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Brain synaptic terminal

The aforementioned results are consistent with the view that the rat brain PCP/"sigma opiate" high-affinity receptor is associated with the voltage-regulated, non inactivating K channels in the pre-synaptic terminals. Thus, we reasoned that the elucidation of the molecular composition of this PCP "receptor" might provide direct information about the subunit composition of these K channels. [Pg.58]

The activity of the malate-aspartate shuttle increases during development in parallel with synaptogenesis, which is consistent with the high activity and importance of this shuttle in neurons and synaptic terminals. Evidence of highly regulated malate-aspartate shuttle in adult human brain has been documented [73 and references therein]. [Pg.542]

McKenna, M. C., Tildon, J. T., Stevenson, J. H. Jr etal. Regulation of energy metabolism in synaptic terminals and cultured rat brain astrocytes differences revealed using aminooxyacetate. Dev. Neurosci. 15 320-329,1993. [Pg.555]

Other drugs, like GHB and Rohypnol , can interact directly with the neurotransmitter receptors to either enhance or block the effects of the brain s own neurotransmitters. Still other drugs can alter the metabolic breakdown or clearance of certain neurotransmitters after they are released from the synaptic terminal, thereby altering how long the neurotransmitter affects the activity of other nearby neurons. [Pg.15]

Indirect mechanisms Nicotine has indirect effects on monoamine systems. A considerable amount of research has examined the relationships between nicotine and dopamine activity in the brain, in light of dopamine s role in reinforcement and nicotine s addictive properties. Nicotine increases dopamine turnover in the striatum and cerebral cortex (Clarke and Reuben 1996 Tani et al. 1997 Nanri et al. 1998). It also increases burst activity in dopamine neurons of the ventral tegmental area (VTA), a primary source of dopamine to the forebrain (Nisell et al. 1995 Fisher et al. 1998). Such a firing pattern in the VTA is associated with processes of reinforcement, learning, and cognitive activity. Nicotine actions on dopaminergic neurons occur at both somatodendritic sites and synaptic terminals. Further, both systemic nicotine and direct administration into the VTA increase dopamine release in the nucleus ac-... [Pg.109]

Roseth S, Fykse EM, Fonnum F (1995) Uptake of L-glutamate into rat brain synaptic vesicles effect of inhibitors that bind specifically to the glutamate transporter. J Neurochem 65 96-103 Ryan TA (1996) Endocytosis at nerve terminals timing is everything. Neuron 17 1035-7 Ryan TA, Smith SJ (1995) Vesicle pool mobilization during action potential firing at hippocampal synapses. Neuron 14 983-9... [Pg.43]

Crump FT, Fremeau RT, Craig AM (1999) Localization of the brain-specific high-affinity 1-proline transporter in cultured hippocampal neurons molecular heterogeneity of synaptic terminals. Mol Cell Neurosci 13 25-39. [Pg.100]

Conklin BR, Farfel Z, Lustig KD et al (1993) Substitution of three amino acids switches receptor specificity of Gq alpha to that of Gi alpha. Nature 363 274-6 Cousin MA, Robinson PJ (2000) Two mechanisms of synaptic vesicle recycling in rat brain nerve terminals. J Neurochem 75 1645-53... [Pg.246]

Glutamate is the primary excitatory neurotransmitter in the brain. Glutamate is formed by the Krebs cycle and is found free and stored in vesicles in synaptic terminals. Its release is calcium dependent, and an uptake system exists in presynaptic terminals and in glia to terminate its action after release. It is possible that glia metabolize glutamate to glutamine and return it to the neuron for reuse. An excessive release of glutamate can be lethal to cells in the immediate vicinity. [Pg.194]

It is interesting to notice that the characterization of the cellular and molecular mechanisms of the star fruit intoxication needs to pass through a group of different experimental protocols among them in vivo and the in vitro bioassays. The correlation between in vivo and in vitro models is then more complex that we should think it is [53]. Thus, the particular case of synaptosomes and GABA and glutamate release and re-uptake, shows neurochemical dynamics associated to star fruit intoxication mechanisms in a preparation which consists of isolated synaptic terminals (44). However, additional studies are needed with brain slices from control brains treated with the AcTx and even the use of ex vivo models in vitro bioassays from tissue after in vivo experiments), for example, in our case, brain slices from treated animals. [Pg.910]

McLaughlin BJ, Wood JG, Saito K, Barber R, Vaughn JE, Roberts E, Wu JY (1974) The fine structural localization of glutamate decarboxylase in synaptic terminals of rodent cerebellum. Brain Res 76 377-391. [Pg.110]

Mizuno N, Konishi A, Nakamura Y (1976) An electron microscope study of synaptic terminals of the spino-olivary fibers in the cat. Brain Res., 104, 303-308. [Pg.347]

Microelectrode suuctures have been created that mimic aspects of brain function. Amatore and coworkers have described assemblies of paired microband electrodes that behave like a neuronal synapse (26). The generator electrode in these devices mimics a synaptic terminal, and the collector electrode functions as a postsynaptic membrane. These artificial synapses can be designed in several configurations to perform Boolean logical operations, such as AND or OR operations. [Pg.177]


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