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Synaptic input

A second less frequent type of synapse forms asymmetric synapses along all portions of the dendrites of pallidal neurons. These inputs have been demonstrated, using anterograde tracing with PHA-L, to arise from the subthalamic nucleus (Kita and Kitai 1987). [Pg.399]

Descending output of the globus pallidus to other components of the basal ganglia is directed principally to the subthalamic nucleus and to the entopeduncular nucleus (internal segment of the globus pallidus in primates) and the substantia nigra (Haber [Pg.399]

Of particular note is the synaptic organization of pallidal projection terminals, particularly those that provide input to the internal pallidal and substantia nigra neurons. Pallidal afferents onto these neurons is directed to the cell soma and proximal dendrites, whereas the striatal afferent input is directed to the same neurons more distal dendrites (Smith and Bolam 1989, 1990, 1991). The organization of these projections will be discussed in more detail below. [Pg.400]


Altered density of voltage-dependent ion currents in neurons Such changes may considerably affect the firing properties of neurons. They may also affect how neurons integrate a given synaptic input. [Pg.126]

The M-channels (M for muscarine) are expressed in the peripheral sympathetic neurons and CNS. In the absence of acetylcholine, the M-channel opens at resting membrane potential and dampens neuronal responsiveness to synaptic inputs. Acetylcholine inhibits M-channel activity by activation of Ml receptor. [Pg.739]

The primary role of the sodium channels is to generate action potentials in excitable cells. In case of neurons, the sodium channel density is high at axon hillocks or axon initial segment where action potentials start to propagate. The sodium channels are also present in dendrites. The sodium channels contribute to amplifying synaptic inputs (particularly those distally located) and are actively involved in back propagation of action potentials into dendrites. Subtle differences in properties of sodium channels influence the dendritic processes of synaptic integration in and complex ways. [Pg.1305]

In the CNS there are many forms of neuronal organisation. One neuron can have many synaptic inputs and a multiplicity of NTs and NT effects are utilised within a complex interrelationship of neurons. There are also positive and negative feedback circuits as well as presynaptic influences all designed to effect changes in excitability and frequency of neuronal firing, i.e. patterns of neuronal discharge. [Pg.22]

Chen W.P., Witkin J.W. and Silverman A.J. (1990). Sexual dimorphism in the synaptic input to gonadotropin-releasing hormone neurons. Endocrinology 126, 695-702. [Pg.196]

Tamiya, R. (1991). Synaptic inputs to histaminergic neurons in the rat posterior hypothalamus. Osaka City Med. J. 37, 107-22. [Pg.176]

Chamberlin, N. L., Arrigoni, E., Chou, T. C. et al. (2003). Effects of adenosine on gabaergic synaptic inputs to identified ventrolateral preoptic neurons. Neuroscience 119 (4), 913-18. [Pg.354]

Analyses of afferents of dentate granule cells from epileptic animals reveal abnormal inhibitory and excitatory synaptic input 633... [Pg.629]

Inflammatory pain results from changes both in primary sensory and dorsal horn neurons. The alterations in primary sensory neurons fall into two broad categories (a) a reduction in threshold and an increase in the response of the peripheral terminals of nociceptors (peripheral sensitization), and (b) an alteration in transmitter content modifying synaptic input to the spinal cord. In the dorsal horn, peripheral inflammation results in an increase in membrane excitability and synaptic efficacy, which is the phenomenon of central sensitization [12]. [Pg.933]

Figure 17.4. Epigenetics in the nervous system. Regulation occurs in response to synaptic inputs and/or other psychosocial-environmental stimuli. The external stimuli result in changes in the transcriptional profile of the neuron and eventually affects neural function(s). Many disorders of human cognition might involve dysfunction of epigenetic tagging. (See color insert.)... Figure 17.4. Epigenetics in the nervous system. Regulation occurs in response to synaptic inputs and/or other psychosocial-environmental stimuli. The external stimuli result in changes in the transcriptional profile of the neuron and eventually affects neural function(s). Many disorders of human cognition might involve dysfunction of epigenetic tagging. (See color insert.)...
Dendritic spine a small sac of membrane that protrudes from the dendrites of some cells and receives synaptic input. [Pg.391]

A. Atropine has little effect on blood pressure in the absence of a circulating muscarinic agonist because the muscarinic receptors on endothelial cells do not receive synaptic input. Therefore, the blood pressure of a healthy patient will not change with treatment with atropine. In contrast, patients being treated with an AQiE inhibitor may have slightly elevated plasma ACh levels, and patients being treated with bethanechol may be hypotensive because of its direct actions on the muscarinic receptors on endothelial cells. [Pg.140]

