Nervous system nerve-muscle

Only in the last few centuries has the link between the brain and behaviour become clear, and only at the end of the nineteenth century was it demonstrated that the nervous system was made up of billions of separate nerve cells or neurons. We now know that during evolution complex networks of such neurons have developed in order to effect certain behaviours. Whilst the neurons of the central, peripheral and autonomic nervous systems vary enormously in form and function, they can be classed into three broad groups sensory neurons which convey information into the central nervous system effector neurons which carry information out of the central nervous system to muscles and other effector organs and interneurons within the central nervous system which link the sensory and effector neurons and also have links with one another. 

The functions of CDF/LIF in vivo appear to differ from those of CNTF. As already described, the tissue distributions of CNTF and CDF/LIF are different. Among the peripheral tissues of rat innervated by sympathetic neurons, detectable amounts of CDF/LIF are expressed only in the foot pad, while CNTF is widely distributed. In the central nervous system, CDF/LIF is restricted to some visual neurons (Yamamori, 1991b), whereas CNTF is predominantly expressed in astrocytes of the optic nerve and olfactory bulb, and at moderate levels in other areas (Stbckli et al., 1991). Conversely, a specific receptor subunit for CNTF (CNTF-a) is expressed only in the nervous system and muscle, whereas gpl30 and LIF-R are expressed in most tissues (Ip et al., 1993). 

The human body has more than 600 muscles. The body s movement is performed by muscle contractions, which are stimulated by the nervous system. This system links muscle tissue to the spinal cord and brain. The network of nerve cells which carries the brain s signals directs the flow of muscular energy. Most muscular activity occurs beyond the range of the conscious mind. The body, working through the neuromuscular network, manages... 

The same author found Z-hyoscine sixteen to eighteen times as active as the d-isomeride in antagonising the action of pilocarpine on the termination of nerves in the salivary glands, -while both isomerides are equally active on nerve ends in striated and unstriated muscle and on the central nervous system. 

The adrenergic dragp produce pharmacologic effects similar to the effects that occur in die body when die adrenergic nerves and the medulla are stimulated. The primary effects of these drugp occur on the heart, the blood vessels, and die smooth muscles, such as die bronchi. A basic knowledge of the nervous system is necessary to understand tiiese drugp and how they work in the body. 

The somatic motor nervous system or voluntary nervous system consists of nerve libers that irmervate skeletal muscle motor end-plates. 

Enteric nerves control intestinal smooth muscle action and are connected to the brain by the autonomic nervous system. IBS is thought to result from dysregulation of this brain-gut axis. The enteric nervous system is composed of two gan-glionated plexuses that control gut innervation the submucous plexus (Meissner s plexus) and the myenteric plexus (Auerbach s plexus). The enteric nervous system and the central nervous system (CNS) are interconnected and interdependent. A number of neurochemicals mediate their function, including serotonin (5-hydroxytryptamine or 5-HT), acetylcholine, substance P, and nitric oxide, among others. 

Both the G- and V-agents have the same physiological action on humans. They are potent inhibitors of the enzyme acetylcholinesterase (AChE), which is required for the function of many nerves and muscles in nearly every multicellular animal. Normally, AChE prevents the accumulation of acetylcholine after its release in the nervous system. Acetylcholine plays a vital role in stimulating voluntary muscles and nerve endings of the autonomic nervous system and many structures within the CNS. Thus, nerve agents that are cholinesterase inhibitors permit acetylcholine to accumulate at those sites, mimicking the effects of a massive release of acetylcholine. The major effects will be on skeletal muscles, parasympathetic end organs, and the CNS. 

The endogenous release of the potent vasoconstrictor neuropeptide Y (NPY) is increased during sepsis and the highest levels are detected in patients with shock (A8). NPY is a 36-amino-acid peptide belonging to the pancreatic polypeptide family of neuroendocrine peptides (T2). It is one of the most abundant peptides present in the brain and is widely expressed by neurons in the central and peripheral nervous systems as well as the adrenal medulla (A3). NPY coexists with norepinephrine in peripheral sympathetic nerves and is released together with norepinephrine (LI9, W14). NPY causes direct vasoconstriction of cerebral, coronary, and mesenteric arteries and also potentiates norepinephrine-induced vasoconstriction in these arterial beds (T8). It appears that vasoconstriction caused by NPY does not counterbalance the vasodilatator effects of substance P in patients with sepsis. The properties of vasodilatation and smooth muscle contraction of substance P are well known (14), but because of the morphological distribution and the neuroendocrine effects a possible stress hormone function for substance P was also advocated (J7). Substance P, which is a potent vasodilatator agent and has an innervation pathway similar to that of NPY, shows a low plasma concentration in septic patients with and without shock (A8). 

The cell bodies of visceral motor neurons are found in the lateral horn. The axons of these neurons form efferent nerve fibers of the autonomic nervous system (ANS). The ANS innervates cardiac muscle, smooth muscle and glands (see Chapter 9). The axons of these neurons exit the spinal cord by way of the ventral root. 

Because baroreceptors respond to stretch or distension of the blood vessel walls, they are also referred to as stretch receptors. A change in blood pressure will elicit the baroreceptor reflex, which involves negative feedback responses that return blood pressure to normal (see Figure 15.6). For example, an increase in blood pressure causes distension of the aorta and carotid arteries, thus stimulating the baroreceptors. As a result, the number of afferent nerve impulses transmitted to the vasomotor center increases. The vasomotor center processes this information and adjusts the activity of the autonomic nervous system accordingly. Sympathetic stimulation of vascular smooth muscle and the heart is decreased and parasympathetic stimulation of the heart is increased. As a result, venous return, CO, and TPR decrease so that MAP is decreased back toward its normal value. 

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