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Sensory excitation

Sensory excitement, involvement, sensuality Enhanced or decreased sensory intensity... [Pg.12]

Color visions were provoked by doses of 0.36-0.44 g. of mescaline sulfate distributed in several subcutaneous injections. The state of intoxication and the visions lasted for 5 to 10 hours. The effects varied widely in different individuals. The most characteristic symptom is that of wonderful visual color hallucinations. Clear consciousness is generally preserved and the subject is fully aware of his condition. Sensory illusions and transposition of sensorial excitation are the interesting factors in this inebriation. Ordinary objects appear to be marvelous. Sounds and music are seen in color. In comparison, the impressions of everyday life seem pale and inert. Color symphonies and new, unknown colors of unimaginable beauty and brilliancy are perceived. Euphoria is not always present. Hallucinations of hearing, taste, or other senses were reported more rarely. Bradycardia, nausea, a feeling of oppression in the chest, faintness, and headache may also occur. [Pg.333]

How do inhibitory transmitters contribute to sensory excitation by hypoxia Hypoxia ubiquitously augments the sensory discharge of the carotid bodies... [Pg.430]

A persistent idea is that there is a very small number of flavor quaUties or characteristics, called primaries, each detected by a different kind of receptor site in the sensory organ. It is thought that each of these primary sites can be excited independently but that some chemicals can react with more than one site producing the perception of several flavor quaUties simultaneously (12). Sweet, sour, salty, bitter, and umami quaUties are generally accepted as five of the primaries for taste sucrose, hydrochloric acid, sodium chloride, quinine, and glutamate, respectively, are compounds that have these primary tastes. Sucrose is only sweet, quinine is only bitter, etc saccharin, however, is slightly bitter as well as sweet and its Stevens law exponent is 0.8, between that for purely sweet (1.5) and purely bitter (0.6) compounds (34). There is evidence that all compounds with the same primary taste characteristic have the same psychophysical exponent even though they may have different threshold values (24). The flavor of a complex food can be described as a combination of a smaller number of flavor primaries, each with an associated intensity. A flavor may be described as a vector in which the primaries make up the coordinates of the flavor space. [Pg.3]

Voltage-gated Ca2+ channels are Ca2+-selective pores in the plasma membrane of electrically excitable cells, such as neurons, muscle cells, (neuro) endocrine cells, and sensory cells. They open in response to membrane depolarization (e.g., an action potential) and permit the influx of Ca2+ along its electrochemical gradient into the cytoplasm. [Pg.295]

These are a subset of sensory neurons having their cell bodies (small to medium size) in dorsal root and in cranial nerve ganglia and possessing nonmyelinated (C-type) or thinly myelinated (A-delta type) fibres. This subset of neurons express transient receptor potential vanilloid type 1 (TRPV1, or vanilloid, or capsaicin receptor) that is excited by capsaicin, the pungent ingredient of chilli. These neurons have been classified as polymodal nociceptors because they can be excited by various noxious stimuli. [Pg.320]

Hi-receptors in the adrenal medulla stimulates the release of the two catecholamines noradrenaline and adrenaline as well as enkephalins. In the heart, histamine produces negative inotropic effects via Hr receptor stimulation, but these are normally masked by the positive effects of H2-receptor stimulation on heart rate and force of contraction. Histamine Hi-receptors are widely distributed in human brain and highest densities are found in neocortex, hippocampus, nucleus accumbens, thalamus and posterior hypothalamus where they predominantly excite neuronal activity. Histamine Hrreceptor stimulation can also activate peripheral sensory nerve endings leading to itching and a surrounding vasodilatation ( flare ) due to an axonal reflex and the consequent release of peptide neurotransmitters from collateral nerve endings. [Pg.589]

Besides all the sensory and texturizing properties, GA has interesting antioxidant properties such as an efficient capacity for deactivation of excited electronic states and moderated radical scavenging capacity. There is increasing experimental evidence that associate the antioxidant function with its protein fraction, mainly by amino acid residues such as histidine, tyrosine and lysine, which are generally considered as antioxidants molecules (Marcuse, 1960,1962 Park et al., 2005). [Pg.18]

