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By B. Redge. Arizona State University West.

These effects of 5-HT3 receptor activation are prevented by co-administration of a D2-receptor antagonist generic 100mg aurogra. This is consistent with evidence that activation of 5-HT3 receptors can increase dopamine release and points to functional interactions between these two groups of neurons that affect the sleep±waking cycle buy aurogra 100 mg on line. Such interactions will certainly confound any attempts to define the specific role of 5-HT in the regulation of sleep and arousal order aurogra 100mg otc. Overall 100 mg aurogra mastercard, 5-HT transmission seems to increase during waking and to decline in sleep although it may only reach its minimal level, in some neurons anyway, during REM 494 NEUROTRANSMITTERS, DRUGS AND BRAIN FUNCTION sleep. Whether its role is simply to prime target cells to enable an increase in the motor activity associated with waking, as has been suggested, remains to be seen. ADENOSINE It is perhaps not surprising that, since adenosine has been presented as an endogenous inhibitor of neuronal function with its antagonists, like theophylline, being stimulants (see Chapter 13), it should have been implicated in sleep induction. In fact EEG studies have shown that administration of an adenosine A1 agonist increases SWS in humans and induces it in sleep-deprived rats while adenosine also inhibits the important cortical activating brainstem cholinergic neurons. After that, it falls sharply within an hour as the animal enters the quiet (lights on) sleepy period (see Huston et al. AMINO ACIDS Since most excitatory transmission is mediated by glutamate this must be involved in the sleep±waking cycle. It certainly mediates the input of the retinohypothalamic tract to the SCN, apart from afferent inputs more generally to the ARAS, etc. So far, specific in vivo manipulation of the direct glutamate input to the SCN has not been possible. The fact that SCN neurons contain GABA, and that this appears to be the neurotransmitter released by the geniculohypothalamic tract onto the SCN, clearly puts it in a prime position for regulation of sleep rhythms. However, its precise role is unclear, not least because it can act as an excitatory, as well as an inhibitory, neurotransmitter in this nucleus and that these varied responses appear to follow a circadian rhythm (see Chapter 11). Again, specific manipulation of this pathway is difficult although GABA enhancement generally (e. SLEEP FACTORS In classical times, sleep was thought to be induced by sleep factors (vapours) emanating from food in the stomach. These are thought to have a pervading influence on sleep throughout the brain, although the stomach is no longer regarded as their source! This view was strongly encouraged by experiments, carried out in the early twentieth century, by Pieron in Paris, who showed that the CSF of sleep-deprived dogs contained a substance that had a somnogenic effect when infused into non-sleep- deprived animals. Since then, many candidate sleep substances have emerged, some of which are more convincing than others. Chemical extraction from thousands of rabbit brains and many gallons of human urine yielded a sleep factor and established it as a muramyl peptide. Unfortunately muramyl peptides are not synthesised by mammalian cells but are components of bacterial cell walls. Apart from the obvious possibility of mere contamination, it is not clear how the substance turned up in the CSF and brain tissue. Despite this setback, and some scepticism about whether somnogenic peptides exist at all, research still continues in this area and many candidates have been suggested. These include well-known peptides such as prolactin, CCK-8, VIP and somatostatin as well as some novel ones such as d-sleep-inducing peptide. IL-6 also reduces REM sleep and SWS in the first half of the sleep cycle but subsequently increases SWS. However, all these responses vary with dose, test species and even time of day. These factors are produced by T-cell lymphocytes but their receptors are associated with neurons, astrocytes, microglia and endothelial cells. Because these agents induce nitric oxide synthase, and there is some evidence that nitric oxide increases waking, possibly through modulation of ACh release in the medial pontine reticular formation, there is no need for them to cross the blood± brain barrier (although there is evidence that they do). Nevertheless, how these factors actually cause changes in the sleep cycle is as yet unclear.

