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Neurones aminergic

Figure 2.4 Flip-flop switch model of wake and slow wave sleep active systems. Mutually inhibitory connections exist between GABAergic/Galaninergic slow wave sleep active neurons in the ventrolateral preoptic area (VLPO) of the anterior hypothalamus and aminergic neurons in the hypothalamus (histamine (HA) neurons in the tuberomammillary nucleus (TMN)) and brainstem (serotonin (5-HT) neurons in the dorsal raphe (DR) and noradrenaline (NA) neurons in the locus coeruleus (LC)). Orexinergic neurons in the perifornical hypothalamus (PFH) stabilize the waking state via excitation of the waking side of the flip-flop switch (aminergic neurons). Figure 2.4 Flip-flop switch model of wake and slow wave sleep active systems. Mutually inhibitory connections exist between GABAergic/Galaninergic slow wave sleep active neurons in the ventrolateral preoptic area (VLPO) of the anterior hypothalamus and aminergic neurons in the hypothalamus (histamine (HA) neurons in the tuberomammillary nucleus (TMN)) and brainstem (serotonin (5-HT) neurons in the dorsal raphe (DR) and noradrenaline (NA) neurons in the locus coeruleus (LC)). Orexinergic neurons in the perifornical hypothalamus (PFH) stabilize the waking state via excitation of the waking side of the flip-flop switch (aminergic neurons).
The normally harmonious music of the aminergic neuronal spheres is contrapuntal to the brain stem cholinergic system, whose modulatory output is generally reciprocal to the aminergic groups and distinctly phasic and burstlike in character (rather than tonic and regular). In fact, the phasic bursts of acetylcholine (ACh) neuronal discharge appear to be strictly and precisely related to eye movement control by the paramedian reticular formation and the oculomotor system. [Pg.91]

Activation-synthesis model. (A) Systems model. (B) Wiring diagram. As a result of disinhibition caused by cessation of aminergic neuronal firing, brainstem reticular systems autoactivate. Their outputs have effects including depolarization of afferent terminals causing phasic presynaptic inhibition and blockade of external stimuli, especially during the bursts of REM, and postsynaptic hyperpolarization... [Pg.182]

As mentioned above, the existence of H3 receptors located presynaptically as heteroreceptors on other aminergic neurons, such as serotonergic, noradrenergic and dopaminergic neurons has been suggested [10-13], However, in a series of experiments we found that neither RmHA nor THIOP affected the ACTH response to serotonergic activation induced by administration of the 5-HT precursor 5-hydroxytryptophan in combination with the 5-HT re-uptake inhibitor fluoxetine [27],... [Pg.48]

The available data indicate that systemic administration of H3 receptor agonists oppose the stimulatory effect of endogenous HA on PRL secretion and that this effect, which is prevented by concomitant blockade of the H3 receptors, occurs on presynaptic histaminergic neurons rather than on other aminergic neurons. At least, the effect is not exerted via activation of H3 heteroreceptors on serotonergic neurons. [Pg.50]

However, receptor autoradiography and in vitro studies have suggested that H3 receptors are located on other aminergic neurons in the brain. Since amines such as serotonin and catecholamines are involved in the regulation of pituitary hormone secretion, it is obvious that an action of the H3 receptor compounds may be exerted via these H3 heteroreceptors. Only few studies have evaluated this heteroreceptor action. It has been excluded that the effect of the H3 receptor agonists is due to an effect on H3 receptors located on serotonergic neurons, while an effect on catecholaminergic neurons has yet not been excluded. [Pg.55]

J.C. Schwartz, J.M. Arrang, M. Garbarg, and H. Pollard, Hist-aminergic Neurons Morphology and Function. T. Watanabe and H. Wada eds. CRC Press Boca Raton. (1991)85. [Pg.264]

Fora basic account of synapses in general, see the text by Threadgold 877). Synapses have been examined in a number of genera, e.g. Diphyllobothrium, Echinococcus and Hymenolepis 277, 726,936,941,943). In the plerocercoid of Diphyllobothrium dendriticum, synapses are formed between neurites in which the presynaptic neurite contains (a) both dense-core vesicles and clear vesicles or b) small clear vesicles only (Fig. 2.10). The former correspond closely to the dense-core vesicles of aminergic neurones, and have been tentatively classified as aminergic synapses (277), whilst the latter are classified as cholinergic synapses. These neurones are discussed further below. [Pg.25]

Gustafsson, M. K. S. Wikgren, M. C. (1981a). Peptidergic and aminergic neurons in adult Diphyllobothrium dendriticum Nitzsch, 1824 (Cestoda, Pseudophyllidea). Zeitschrift fur Parasitenkunde, 64 121-34. [Pg.323]

Mann, J.J., Stanley, M., Gerson, S. and Rossor, M. (1980) Mental symptoms in Huntington s disease and a possible primary aminergic neuron lesion. Science 210 1369-1371. [Pg.495]

Imipramine blocked the uptake of dopamine at central aminergic neurons in the rat Lithium inhibited the electrically-induced release of NE and 5" in brain slices 3 and did not interfere with the transfer rate of Ma from blood to brain tissue. Data were reported which suggested that the therapeutic effect of electroshock treatment may be due to increased levels of brain amines 5 or to an increase in NE turnover rate . In a study of catecholamine turnover rates in mouse brain it was found that neuroleptics have a predominant influence on dopamine metabolism while antidepressants selectively affect NE metabolism, a higher rate of NE synthesis was found in the forebrain of "mouse-killing" rats over that of controls Imipramine blocked the muricidal behaviour9 and also lowered NE turnover . [Pg.16]


See other pages where Neurones aminergic is mentioned: [Pg.31]    [Pg.34]    [Pg.35]    [Pg.46]    [Pg.397]    [Pg.517]    [Pg.125]    [Pg.129]    [Pg.138]    [Pg.154]    [Pg.184]    [Pg.25]    [Pg.17]    [Pg.464]    [Pg.125]    [Pg.129]    [Pg.138]    [Pg.154]    [Pg.1077]    [Pg.144]    [Pg.145]    [Pg.790]    [Pg.443]   
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