scholarly journals Neurophysiological effects of corticotropin-releasing factor in the undergoing sections of the olfactory area of the rat cerebral cortex

2003 ◽  
Vol 49 (1) ◽  
pp. 51-53 ◽  
Author(s):  
A. A. Mokrushin ◽  
V. G. Shalyapina
Keyword(s):  
Cerebral Cortex ◽  
Olfactory Cortex ◽  
Corticotropin Releasing Factor ◽  
Posttetanic Potentiation ◽  
Postsynaptic Potentials ◽  
Corticotrophin Releasing Factor ◽  
Inhibitory Postsynaptic Potentials ◽  
Cortex Slices ◽  
Focal Potentials

Application of corticotrophin-releasing factor (CPF) in concen­trations of 10-9-10-8 M on the rat olfactory cortex slices induced activation of the pre- and postsynaptic excitatory components of the focal potentials recorded in the slices. The amplitude and du­ration of α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic and N-methyl-D-aspartate components of postsynaptic evoking potentials increased upon exposure to CRF, while the amplitude of GABAB-mediated inhibitory postsynaptic potentials was sup­pressed. At higher concentrations of CRF (10-8 M) epileptiform charges were recorded in the cells. CRF effects were reversible and eliminated after washing. A long (90 min) exposure induced the phenomena similar to long-term posttetanic potentiation. The findings suggest that CRF has pronounced activating properties and ajfects the glutamatergic and GABAergic systems.

2-Deoxyglucose–Induced Long-Term Potentiation of Monosynaptic IPSPs in CA1 Hippocampal Neurons

2000 ◽  
Vol 83 (2) ◽  
pp. 879-887 ◽  
Author(s):  
Krešimir Krnjević ◽  
Yong-Tao Zhao
Keyword(s):  
Hippocampal Neurons ◽  
Long Term Potentiation ◽  
Inhibitory Synapses ◽  
Current Clamp ◽  
Glutamate Antagonists ◽  
Postsynaptic Potentials ◽  
Postsynaptic Currents ◽  
Inhibitory Postsynaptic Potentials ◽  
Term Potentiation

In previous experiments on excitatory synaptic transmission in CA1, temporary (10–20 min) replacement of glucose with 10 mM 2-deoxyglucose (2-DG) consistently caused a marked and very sustained potentiation (2-DG LTP). To find out whether 2-DG has a similar effect on inhibitory synapses, we recorded pharmacologically isolated mononosynaptic inhibitory postsynaptic potentials (IPSPs; under current clamp) and inhibitory postsynaptic currents (IPSCs; under voltage clamp); 2-DG was applied both in the presence and the absence of antagonists of N-methyl-d-aspartate (NMDA). In spite of sharply varied results (some neurons showing large potentiation, lasting for >1 h, and many little or none), overall there was a significant and similar potentiation of IPSP conductance, both for the early (at ≈30 ms) and later (at ≈140 ms) components of IPSPs or IPSCs: by 35.1 ± 10.25% (mean ± SE; for n = 24, P = 0.0023) and 36.5 ± 16.3% (for n = 19, P = 0.038), respectively. The similar potentiation of the early and late IPSP points to a presynaptic mechanism of LTP. Overall, the LTP was statistically significant only when 2-DG was applied in the absence of glutamate antagonists. Tetanic stimulations (in presence or absence of glutamate antagonists) only depressed IPSPs (by half). In conclusion, although smaller and more variable, 2-DG–induced LTP of inhibitory synapses appears to be broadly similar to the 2-DG–induced LTP of excitatory postsynaptic potentials previously observed in CA1.

scholarly journals Cholinergic Agonist Carbachol Enables Associative Long-Term Potentiation in Piriform Cortex Slices

1998 ◽  
Vol 80 (5) ◽  
pp. 2467-2474 ◽  
Author(s):  
Madhvi M. Patil ◽  
Christiane Linster ◽  
Eugene Lubenov ◽  
Michael E. Hasselmo
Keyword(s):  
Piriform Cortex ◽  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Afferent Input ◽  
Cholinergic Agonist ◽  
Inhibitory Postsynaptic Potentials ◽  
Term Potentiation ◽  
Cortex Slices ◽  
Association Fibers

Patil, Madhvi M., Christiane Linster, Eugene Lubenov, and Michael E. Hasselmo. Cholinergic agonist carbachol enables associative long-term potentiation in piriform cortex slices. J. Neurophysiol. 80: 2467–2474, 1998. Pyramidal cells in piriform (olfactory) cortex receive afferent input from the olfactory bulb as well as intrinsic association input from piriform cortex and other cortical areas. These two functionally distinct inputs terminate on adjacent apical dendritic segments of the pyramidal cells located in layer Ia and layer Ib of piriform cortex. Studies with bath-applied cholinergic agonists have shown suppression of the fast component of the inhibitory postsynaptic potentials (IPSPs) evoked by stimulation of the association fibers. It was previously demonstrated that an associative form of LTP can be induced by coactivation of the two fiber systems after blockade of the fast, γ-aminobutyric acid-A–mediated IPSP. In this report, we demonstrate that an associative form of long-term potentiation can be induced by coactivation of afferent and intrinsic fibers in the presence of the cholinergic agonist carbachol.

29. Phospholipid methylation during long-term potentiation in rat olfactory cortex slices

1994 ◽  
Vol 52 (1) ◽  
pp. A13-A14
Author(s):  
I.A. Gerassimova ◽  
A.A. Mokrushin ◽  
L.I. Pavlinova ◽  
N.A. Emelyanov
Keyword(s):  
Long Term Potentiation ◽  
Olfactory Cortex ◽  
Term Potentiation ◽  
Cortex Slices

scholarly journals Pre-motor versus motor cerebral cortex neuromodulation for chronic neuropathic pain

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Igor Lavrov ◽  
Timur Latypov ◽  
Elvira Mukhametova ◽  
Brian Lundstrom ◽  
Paola Sandroni ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Cerebral Cortex ◽  
Motor Cortex ◽  
Initial Assessment ◽  
Motor Cortex Stimulation ◽  
Chronic Neuropathic Pain ◽  
Long Term Effect ◽  
Stimulation Of

AbstractElectrical stimulation of the cerebral cortex (ESCC) has been used to treat intractable neuropathic pain for nearly two decades, however, no standardized approach for this technique has been developed. In order to optimize targeting and validate the effect of ESCC before placing the permanent grid, we introduced initial assessment with trial stimulation, using a temporary grid of subdural electrodes. In this retrospective study we evaluate the role of electrode location on cerebral cortex in control of neuropathic pain and the role of trial stimulation in target-optimization for ESCC. Location of the temporary grid electrodes and location of permanent electrodes were evaluated in correlation with the long-term efficacy of ESCC. The results of this study demonstrate that the long-term effect of subdural pre-motor cortex stimulation is at least the same or higher compare to effect of subdural motor or combined pre-motor and motor cortex stimulation. These results also demonstrate that the initial trial stimulation helps to optimize permanent electrode positions in relation to the optimal functional target that is critical in cases when brain shift is expected. Proposed methodology and novel results open a new direction for development of neuromodulation techniques to control chronic neuropathic pain.

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