Changes of extracellular potassium concentration during spontaneous activity in the mesencephalic reticular formation of the rat.
Explore the source record for details and available documents.
Action Potentials↗
Biomedical subjects
E Syková
Publications and source records attributed to E Syková.
Changes of extracellular potassium concentration induced by neuronal activity in the sinal cord of the cat.
1. Changes of extracellular K(+) concentration, [K](e), arising in the spinal cord of the cat in response to an afferent stimulation were studied by means of K(+)-specific micro-electrodes.2. In the most active areas of the spinal cord a single volley in a large afferent input like the common peroneal nerve or the posterior tibial nerve produced a transient increase in [K](e) of 0.05-0.1 mM, which reached its peak in 0.2-0.3 sec and it declined in about 3 sec.3. Much higher increases in [K](e) were found during repetitive stimulation of an afferent input. The highest increase (by 3 mM) was at 100 Hz, but even at 1 Hz a significant increase of 0.25 mM was observed. Equilibration of accumulated K(+) was slow with a time constant of about 6 sec, which is much longer than could be expected for the same process in free solution.4. A characteristic distribution of increased [K](e) was found in the spinal cord in response to 100 Hz afferent stimulation. The highest increase of 3 mM was found in and around the intermediate nucleus, but at depths between 0.9-1.8 mm the [K](e) increase exceeded 1 mM.5. In the ventral horns afferent stimulation (100 Hz) increased [K](e) by 0.25 mM, while the same stimulation of the ventral root resulted in a [K](e) increase of less than 0.05 mM.6. The consequences of K(e) (+) accumulation after neuronal discharge are discussed in respect to its possible role in the depolarization of primary afferent terminals.
Animals↗
Extracellular ionic and volume changes: the role in glia-neuron interaction.
Activity-related changes in extracellular K+ concentration ([K+]e), pH (pHe) and extracellular volume were studied by means of ion-selective microelectrodes in the adult rat spinal cord in vivo and in neonatal rat spinal cords isolated from pups 3-14 days of age (P3-P14). Concomitantly with the ionic changes, the extracellular space (ECS) volume fraction (alpha), ECS tortuosity (lambda) and non-specific uptake (kappa'), three parameters affecting the diffusion of substances in nervous tissue, were studied in the rat spinal cord gray matter. In adult rats, repetitive electrical nerve stimulation (10-100 Hz) elicited increases in [K+]e of about 2.0-3.5 mM, followed by a post-stimulation K(+)-undershoot and triphasic alkaline-acid-alkaline changes in pHe with a dominating acid shift. The ECS volume in the adult rat occupies about 20% of the tissue, alpha = 0.20 +/- 0.003, lambda = 1.62 +/- 0.02 and kappa' = 4.6 +/- 0.4 x 10(-3) s-1 (n = 39). In contrast, in pups at P3-P6, the [K+]e increased by as much as 6.5 mM at a stimulation frequency of 10 Hz, i.e. K+ ceiling level was elevated, and there was a dominating alkaline shift. An increase in [K+]e as large as 1.3-2.5 mM accompanied by an alkaline shift was evoked by a single electrical stimulus. The K+ ceiling level and alkaline shifts decreased with age, while an acid shift, which was preceded by a small initial alkaline shift, appeared in the second postnatal week. In pups at P1-P2, the spinal cord was X-irradiated to block gliogenesis. The typical decrease in [K+]e ceiling level and the development of the acid shift in pHe at P10-P14 were blocked by X-irradiation. Concomitantly, continuous development of glial fibrillary acidic protein positive reaction was disrupted and densely stained astrocytes in gray matter at P10-P14 revealed astrogliosis. The alkaline, but not the acid, shift was blocked by Mg2+ and picrotoxin (10(-6) M). Acetazolamide enhanced the alkaline but blocked the acid shift. Furthermore, the acid shift was blocked, and the alkaline shift enhanced, by Ba2+, amiloride and SITS. Application of glutamate or gamma-aminobutyric acid evoked an alkaline shift in the pHe baseline at P3-P14 as well as after X-irradiation. The results suggest that the activity-related acid shifts in pHe are related to membrane transport processes in mature glia, while the alkaline shifts have a postsynaptic origin and are due to activation of ligand-gated ion channels.(ABSTRACT TRUNCATED AT 400 WORDS)
4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
Diffusion constraints and neuron-glia interaction during aging.
Changes in brain extracellular space (ECS) volume, composition, and geometry are a consequence of neuronal activity, of glial K+, pH, and amino acid homeostasis, and of changes in glial cell morphology, proliferation, and function. They occur as a result of repetitive neuronal activity, seizures, anoxia, injury, inflammation, and many other pathological states in the CNS, and may significantly affect signal transmission in the CNS. Activity-related or CNS damage-related cellular swelling is compensated for by ECS volume shrinkage and, as a consequence, by a decrease in the apparent diffusion coefficients (ADCs) of neuroactive substances diffusing in the ECS. Changes in cellular morphology, such as occur during aging, could also result in changes of ECS volume and geometry. We provide evidence for limited diffusion in rat cortex, corpus callosum, and hippocampus in the aging brain that correlates with changes in glial volume and the extracellular matrix. In all structures, the mean ECS volume fraction alpha (alpha = ECS volume/total tissue volume) and nonspecific uptake k' are significantly lower in aged rats (26-32 months old) than in young adult brain. Compared to young adult brain, in the aged brain we found an increase in GFAP staining and hypertrophied astrocytes with thicker processes which, in the hippocampus, lost their radial organization. The tortuosity (lambda = square root of D/ADC) was lower in the cortex and CA3 region. Immunohistochemical staining for fibronectin and chondroitin sulfate proteoglycans revealed a substantial decrease that could account for a decrease in diffusion barriers. Diffusion parameters alpha, lambda, and k' in the aging brain after cardiac arrest changed substantially faster than in the young adult brain, although the final values were not significantly different. This suggests that the smaller extracellular space during aging results in a greater susceptibility of the aging brain to anoxia/ischemia, apparently due to a faster extracellular acidosis and accumulation of K+ and toxic substances, for example, glutamate. We conclude that during aging the movement of substances is more hindered in the narrower clefts. This is partly compensated for by a decrease in the diffusion barriers that may be formed by macromolecules of the extracellular matrix. Diffusion parameters can affect the efficacy of synaptic as well as extrasynaptic transmission by a greater accumulation of substances, because they diffuse away from a source more slowly, or induce damage to nerve cells if these substances reach toxic concentrations. Diffusion parameters are also of importance in the "crosstalk" between synapses, which has been hypothesized to be of importance during LTP and LTD. We can, therefore, assume that the observed changes in ECS diffusion parameters during aging can contribute to functional deficits and memory loss.
Aging↗