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Thus aurogra 100 mg with visa, any two sounds having a tenfold difference in in- The Nature of Sound generic aurogra 100 mg without prescription. Sound waves are mechanical dis- tensity have a decibel difference of 20; a 100-fold differ- turbances that travel through an elastic medium (usually air ence would mean a 40 dB difference and a 1 generic aurogra 100 mg otc,000-fold dif- or water) cheap aurogra 100 mg without a prescription. Usually the reference value is brating structure that alternately compresses and rarefies assumed to be constant and standard, and it is not expressed the air (or water) in contact with it. As the cone moves back, the space between the shown in the table expresses a relative range of 10 million- disturbed molecules is increased; this is known as rarefac- fold. The compression (or rarefaction) of air molecules in auditory system allow encoding of most of this wide range one region causes a similar compression in adjacent re- into biologically useful information. Continuation of this process causes the disturbance Sinusoidal sound waves contain all of their energy at (the sound wave) to spread away from the source. Complex The speed at which the sound wave travels is deter- sound waves, such as those in speech or music, consist of mined by the elasticity of the air (the tendency of the mol- the addition of several simpler waveforms of different fre- ecules to spring back to their original positions). The human ear is capable of hear- the sound source is moving back and forth at a constant rate ing sounds over the range of 20 to 16,000 Hz, although the of alternation (i. Auditory sensitivity varies compression wave will pass a given point once for every cy- with the frequency of the sound; we hear sounds most read- cle of the source. Because the propagation speed is constant ily in the range of 1,000 to 4,000 Hz and at a sound pres- in a given medium, the compression waves are closer to- sure level of around 60 dB. Not surprisingly, this is the fre- gether at higher frequencies; that is, more of them pass the quency and intensity range of human vocalization. A tone of 1,000 cycles per second, travel- by the masking sound, which would reduce the number of ing through the air, has a wavelength of approximately available receptor cells. The pinna, the visible portion of the outer water are greater than those in air, the speed of sound in ear, is not critical to hearing in humans, although it does water is about 4 times as great, and the wavelength is cor- respondingly increased. Since the wavelength depends on the elasticity of the medium (which varies according to temperature and pressure), it is more convenient to TABLE 4. Sound fre- Common Sounds quency is usually expressed in units of Hertz (Hz or cy- Sound cles per second). Pressure Pressure Relative Another fundamental characteristic of a sound wave is 2 (dynes/cm ) Level (dB) Sound Source Pressure its intensity or amplitude. This may be thought of as the relative amount of compression or rarefaction present as 0. Be- 200 120 Loud thunder 1,000,000 cause the human ear is sensitive to sounds over a million- 2,000 140 Pain and damage 10,000,000 fold range of sound pressure levels, it is convenient to ex- press the intensity of sound as the logarithm of a ratio Modified from Gulick WL, Gescheider GA, Frisina RD. New referenced to the absolute threshold of hearing for a tone York: Oxford University Press, 1989, Table 2. The superior and lateral lig- Vestibular nerve Incus aments lie roughly in the plane of the ossicular chain and an- Facial nerve chor the head and shaft of the malleus. The anterior ligament Cochlear attaches the head of the malleus to the anterior wall of the nerve middle ear cavity, and the posterior ligament runs from the head of the incus to the posterior wall of the cavity. The sus- pensory ligaments allow the ossicles sufficient freedom to function as a lever system to transmit the vibrations of the tympanic membrane to the oval window. This mechanism is especially important because, although the eardrum is sus- pended in air, the oval window seals off a fluid-filled cham- ber. Transmission of sound from air to liquid is inefficient; if Pinna sound waves were to strike the oval window directly, 99. Al- though it varies with frequency, the ossicular chain has a Outer ear Middle Inner ear ear lever ratio of about 1. The brane is coupled to the smaller area of the oval window (ap- structures of the middle and inner ear are en- proximately a 17:1 ratio). These conditions result in a pres- cased in the temporal bone of the skull.

