Biomedical subjects

G Matthews

Publications and source records attributed to G Matthews.

At least 145 records · Page 8Linked to original sources

PubMed1978

Evoked depolarizing and hyperpolarizing potentials in reticulospinal axons of lamprey.

1. Intracellular recordings were made from reticulospinal axons (Müller axons) in the lamprey spinal cord. Electrical stimuli applied to the spinal cord surface elicited depolarizing and hyperpolarizing 'synaptic-like' potentials in Müller axons. The physiological basis of these evoked potentials was investigated. 2. The depolarizing response was not the result of increased extracellular K, as demonstrated by the constancy of the undershoot of the axonal action potential during the depolarization, by the failure of the response to summate during repetitive stimulation and by the failure of the response amplitude to vary as predicted when the [K] of the saline was varied. 3. When the membrane potential of the axon was varied by passing current through a micro-electrode, the amplitude of the depolarizing evoked potential decreased at membrane potentials positive to the resting potential and increased up to a maximum when the axon was hyperpolarized by about 10 mV. The extrapolated 'reversal potential' for the depolarizing response was about 15 mV positive to the normal -80 mV resting potential of the axon. However, the amplitude of the response did not continue to grow with hyperpolarizations greater than 10 mV, and, thus, the response did not behave as would a normal depolarizing synaptic potential. 4. Müller axons make numerous electrical synapses with spinal motoneurones and interneurones, and this suggested that the depolarizing response might be a coupling potential. In agreement with this idea, quantitative correspondence was found between changes in the input resistance of the axon produced by the depolarizing response and the variation in the depolarizing response amplitude. Thus, although the depolarizing response mimicked in some ways the behaviour of an excitatory synaptic potential, we conclude that it is a coupling potential. 5. The hyperpolarizing response also appeared to be a coupling potential. Its amplitude was not changed by hyperpolarizing the axon up to 30 mV and was decreased by depolarizing the axon sufficiently to decrease the axon's input resistance. 6. It is proposed that both depolarizing and hyperpolarizing evoked potentials in lamprey Müller axons are a result of passive flow of current from cells activated by the spinal cord stimulus and electrically coupled to Müller axons.

Animals↗

PubMed1978

Sustained depolarizing potentials in reticulospinal axons during evoked seizure activity in lamprey spinal cord.

1. Intracellular recordings were made from lamprey reticulospinal axons (Müller axons) during seizures evoked by electrical stimulation of the isolated spinal cord in saline containing either 0 Cl or 1 mM picrotoxin. The seizures had tonic and clonic-phases similar to ictal seizures in mammalian brain. 2. During seizures Müller axons were depolarized by 10-15 mV. These seizure-depolarizations were not due to any direct effect of the evoking stimulus on the Müller axons themselves nor were they initiated by an accumulation or extracellular potassium. 3. A decrease in axonal input resistance occurred during a seizure-depolarization. Also, the amplitude of a seizure-depolarization was decreased by depolarizing the axon 5-15 mV with injected current. Further, hyperpolarizing the axon increased the amplitude of the seizure-depolarization, but the growth flattened out beyond 30-40 mV of hyperpolarization. The decrease in input resistance during the seizure-depolarization and the dependence of the response amplitude on axonal membrane potential suggested that the seizure-depolarization was an excitatory synaptic potential. However, the failure of the seizure-depolarization amplitude to continue to grow at membrane potentials greater than 30 mV negative to the resting potential was not consistent with this interpretation. 4. A synaptic conductance change as the cause of the seizure-depolarization was ruled out by setting the axonal membrane potential at different levels with injected current and monitoring the input resistance of the axon before and during seizure-depolarizations. It was found that no change in input resistance occurred during the seizure-depolarization when the axon was hyperpolarized more than approximately 30 mV, the same potential at which the growth in the response amplitude ceased. From analysis of these data and the passive current-voltage properties of Müller axons it is concluded that the seizure-depolarization is not a chemical synaptic potential, but rather the result of the passive injection of depolarizing current into the axons. 5. The source of the depolarizing current which flows into Müller axons during seizures is probably paroxysmal action-potential activity in spinal motoneurons and interneurons, many of which are electrically coupled to Müller axons.

Action Potentials↗

PubMed1978

Properties of the membrane current of rod outer segments.

The membrane current of single rod outer segments in pieces of isolated toad retina was recorded with a glass suction electrode. Light evoked a slow net outward photocurrent consisting of a reduction in the steady inward dark current. In very dim light, the photocurrent broke up into discrete shot effects with a rounded shape and an amplitude of about 1 pA. These events were shown to result from photoisomerization of single rhodopsin molecules. The current in darkness showed fluctuations consisting of (a) discrete events apparently resulting from thermal isomerization of rhodopsin molecules, and (b) smaller amplitude shot effects shaped by two of the four rate processes of the light response.

Animals↗

PubMed1977

Electrical stimulation of the rat diencephalon: differential effects of interrupted stimulation on on- and off-responding.

