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

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.

Changes in extracellular [K+] and [Ca2+] induced by anoxia in neonatal rabbit medulla

Ion-selective microelectrodes were used to record levels of extracellular K+ and Ca2+ concentrations ([K+]o and [Ca2+]o, respectively) and the changes evoked by anoxia in the medulla of anesthetized ventilated newborn rabbits, 1-14 days of age. Resting levels of [K+]o showed significant decline with increasing age. The mean initial level of [K+]o was 6.5 +/- 0.3 mM for the 1st neonatal wk and 5.1 +/- 0.4 mM for the 2nd wk. Brief periods of N2 inhalation (1-3 min) induced reversible increases in [K+]o that were smaller with progression of maturity. The duration of the initial increase (phase I) in [K+]o was twofold greater during the 1st wk than the 2nd wk. At the maximal steady-state level of change (phase III), [K+]o increased by 1.8 +/- 0.2 mM during wk 1 and by 0.9 +/- 0.1 mM during wk 2. Large transient bursts of increase were frequently observed during both early and recovery phases of the sustained [K+]o accumulation. Resting levels of [Ca2+]o also showed age dependence. The mean values during early neonatal days 1-3, compared with days 7-10, were 3.7 +/- 0.3 and 2.4 +/- 0.6 mM, respectively. Anoxia evoked multiphasic decreases in [Ca2+]o that were largest in the youngest pups. Early transient falls of 0.5 +/- 0.1 mM occurred at times similar to those for the earliest increases of [K+]o and negative focal potentials; larger decreases (0.9 +/- 0.2 mM) were recorded after reoxygenation.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain extracellular potassium and genera anaesthetics

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.

Correlation Between Extracellular Focal Potentials and K+ Potentials Evoked by Primary Afferent Activity

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.

Factors Determining the Decay of K+ Potentials and Focal Potentials in the Central Nervous System

Post-tetanic undershoots in extracellular focal potential (ΔV) and K+ potential (EK) can be recorded in the cuneate nucleus and dorsal horn of Dial-anaesthetized or decerebrate cat. They are seen best at depths where the largest ΔEK and ΔV are recorded and they increase with the frequency and duration of stimulation. The very different time courses of undershoots of ΔV and ΔEK indicate two hyperpolarizing influences: first, electrogenic pumping, and later, a reduced external K+ concentration. The importance of active K+ removal in determining the amplitude and duration of ΔEK and ΔV is illustrated by their marked potentiation (as well as the disappearance of post-tetanic undershoots) induced by a lowering of blood pressure or local application of strophanthidin.