Brain extracellular potassium and genera anaesthetics

1978 ◽  
Vol 56 (5) ◽  
pp. 863-872 ◽  
Author(s):  
M. E. Morris

General anaesthetic agents (halothane, trichlorethylene, methohexital, pentobarbital, and alphaxalone–alphadolone) depress the extracellular accumulations (ΔEk) and associated focal potentials (ΔV) which are evoked in the cuneate nucleus by tetanic stimulation of peripheral nerves. Depressions of ΔV are significantly greater than those of ΔEk; at the same time there is a dissociation of the relation between ΔV and ΔEk. There are no detectable changes in the resting levels of K+ or the small voltage shifts evoked by low-frequency intranuclear stimulation with a microelectrode. When anaesthesia produces severe hypotension, augmentations of [K+]0 occur which can be attributed to depression of electrogenic Na–K pumping. A possible explanation of the reduction in K+ release resulting from afferent fibre activity would be failure of conduction caused by membrane stabilization or hyperpolarization.

1975 ◽  
Vol 53 (5) ◽  
pp. 912-922 ◽  
Author(s):  
K. Krnjević ◽  
M. E. Morris

There is a clear, positive correlation in amplitude between changes in potassium potentials (ΔEK) and focal potentials (ΔV) evoked by tetanic stimulation of afferent nerves in the cuneate nucleus and dorsal horn of cats under Dial anaesthesia or after decerebration. Data obtained with stimulations at various frequencies and intensities, or recording at different positions give a relatively constant slope of ΔV/ΔEK (varying between 0.2 and 0.6 in different experiments). These observations are fully consistent with the possibility that ΔV mainly reflects changes in extracellular potassium concentration caused by the release of K+ from active terminals. Differences in time course of ΔEK and ΔV evoked by single stimuli are a steep function of distance and therefore can be ascribed to the slowness of diffusion, without excluding the possibility of an early additional depolarizing effect by another mechanism.


2007 ◽  
Vol 35 (06) ◽  
pp. 987-993 ◽  
Author(s):  
Byeol-Rim Kang ◽  
Chang-Beohm Ahn ◽  
Byung-Tae Choi

We investigated whether the 2 Hz electroacupuncture (EA) analgesia is associated with phosphorylation of N-methyl-D-aspartate receptor (NMDAR) NR-1 subunits and NMDAR antagonism in the lumbar spinal cord of rats. EA stimulation produced an increase of serine phosphorylation of NMDAR NR-1 subunits in the spinal cord as compared with normal conditions. However, the intrathecal injection of NMDAR antagonist D-2-amino-5-phosphonopentanoic acid significantly prevented serine phosphorylation of NMDAR NR-1 subunits induced by EA stimulation in the dorsal horn of spinal cord. These results indicate that EA analgesia by stimulation of peripheral nerves may be involved in an increase of NR-1 serine phosphorylation in the dorsal horn of the spinal cord.


2021 ◽  
Vol 11 (5) ◽  
pp. 639
Author(s):  
David Bergeron ◽  
Sami Obaid ◽  
Marie-Pierre Fournier-Gosselin ◽  
Alain Bouthillier ◽  
Dang Khoa Nguyen

Introduction: To date, clinical trials of deep brain stimulation (DBS) for refractory chronic pain have yielded unsatisfying results. Recent evidence suggests that the posterior insula may represent a promising DBS target for this indication. Methods: We present a narrative review highlighting the theoretical basis of posterior insula DBS in patients with chronic pain. Results: Neuroanatomical studies identified the posterior insula as an important cortical relay center for pain and interoception. Intracranial neuronal recordings showed that the earliest response to painful laser stimulation occurs in the posterior insula. The posterior insula is one of the only regions in the brain whose low-frequency electrical stimulation can elicit painful sensations. Most chronic pain syndromes, such as fibromyalgia, had abnormal functional connectivity of the posterior insula on functional imaging. Finally, preliminary results indicated that high-frequency electrical stimulation of the posterior insula can acutely increase pain thresholds. Conclusion: In light of the converging evidence from neuroanatomical, brain lesion, neuroimaging, and intracranial recording and stimulation as well as non-invasive stimulation studies, it appears that the insula is a critical hub for central integration and processing of painful stimuli, whose high-frequency electrical stimulation has the potential to relieve patients from the sensory and affective burden of chronic pain.


