as the effect on the heart by the vagus nerve). Secreted by many neurons, including those in the motor area of the brain, basal ganglia, skeletal muscle motor neurons, all preganglionic autonomic nervous system neurons, all postganglionic parasympathetic neurons, and some postganglionic sympathetic neurons. 

Purkinje cells is demonstrated in Figure 12.1 and, like all cardiac myocytes, can be divided into four phases. Phase 4 (pacemaker potential) involves the slow influx of sodium ions, depolarizing the cell until the threshold potential is reached. Once the threshold potential is reached, the fast sodium current is activated, resulting in a rapid influx of sodium ions causing cell depolarization (phase 0 rapid depolarization). Phase 1 (partial repolarization) involves the inactivation of sodium channels and a transient outward current. Phase 2 (plateau phase) results from the slow influx of calcium ions. Repolarization (phase 3) occurs as a result of outflow of potassium ions from the cell and restores the resting potential. There are variations between the different areas of the heart, specifically the nodal tissues do not possess fast sodium channels and slow L-t5rpe calcium channels generate phase 0 current (Fig. 12.1). Phase 4 activity varies between nodal areas the sinoatrial node depolarizes more rapidly than the atrioventricular (AV) node. Automaticity is under autonomic nervous system control. Parasympathetic neurons... 

The predominant action of cannabinoid receptor agonists on the GI tract is an inhibitory effect on gastrointestinal motility, reminiscent of the neuromodulatory response to presynaptic p-opioid receptor or 02 -adrenoceptor activation of cholinergic, postganglionic parasympathetic neurons. The mechanisms underlying this effect have been studied chiefly in the GI tract of small rodents, but also in man and the pig. Here we shall review the findings of studies carried out in vitro (Sect. 3.1, below) and in vivo (Sect. 3.2). 

Ciliary neurotrophic factor (CNTF) is a naturally occurring protein with a molecular mass of approximately 22 kDa. It was initially identified by its ability to support the survival of parasympathetic neurons of the chick ciliary ganglion in vitro (Adler et al., 1979) and subsequently purified to homogeneity from sciatic nerves (Lin et al., 1989 Stbckli et al., 1989). CNTF enhances the survival of... 

Scott, S.A. and Davies, A.M. (1990) Inhibition of protein synthesis prevents cell death in sensory and parasympathetic neurons deprived of neurotrophic factor in vitro. J. Neurobiol. 21 630-638. 

While the identity of the factor(s) are as yet unknown, there is now evidence that a soluble factor can direct the differentiation of parasympathetic neurons from precursor cells in the neural crest. By the use of monoclonal antibodies to cell surface antigens, Barald and coworkers have identified a subpopulation of cephalic neural crest cells which are committed to a cholinergic neurogenic fate (Barald, 1988a,b). The monoclonal antibodies rec-... 

Crouch, M.F. and Hendry, I.A. (1991) Co-activation of insulin-like growth factor-I receptors and protein kinase C results in parasympathetic neuronal survival. J. Neurosci. Res. 28 115-120. 

Bonyhady, R.E., Hendry, I.A., Hill, C.E. and McLennan, I.S. (1980) Characterization of a cardiac muscle factor required for the survival of cultured parasympathetic neurons. Neurosci. Lett. 18 197-201. 

Helfand, S.L., Smith, G.A. and Wessells, N.K. (1976) Survival and development in culture of dissociated parasympathetic neurons from ciliary ganglia. Dev. Biol. 50 541-547. 

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