No abstract

Summary: Extracellular space (ECS) volume fraction(IX), ECS tortuosity (A), and nonspecific uptake (k'), three parameters affecting the diffusion of substances in ner vous tissue, were studied during ischemia and anoxia in the rat spinal cord gray matter in vivo. Progressive isch emia evoked by exsanguination, as well as anoxia evoked by respiratory or cardiac arrest, produced prominent ex tracellular K + and pH changes closely related to a de crease in blood pressure and amplitude of field potentials. With use of ion-selective microelectrodes, the changes in the diffusion parameters were measured by quantitative analysis of concentration-time profiles of tetramethylam monium (TMA +) applied by iontophoresis concomitantly with ionic shifts. Under normoxic conditions (in rats with blood pressure of 80-110 mm Hg) diffusion parameters in the dorsal hom gray matter at depth 500-900 fLm were as follows: IX = 0.20 ± 0.019, A = 1.62 ± 0.12, k' = 4.6 ± 2.5 x 10-3 s -1 (mean ± SD, n = 39). Extracellular K +, pH, and diffusion properties gradually changed during progressive ischemia. As the blood pressure fell to 50-60 mm Hg and field potential amplitude to 20-60%, K + rose to 6-12 mM, pHe fell by -0.05-0.1 pH unit, and volume fraction of the ECS significantly decreased, to IX = 0.16 ± 0.019 (n = 22). Even though the tortuosity remained vir tually constant, the nonspecific uptake significantly de creased to k' = 3.4 ± 1.8 x 10-3 S-I. As the blood pressure fell to 20-30 mm Hg and field potential ampli tude to 0-6%, K + rose to 60-70 mM, pHe fell by -0.6-0.8 pH unit, and all three diffusion parameters significantly 301changed. The ECS volume fraction decreased to a = 0.05 ± 0.021, tortuosity increased to A = 2.00 ± 0.24, and TMA + uptake decreased to k' = 1.5 ± 1.6 x 10 -3 S -1 (n = 12). No further increase in extracellular K + or changes in the IX were found during and up to 120 min after the death of the animal. However, there was a further signif icant increase in A = 2.20 ± 0.14 and decrease in k' = 0.4 ± 0.3 x 10-3 s -1 (n = 24). The acid shift reached its maximum level at -5-10 min after respiratory arrest and then the pHe gradually increased by -0.2 unit. Full re covery to "normoxic" diffusion parameters was achieved after reinjection of the blood or after an injection of nor adrenaline during severe ischemia, if this resulted in a rise in blood pressure above 80 mm Hg and a decrease in extracellular K + below 12 mM. At -10 and 30 min after this recovery, the ECS volume fraction significantly in creased above "normoxic" values, to IX = 0.25 ± 0.016 (n = 7) and IX = 0.30 ± 0.021 (n = 6), respectively. The A and k' were not significantly different from the values found under normoxic conditions. Our data represent the first detailed in vivo measurements of diffusion parame ters IX, A, and k' during and after progressive ischemia and anoxia. The observed substantial changes in the diffusion parameters could affect the diffusion and aggravate the accumulation of ions, neurotransmitters, metabolic sub stances, and drugs ...

No abstract

No abstract

No abstract

No abstract

No abstract

Studies with neonate chicks, trained on a passive avoidance task, suggest that at least two shorter-term memory stages precede long-term, protein synthesis-dependent memory consolidation. Posttetanic neuronal hyperpolarization arising from two distinct mechanisms is postulated to underlie formation of these two early memory stages. Maintenance of the second of these stages may involve a prolonged period of hyperpolarization brought about by phosphorylation of particular proteins. A triggering mechanism for long-term consolidation is postulated to occur at a specific time during the second stage, and may involve reinforcement-contingent release of neuronal noradrenaline stimulating cAMP-dependent intracellular processes. The possibility that astroglia may have a critical role to play in these early stages of memory processing is raised.