Wooley, C.S., Weiland, N.G., McEwen, B.S., and Schwartzkroin, P.A. (1997) Estradiol increases sensistivity of hippocampal CAl pyramidal cells to NMDA receptor-mediated synaptic input correlation with dendritic spine density. J Neurosci 17 1848— 1859. [Pg.19]

Neuron A, shown at left, receives synaptic inputs from many neurons and sends its axon to make synapses with neuron B and others. Extensions called dendrites branch out from the cell body—the soma—and are the sites of many synapses. [One synapse is shown magnified.)... [Pg.74]

Finnegan TF, Chen SR, Pan HL (2005) Effect of the p opioid on exdtatory and inhibitory synaptic inputs to periqueductal gray-projecting neurons in the amygdala. J Pharmacol Exp Ther 312 441-8... [Pg.430]

Neural production and release of ECs is likely to be stimulated by repetitive firing of neurons or repetitive synaptic input to a neuron rather than the prolonged depolarization used to initiate DSE/I. Investigators have now discovered a number of patterns of neuronal activity that generate short-lasting EC-dependent synaptic depression in different brain regions. The majority of these involve activation of neurotransmitter receptors or brief periods of repetitive synaptic activation (see Chevaleyre et al. 2006 for review). [Pg.451]

It is tempting to speculate that disinhibitory effects of endocannabinoids would promote learning, while endocannabinoid-mediated reductions in excitatory tran-mission underly amnestic effects. Thus, the role of the endocannabinoid system in learning and memory would depend on which synaptic inputs within a given brain region contain the receptor, and which inputs are activated during a given phase of... [Pg.464]

Walsh JP (1993) Depression of excitatory synaptic input in rat striatal neurons. Brain Res 608(1) 123-8... [Pg.478]

Derbenev AV, Monroe MJ, Glatzer NR, Smith BN (2006) Vanilloid-mediated heterosynaptic facilitation of inhibitory synaptic input to neurons of the rat dorsal motor nucleus of the vagus. J Neurosci 26 9666-72... [Pg.517]

Fuder H, Muscholl E (1995) Heteroreceptor-mediated modulation of noradrenaline and acetylcholine release from peripheral nerves. Rev Physiol Biochem Pharmacol 126 265 412 Funahashi M, Mitoh Y, Matsuo R (2004a) Activation of presynaptic 5-HT3 receptors facilitates glutamatergic synaptic inputs to area postrema neurons in rat brain slices. Methods Find Exp Clin Pharmacol 26 615-22... [Pg.518]

Within the AL several types of synaptic interactions take place. Both LNs and PNs receive synaptic input direct from ORNs. ORNs also receive input synapses, but only from LNs. PNs and LNs synapse with each other and also with neurons of the same type. The incoming ORN signal can thus be transferred to the output neurons (PNs) via a number of possible paths. [Pg.701]

Blasco-Ibanez, J. M., and Freund, T. F. (1995). Synaptic input of horizontal interneurons in stratum oriens of the hippocampal CA1 subfield Structural basis of feed-back activation. Eur. J. Neurosci. 7, 2170-2180. [Pg.347]

Stanford IM, Lacey MG. Differential actions of serotonin, mediated by 5-HT1B and 5-HT2C receptors, on GABA-mediated synaptic input to rat substantia nigra pars reticulata neurons in vitro. J Neurosci 1996 16 7566-7573. [Pg.305]

Li Y, Bayliss DA. Presynaptic inhibition by 5-HT1B receptors of glutamatergic synaptic inputs onto serotonergic caudal raphe neurones in rat. J Physiol 1998 510 121-134. [Pg.399]


See other pages where Synaptic input is mentioned: [Pg.993]    [Pg.240]    [Pg.6]    [Pg.282]    [Pg.633]    [Pg.922]    [Pg.926]    [Pg.933]    [Pg.933]    [Pg.934]    [Pg.118]    [Pg.124]    [Pg.328]    [Pg.31]    [Pg.126]    [Pg.103]    [Pg.343]    [Pg.521]    [Pg.334]    [Pg.437]    [Pg.470]    [Pg.511]    [Pg.684]    [Pg.385]    [Pg.386]   
See also in sourсe #XX -- [ Pg.67 ]




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