Biosynthesis of taurine and enhancement of decar☐ylation of cysteine sulphinate and glutamate by the electrical stimulation of rat brain slices

1973 ◽  
Vol 55 (1) ◽  
pp. 173-178 ◽  
Author(s):  
S.S. Oja ◽  
M.-L. Karvonen ◽  
P. La¨hdesma¨ki
1995 ◽  
Vol 67 (4) ◽  
pp. 399-402
Author(s):  
Kaoru Kondo ◽  
Hitoshi Hashimoto ◽  
Kazuko Sakata ◽  
Hiroshi Saga ◽  
Jun-ichi Kitanaka ◽  
...  

2002 ◽  
Vol 950 (1-2) ◽  
pp. 186-194 ◽  
Author(s):  
Marisol R Lamprea ◽  
Fernando P Cardenas ◽  
Daniel Machado Vianna ◽  
Vanessa M Castilho ◽  
Sara Eugenia Cruz-Morales ◽  
...  

1994 ◽  
Vol 266 (3) ◽  
pp. R658-R667 ◽  
Author(s):  
K. Sugaya ◽  
W. C. De Groat

An in vitro neonatal (1-7 day) rat brain stem-spinal cord-bladder (BSB) preparation was used to examine the central control of micturition. Isovolumetric bladder contractions occurred spontaneously or were induced by electrical stimulation of the ventrolateral brain stem, spinal cord, bladder wall (ES-BW), or by perineal tactile stimulation (PS). Transection of the spinal cord at the L1 segment increased the amplitude of ES-BW- and PS-evoked contractions, and subsequent removal of the spinal cord further increased spontaneous and ES-BW-evoked contractions but abolished PS-evoked contractions. Hexamethonium (1 mM), a ganglionic blocking agent, mimicked the effect of cord extirpation. Tetrodotoxin (1 microM) blocked ES-BW- and PS-evoked contractions but enhanced spontaneous contractions. Bicuculline methiodide (10-50 microM), a gamma-aminobutyric acid A receptor antagonist, increased the amplitude of spontaneous, ES-BW- and PS-evoked contractions. These results indicate that PS-evoked contractions are mediated by spinal reflex pathways, whereas spontaneous and ES-BW-evoked contractions that are elicited by peripheral mechanisms are subject to a tonic inhibition dependent on an efferent outflow from the spinal cord. PS-evoked micturition is also subject to inhibitory modulation arising from sites rostral to the lumbosacral spinal cord. Although electrical stimulation of bulbospinal excitatory pathways can initiate bladder contractions in the neonatal rat, these pathways do not appear to have an important role in controlling micturition during the first postnatal week.


Science ◽  
1986 ◽  
Vol 232 (4746) ◽  
pp. 85-87 ◽  
Author(s):  
Kelso ◽  
TH Brown

An electrophysiological stimulation paradigm similar to one that produces Pavlovian conditioning was applied to synaptic inputs to pyramidal neurons of hippocampal brain slices. Persistent synaptic enhancement was induced in one of two weak synaptic inputs by pairing high-frequency electrical stimulation of the weak input with stimulation of a third, stronger input to the same region. Forward (temporally overlapping) but not backward (temporally separate) pairings caused this enhancement. Thus hippocampal synapses in vitro can undergo the conditional and selective type of associative modification that could provide the substrate for some of the mnemonic functions in which the hippocampus is thought to participate.


2005 ◽  
Vol 1 ◽  
pp. 1744-8069-1-2 ◽  
Author(s):  
Shui-Wang Ying ◽  
Peter A Goldstein

Propofol is a widely used intravenous general anesthetic. Propofol-induced unconsciousness in humans is associated with inhibition of thalamic activity evoked by somatosensory stimuli. However, the cellular mechanisms underlying the effects of propofol in thalamic circuits are largely unknown. We investigated the influence of propofol on synaptic responsiveness of thalamocortical relay neurons in the ventrobasal complex (VB) to excitatory input in mouse brain slices, using both current- and voltage-clamp recording techniques. Excitatory responses including EPSP temporal summation and action potential firing were evoked in VB neurons by electrical stimulation of corticothalamic fibers or pharmacological activation of glutamate receptors. Propofol (0.6 – 3 μM) suppressed temporal summation and spike firing in a concentration-dependent manner. The thalamocortical suppression was accompanied by a marked decrease in both EPSP amplitude and input resistance, indicating that a shunting mechanism was involved. The propofol-mediated thalamocortical suppression could be blocked by a GABAA receptor antagonist or chloride channel blocker, suggesting that postsynaptic GABAA receptors in VB neurons were involved in the shunting inhibition. GABAA receptor-mediated inhibitory postsynaptic currents (IPSCs) were evoked in VB neurons by electrical stimulation of the reticular thalamic nucleus. Propofol markedly increased amplitude, decay time, and charge transfer of GABAA IPSCs. The results demonstrated that shunting inhibition of thalamic somatosensory relay neurons by propofol at clinically relevant concentrations is primarily mediated through the potentiation of the GABAA receptor chloride channel-mediated conductance, and such inhibition may contribute to the impaired thalamic responses to sensory stimuli seen during propofol-induced anesthesia.


Sign in / Sign up

Export Citation Format

Share Document