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The application of adenosine order aurogra 100mg without prescription, ATP discount aurogra 100mg fast delivery, or other purinergic analogs also mimics slow IPSPs discount 100 mg aurogra free shipping. Inhibitory actions of adenosine 1 agonists result Presynaptic inhibition aurogra 100 mg. Different neuro- transmitters act through the presynaptic inhibitory receptors to suppress axonal release of the transmitters for slow and fast EP- Presynaptic Inhibitory Receptors Are Found at SPs. Presynaptic autoreceptors are involved in a special form of Enteric Synapses and Neuromuscular Junctions presynaptic inhibition whereby the transmitter for slow or fast EPSPs accumulates at the synapse and acts on the autoreceptor to Presynaptic inhibition (Fig. The mechanisms for controlling orderly Paralytic ileus, another form of pseudoobstruction, propulsive motility fail while the intestinal lumen is free is characterized by prolonged motor inhibition. This syndrome may result from abnor- trical slow waves are normal, but muscular action poten- malities of the muscles or ENS. Prolonged ileus com- colicky abdominal pain, nausea and vomiting, and abdom- monly occurs after abdominal surgery. Failure of propulsive motility re- nism is presynaptic inhibition and the closure of synaptic flects the loss of the neural networks that program and gates (see Fig. Continuous discharge of the inhibitory motor neurons This disorder can occur in varying lengths of intestine or in accompanies suppression of the motor circuits. Contractile behav- ity of the inhibitory motor neurons prevents the circular ior of the circular muscle is hyperactive but disorganized in muscle from responding to electrical slow waves, which the denervated segments. The phenomenon is known to occur mine H3 presynaptic receptors to suppress fast EPSPs. The release of histamine from action of cholecystokinin in the ENS of the gallbladder. At nora- Presynaptic inhibition operates normally as a mechanism drenergic inhibitory synapses in the submucous plexus, it for selective shutdown or deenergizing of a microcircuit (see involves the elevation of cAMP in the postganglionic Clinical Focus Box 26. Preventing transmission among sympathetic fiber and appears as an enhancement of the the neural elements of a circuit inactivates the circuit. For slow IPSPs evoked by the stimulation of sympathetic example, a major component of shutdown of gut function postganglionic fibers. Presynaptic facilitation is the mechanism of action of some prokinetic drugs. Such drugs act to facilitate nicotinic transmission at the fast ex- Presynaptic Facilitation Enhances the citatory synapses in the enteric neural networks that con- Synaptic Release of Neurotransmitters trol propulsive motor function. In both the stomach and the intestine, increases in EPSP amplitudes and rates of rise de- and Increases the Amplitude of EPSPs crease the probability of transmission failure at the Presynaptic facilitation refers to an enhancement of synapses, thereby increasing the speed of information synaptic transmission resulting from the actions of chem- transfer. This mechanism “energizes” the network circuits Control EPSP Presynaptic receptors (facilitative) Stimulus artifact Neurotransmitter Enhanced EPSP 20 mV (e. Postsynaptic Action potential Presynaptic facilitation en- receptors threshold hances release of ACh and in- (nicotinic) creases the amplitude of fast EP- SPs at a nicotinic synapse. CHAPTER 26 Neurogastroenterology and Gastrointestinal Motility 461 and enhances propulsive motility (i. ENTERIC MOTOR NEURONS IJP EJP Substance P Motor neurons innervate the muscles of the digestive tract VIP NO ACh and, like spinal motor neurons, are the final pathways for (–) (+) (–) (+) signal transmission from the integrative microcircuits of the minibrain-in-the-gut (see Figs. The mo- Muscle Muscle tor neuron pool of the ENS consists of excitatory and in- FIGURE 26. The motor neuron pool of the ENS consists of both excita- transmitters released from axons of motor neurons act on tory and inhibitory neurons. Neuromuscular junctions in the digestive inhibitory motor neurons evokes IJPs. Release of ACh or sub- tract are simpler structures than the motor endplates of stance P from excitatory motor neurons evokes EJPs. Most motor axons in the tive intestinal peptide; NO, nitric oxide; IJP, inhibitory junction digestive tract do not release neurotransmitter from termi- potential; EJP, excitatory junction potential. The neurotransmitter is released from the varicosities all along the axon during propagation of the ac- tion potential.

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