Pain production is the most common injury inflicted on man. This noxious stimulus is perceived almost instantly after skin - tentacle contact. A subpopulation (30 - 40%) of visceral sensory C fibers denoting noscioception have been shown to be selectively excited experimentally in nerve ganglia preparations by a component of... [Pg.334]

In addition to changes within the nerve, sympathetic afferents become able to activate sensory afferents via as yet poorly characterised a-adrenoceptors. These interactions between adjacent sensory and autonomic nerve axons and between ganglion cells result in excitation spreading between different nerve fibres. These peripheral ectopic impulses can cause spontaneous pain and prime the spinal cord to exhibit enhanced evoked responses to stimuli, which themselves have greater effects due to increased sensitivity of the peripheral nerves. [Pg.460]

Opioids act in the brain and within the dorsal horn of the spinal cord, where their actions are better understood. The actions of opioids important for analgesia and their side-effects involve pre- and postsynaptic effects (1) reduced transmitter release from nerve terminals so that neurons are less excited by excitatory transmitters, and (2) direct inhibitions of neuronal firing so that the information flow from the neuron is reduced but also inhibitions of inhibitory neurons leading to disinhibition. This dual action of opioids can result in a total block of sensory inputs as they arrive in the spinal cord (Fig. 21.5). Thus any new drug would have to equal this dual action in controlling both transmitter release and neuronal firing. [Pg.469]

TRPVl also plays a central role in intercellular pro-inflammatory feedback loops. An important example is mast cells and sensory nerves. Mast cells release tryptase that, in turn, activates the protease-activated receptor PAR-2 activation of PAR-2 then opens TRPVl via PKC [50]. In keeping with this, PAR-2 agonists reduce the heat activation threshold of TRPVl from 42 °C to below body temperature [51]. Excited nerve endings release SP that, as a positive feedback, binds to neurokinin NKl receptors on mast cells. Mast cells also express TRPVl [52]. Consequently, endovanilloids can act in concert to stimulate mast cells and activate capsaicin-sensitive nerve endings. Of relevance is the finding that PAR-2 is up-regulated in the bladder during experimental cystitis [53]. [Pg.150]

In the vertebrate CNS monoamines have been associated with a number of physiological functions (reviewed in Kandel et al., 1991). Serotonin has functions associated with mood, pain, sleep, learning, and memory. Dopamine has functions associated with schizophrenia, Parkinson s disease, and cocaine addiction. In vertebrates, dopamine is further metabolized into two additional neurotransmitters, norepinephrine and epinephrine. Norepinephrine increases the excitability of cells in response to sudden sensory input such as fear. Epinephrine has been identified in specific neurons of the brain, but the function of these cells is unknown. In addition, AADC has also been found in a class of neurons that do not have any of the four neurotransmitters discussed above (Jaeger et al., 1983). These neurons may use one of the trace amines, tyramine, tryptamine, or phenylethylamine, as a neurotransmitter. [Pg.60]

Interneurons are found in all areas of the spinal cord gray matter. These neurons are quite numerous, small, and highly excitable they have many interconnections. They receive input from higher levels of the CNS as well as from sensory neurons entering the CNS through the spinal nerves. Many intemeurons in the spinal cord synapse with motor neurons in the ventral hom. These interconnections are responsible for the integrative functions of the spinal cord including reflexes. [Pg.67]


See other pages where Sensory excitation is mentioned: [Pg.29]    [Pg.19]    [Pg.22]    [Pg.332]    [Pg.11]    [Pg.203]    [Pg.204]    [Pg.204]    [Pg.424]    [Pg.427]    [Pg.431]    [Pg.619]    [Pg.29]    [Pg.19]    [Pg.22]    [Pg.332]    [Pg.11]    [Pg.203]    [Pg.204]    [Pg.204]    [Pg.424]    [Pg.427]    [Pg.431]    [Pg.619]    [Pg.513]    [Pg.76]    [Pg.295]    [Pg.304]    [Pg.161]    [Pg.74]    [Pg.183]    [Pg.203]    [Pg.207]    [Pg.218]    [Pg.220]    [Pg.340]    [Pg.385]    [Pg.205]    [Pg.492]    [Pg.269]    [Pg.650]    [Pg.146]    [Pg.148]    [Pg.9]    [Pg.80]    [Pg.104]    [Pg.104]   
See also in sourсe #XX -- [ Pg.619 ]




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Sensory excitation nerves

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