1,721,022 research outputs found

    Colture cellulari e loro applicazioni in neurobiologia

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    La comprensione delle complesse interazioni tra il genoma e l'ambiente, che portano alla formazione di un nuovo individuo e quindi del suo sistema nervoso, e la fisiologia di quest'ultimo, a maturazione completata, è condizione indispensabile per affrontare lo studio delle malattie neurologiche e probabilmente anche per la comprensione di alcune patologie psichiatrich

    Blockade of 5-hydroxytryptamine (serotonin)-2 receptors alters interleukin-1-induced changes in rat sleep

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    Recent data suggest that interleukin-1-induced enhancement of non-rapid eye movement sleep is mediated, in part, by the serotonergic system. To determine if sleep changes induced by interleukin-1 are mediated by a specific serotonergic receptor subtype, we evaluated interleukin-1 effects on sleep in rats pretreated with the 5-hydroxytryptamine (serotonin)-2 receptor antagonist ritanserin. Ritanserin (0.63 mg/kg, intraperitoneally) by itself did not alter sleep-wake behavior, although it did reduce cortical brain temperature. Interleukin-1 (5 ng, intracerebroventricularly) enhanced non-rapid eye movement sleep, suppressed rapid eye movement sleep, and induced a moderate febrile response. Pretreatment with ritanserin completely blocked the febrile response to interleukin-1 and abolished the interleukin-1-induced enhancement in non-rapid eye movement sleep that occurred during postinjection hours 3-4, without altering interleukin-1 effects on rapid eye movement sleep. The present data suggest that serotonin may partially mediate interleukin-1 effects on sleep by interacting with 5-hydroxytryptamine (serotonin)-2 receptors. These results also suggest that interactions between the serotonergic system and interleukin-1 may be important in regulating sleep-wake behavior. (C) 1999 IBRO. Published by Elsevier Science Ltd

    Muramyl dipeptide and IL-1 effects on sleep and brain temperature after inhibition of serotonin synthesis

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    The role of the interactions between serotonin (5-HT) and muramyl dipeptide (MDP) and interleukin-1 (IL-1) in sleep control and thermoregulation was evaluated To this purpose, MDP and IL-1 were injected intracerebroventricularly at dark onset into freely moving rats pretreated twice intraperitoneally with para-chlorophenylalanine (PCPA) (300 mg/kg), which depletes brain 5-HT and causes insomnia. Fever and slow-wave sleep (SWS) enhancement induced by 150 pmol MDP were completely blocked in PCPA-pretreated rats. Only the first phase of the biphasic increase in SWS induced by 2.5 ng IL-1 was suppressed by PCPA pretreatment, whereas fever remained unaffected. These results suggest that 1) MDP effects on both sleep-wake activity and brain cortical temperature are mediated by the serotonergic system; 2) the mechanisms mediating the first and the second phases of IL-1-induced SWS excess are different: 5-HT could be involved in the first phase, but not in the second one; and 3) the 5-HT system does not appear to be involved in IL-l-induced fever

    L’encefalina inibisce l’influsso di Ca2+ attraverso i canali del Ca2+ voltaggio-dipendenti in neuroni sensoriali periferici e centrali di mammifero.

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    RIASSUNTO E' stato studiato l'effetto della D-ala2-D-leu5-encefalina (DADLE) 400 nM sulle correnti di calcio HVA (High Voltage Activated) e LVA (Low Voltage Activated). Gli esperimenti sono stati condotti su neuroni dei gangli delle radici dorsali e del talamo ventrobasale di ratto con la tecnica del patch-clamp whole-cell. La DADLE inibiva le correnti di Ca2+ HVA sia dei neuroni periferici (-59% +/-2.47 SEM n = 39 su 43 registrati) che centrali (-67% +/-3.2 n = 22 su 27), mentre solo nei neuroni talamici le correnti di Ca2+ LVA erano sensibili all' effetto della DADLE (-40% +/-3.3 n = 4 su 11). Nei neuroni periferici si potevano distinguere due tipi di modulazione: una dipendente e l'altra indipendente dal voltaggio. I risultati suggeriscono due distinti ruoli funzionali della inibizione esercitata dalla DADLE sulle correnti di Ca2+ HVA dei neuroni periferici. La DADLE potrebbe esercitare inoltre un ruolo significativo nel controllo della scarica ritmica dei neuroni di relè talamici

    CHANGES IN SPONTANEOUS ACTIVITY OF MEDIALIS DORSALIS THALAMIC NEURONS DURING SLEEP AND WAKEFULNESS

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    In chronic unanaesthetized cats unitary activity of medialis dorsalis (MD) thalamic neurones was recorded during wakefulness (W), slow wave (SWS) and desynchronized (DS) sleep. The discharge pattern of these neurones changes during SWS compared to W. Comparison between desynchronization of W and DS shows a change in the mean frequency, being higher in W than in DS. The results suggest that MD neurones participate in the organization of the sleep-wakefulness cycle