1988 ◽  
Vol 73 (3) ◽  
pp. 481-488 ◽  
Author(s):  
T. Winkler ◽  
E. St�lberg

1991 ◽  
Vol 65 (1) ◽  
pp. 20-32 ◽  
Author(s):  
Y. Komatsu ◽  
S. Nakajima ◽  
K. Toyama

1. Intracellular recording was made from layer II-III cells in slice preparations of kitten (30-40 days old) visual cortex. Low-frequency (0.1 Hz) stimulation of white matter (WM) usually evoked an excitatory postsynaptic potential (EPSP) followed by an inhibitory postsynaptic potential (IPSP). The postsynaptic potentials (PSPs) showed strong dependence on stimulus frequency. Early component of EPSP and IPSP evoked by weak stimulation both decreased monotonically at frequencies greater than 0.5-1 Hz. Strong stimulation similarly depressed the early EPSP at higher frequencies (greater than 2 Hz) and replaced the IPSP with a late EPSP, which had a maximum amplitude in the stimulus frequency range of 2-5 Hz. 2. Very weak WM stimulation sometimes evoked EPSPs in isolation from IPSPs. The falling phase of the EPSP revealed voltage dependence characteristic to the responses mediated by N-methyl-D-aspartate (NMDA) receptors and was depressed by application of an NMDA antagonist DL-2-amino-5-phosphonovalerate (APV), whereas the rising phase of the EPSP was insensitive to APV. 3. The early EPSPs followed by IPSPs were insensitive to APV but were replaced with a slow depolarizing potential by application of a non-NMDA antagonist 6,7-dinitro-quinoxaline-2,3-dione (DNQX), indicating that the early EPSP is mediated by non-NMDA receptors. The slow depolarization was mediated by NMDA receptors because it was depressed by membrane hyperpolarization or addition of APV. 4. The late EPSP evoked by higher-frequency stimulation was abolished by APV, indicating that it is mediated by NMDA receptors, which are located either on the recorded cell or on presynaptic cells to the recorded cells. 5. Long-term potentiation (LTP) of EPSPs was examined in cells perfused with solutions containing 1 microM bicuculline methiodide (BIM), a gamma-aminobutyric acid (GABA) antagonist. WM was stimulated at 2 Hz for 15 min as a conditioning stimulus to induce LTP, and the resultant changes were tested by low-frequency (0.1 Hz) stimulation of WM. 6. LTP of early EPSPs occurred in more than one-half of the cells (8/13) after strong conditioning stimulation. The rising slope of the EPSP was increased 1.6 times on average. 7. To test involvement of NMDA receptors in the induction of LTP in the early EPSP, the effect of conditioning stimulation was studied in a solution containing 100 microM APV, which was sufficient to block completely synaptic transmission mediated by NMDA receptors. LTP occurred in the same frequency and magnitude as in control solution.


1993 ◽  
Vol 69 (3) ◽  
pp. 953-964 ◽  
Author(s):  
P. W. Glimcher ◽  
D. L. Sparks

1. The first experiment of this study determined the effects of low-frequency stimulation of the monkey superior colliculus on spontaneous saccades in the dark. Stimulation trains, subthreshold for eliciting short-latency fixed-vector saccades, were highly effective at biasing the metrics (direction and amplitude) of spontaneous movements. During low-frequency stimulation, the distribution of saccade metrics was biased toward the direction and amplitude of movements induced by suprathreshold stimulation of the same collicular location. 2. Low-frequency stimulation biased the distribution of saccade metrics but did not initiate movements. The distribution of intervals between stimulation onset and the onset of the next saccade did not differ significantly from the distribution of intervals between an arbitrary point in time and the onset of the next saccade under unstimulated conditions. 3. Results of our second experiment indicate that low-frequency stimulation also influenced the metrics of visually guided saccades. The magnitude of the stimulation-induced bias increased as stimulation current or frequency was increased. 4. The time course of these effects was analyzed by terminating stimulation immediately before, during, or after visually guided saccades. Stimulation trains terminated at the onset of a movement were as effective as stimulation trains that continued throughout the movement. No effects were observed if stimulation ended 40–60 ms before the movement began. 5. These results show that low-frequency collicular stimulation can influence the direction and amplitude of spontaneous or visually guided saccades without initiating a movement. These data are compatible with the hypothesis that the collicular activity responsible for specifying the horizontal and vertical amplitude of a saccade differs from the type of collicular activity that initiates a saccade.


1981 ◽  
Vol 44 (4) ◽  
pp. 207-217 ◽  
Author(s):  
Don M. Long ◽  
Donald Erickson ◽  
James Campbell ◽  
Richard North

Sign in / Sign up

Export Citation Format

Share Document