    Low-voltage activated calcium channels are differently affected by nimodipine

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    Voltage-dependent Ca2+ channels in adult rat sensory neurones were studied as far as their characterization and nimodipine effects are concerned, using patch-clamp whole-cell technique. Low-voltage activated (LVA) Ca2+ currents were identified according to activation and inactivation kinetics and sensitivity to amiloride. Nimodipine (10 nM) caused a decrease in LVA Ca2+ current amplitude (-40% +/- 2.2 s.e.m., n = 11 out of 30 with LVA Ca2+ currents). Conversely, in 6 neurones out of 30 nimodipine increased the Ca2+ current amplitude (+ 10% +/- 2). In some unaffected neurones (n = 5) nimodipine was also tested at higher concentrations (up to 5 microM) without any appreciable effect. In conclusion, nimodipine was partly able to block LVA calcium channels even at nanomolar concentrations. Supposing nimodipine acts directly on the channel, it can be assumed that there may be different types of LVA calcium channels in sensory neurones

    CHANGES IN SLEEP WAKING CYCLE INDUCED BY LESIONS OF MEDIALIS DORSALIS THALAMIC NUCLEI IN THE CAT

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    Bilateral lesions of medialis dorsalis (MD) thalamic nuclei in chronically implanted cats disrupt the sleep-waking cycle by inducing a reduction of both slow-wave and desynchronized sleep and a corresponding increase of wakefulness. Bilateral lesions of the anterior thalamic group produce some postural deficits but no changes in the percentage of sleep and wakefulness. The hypothesis that MD lesions alter the sleep processes by interrupting an anterior forebrain-MD-cortical link has been put forward

    Sleep is differently modulated by basal forebrain GABA(A) and GABA(B) receptors

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    There is evidence that GABA plays a major role in sleep regulation. GABA(A) receptor agonists and different compounds interacting with the GABA(A) receptor complex, such as barbiturates and benzodiazepines, can interfere with the sleep/wake cycle. On the other hand, there is very little information about the possible role of GABA(B) receptors in sleep modulation. The nucleus basalis of Meynert (NBM), a cholinergic area in the basal forebrain, plays a pivotal role in the modulation of sleep and wakefulness, and both GABA(A) and GABA(B) receptors have been described within the NBM. This study used unilateral infusions in the NBM to determine the effects of 3-hydroxy-5-aminomethylisoxazole hydrobromide (muscimol hydrobromide, a GABA(A) receptor subtype agonist) and beta-(aminomethyl)-4-chlorobenzenepropanoic acid (baclofen, a GABA(B) receptor subtype agonist) on sleep parameters in freely moving rats by means of polygraphic recordings. Muscimol (0.5 nmol) and baclofen (0.7 nmol) induced an increase in slow-wave sleep and an inhibition of wakefulness. Muscimol, but not baclofen, also caused a decrease in desynchronized sleep parameters. The results reported here indicate that 1) the NBM activation of both GABA(A) and GABA(B) receptors influences the sleep/wake cycle, and 2) GABA(A) but not GABA(B) receptors are important for desynchronized sleep modulation, suggesting that the two GABAergic receptors play different roles in sleep modulation

    Stimulation of NMDA and AMPA receptors in the rat nucleus basalis of Meynert affects sleep

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    The nucleus basalis of Meynert (NBM), a heterogeneous area in the basal forebrain involved in the modulation of sleep and wakefulness, is rich in glutamate receptors, and glutamatergic fibers represent an important part of the input to this nucleus. With the use of unilateral infusions in the NBM, the effects of two different glutamatergic subtype agonists, namely N-methyl-D-aspartic acid (NMDA and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) hydrobromide, on sleep and wakefulness parameters were def;ermined in fi eely moving rats by means of polygraphic recordings. NMDA (5 nmol) and AMPA (0.4 nmol) induced an increase in wakefulness and an inhibition of slow-wave sleep. AMPA, but not NMDA, also caused a decrease in desynchronized sleep. These AMPA- and NMDA-mediated effects were counteracted by a pretreatment with the specific NMDA antagonist 2-amino-5-phosphonopentanoic acid (20 nmol) and the specific AMPA antagonist 6,7-dinitroquinoxaline-2,3-dione (2 nmol), respectively. The results reported here indicate that 1) the NBM activation of both NMDA and AMPA glutamate receptors exert a modulatory influence on sleep and wakefulness, and 2) AMPA, but not NMDA receptors, are involved in the modulation of desynchronized sleep, suggesting a different role for NBM NMDA and non-NMDA receptors in sleep modulation

    Responses of VPL thalamic neurones to peripheral stimulation in wakefulness and sleep

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    In unanaesthetized, undrugged, normally respiring cats extracellular recordings were obtained from ventroposterolateral thalamic units through different states of the sleep-waking cycle. An air-puff peripheral stimulation was used to activate the recorded neurones. State-dependent changes of the response of thalamic neurones were shown, comparing slow-wave sleep (SWS) to wakefulness (W). During SWS an increase was observed in the strength of the discharge suppression, which follows the excitatory peak in the typical response pattern. Also the cell excitability is further reduced in slow-wave sleep during the 150-200 ms period following an excitatory response, suggesting that an enhancement of the post-excitatory inhibition could be involved in the generation of the slow 5-6 Hz rhythms, observed during thalamic and cortical synchronization
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