Rats were trained to turn on and to turn off electrical stimulation of the hypothalamus. Breaking trains of stimulation into bursts of pulses separated by intervals of no-stimulation attenuated off-responding more than on-responding. Current intensity was raised in an attempt to maintain a constant level of performance when either burst duration was decreased or interburst interval was increased. Current increases necessary to maintain on-responding were consistently smaller than the increments required to maintain off-responding. At shorter burst durations, off-responding usually ceased while on-responding continued. Four interpretations of the results are discussed: (1) temporal integration characteristics of the underlying neural systems, (2) reward adaptation, (3) electrode location, and (4) procedural artifacts. Only the first explanation which holds that the buildup of activity in the rewarding system is more rapid than in the aversive system is consistent with all the results. If correct, this conclusion indicates that multiple effects of electrical stimulation at a single brain site can be differentiated by manipulating the temporal pattern of the stimulation.

Adaptation, Physiological↗

PubMed1977

Neural substrate for brain stimulation reward in the rat: cathodal and anodal strength-duration properties.

The trade-off between current strength and duration of a stimulating pulse was studied for the rewarding and priming effects of brain stimulation reward (BSR). With cathodal pulses, strenght-duration functions for BSR had chronaxies of .8-3 msec. No differences were observed between the results for rewarding and priming effects. With anodal pulses. strength-duration curves were parallel to the cathodal curves at pulse durations of .1-5 msec, but at pulse durations greater than 5 msec the anodal curves showed a greater drop in required current intensity than did the cathodal curves. The parallel portion of the anodal curves was interpreted as due to anode-make excitation, and the drop at longer pulse durations was interpreted as due to anode-break excitation. Cathodal strength-duration functions for the motor effect elicited through the BSR electrodes had chronaxies of .15-.48 msec. Measurements of the latency of the muscle twitch confirmed that anode-make and anode-break excitation occurred, the latter becoming evident at pulse durations as brief as .3-.4 msec. The results provide quantitative characterization of cathodal and anodal strength-duration properties of the neural substrate for BSR and are discussed in terms of their value in guiding electrophysiological investigation of that substrate.

Animals↗

PubMed1977

Effects of guanidine on transmitter release and neuronal excitability.

1. Guanidine hydrochloride (CH5N3-HCl) was applied to frog neuromuscular junctions blocked by reduced external Ca2+, or increased external Mg2+ concentration, or by both. Guanidine produced a dose-dependent increase in the average number of quanta released by presynaptic action potentials, the threshold dose being 0-1-0-2 mM. No post-synaptic effects were observed. 2. Guanidine also increased the excitability of the motor nerve fibres, as evidenced by multiple firing to single electrical stimuli and finally by spontaneous action potentials. These effects were studied in greater detail in giant axons (Müller axons) in the spinal cord of lamprey. Exposure to guanidine produced in these axons a progressive increase in excitability, manifested by repetitive firing to a single electrical stimulus, spontaneous membrane potential oscillations and spontaneous bursts of action potentials. Guanidine had no effect on the resting potential. 3. The effect of guanidine on the excitability of Müller axons was mimicked in every detail simply by reducing the divalent cation concentration of the bathing solution. 4. Guanidine also produced dose-dependent increases in the duration of action potentials in Müller axons. This effect always preceded in time the appearance of the excitability effects and was not mimicked by reducing the divalent cation concentration. It is suggested that the broadening of the action potential is separate from the excitability effects and may reflect a decrease of delayed rectification. 5. Guanidine (0-3 mM) increased the frequency of miniature end-plate potentials (min. e.p.p.) in solutions containing 2-11 mM-K+ in such a way as to shift the relationship between min. e.p.p. frequency and extracellular K+ toward lower values of K+. This effect was interpreted to mean that guanidine produced a depolarization of the nerve terminal which summed with the depolarization produced by a given concentration of K+. The calculated depolarization produced by 0-3 mM guanidine was 5-7 mV. 6. The effects of guanidine on evoked transmitter release, excitability, and min. e.p.p. frequency are consistent with a hypothesis which states that guanidine binds at or near fixed negative changes on the outside of nerve membrane and reduces the screening effect of divalent cations.

Action Potentials↗

PubMed1977

On the effect of calcium on the frequency of miniature end-plate potentials at the frog neuromuscular junction.

1. The effect of the extracellular Ca concentration on the frequency of miniature end-plate potentials (min. e.p.p.s) at the frog neuromuscular junction was studied. 2. In saline containing elevated K (5 or 11 mM), the frequency of min. e.p.p.s increased as Ca concentration was increased from 0-1 to 1-3 mM. However, with further increases of Ca concentration up to 10 mM, min. E.P.P. frequency declined. 3. In saline containing the normal concentration of K (2 mM), increasing Ca concentration from 0-1 to 10 mM produced a slight, monotonic increase in min. e.p.p. frequency. 4. The non-monotonic effect of Ca on min. e.p.p. frequency in preparations depolarized by elevated K is consistent with the existence of two opposing effects of Ca on transmitter release. Firstly, raising the external concentration of Ca increases the electrochemical potential for Ca entry, which tends to increase Ca influx and transmitter release. Secondly, increasing external Ca concentration increases electrostatic screening of fixed negative charges on the outer surface of the nerve terminal membrane. Such an increase in screening of charges near voltage-sensitive Ca gates would produce a hyperpolarization across the gates and they would tend to close, an effect which would tend to decrease Ca influx. The monotonic increase in min. e.p.p. frequency with increasing Ca concentration in 2 mM-K is consistent with the voltage insensitivity of the Ca gates at potentials close to the normal resting potential.

Animals↗

PubMed1975

Sodium restriction and thiazide diuretics in the treatment of hypertension.

In a group of hypertensive patients it has been shown that moderate sodium chloride restriction has a hypotensive effect that is similar to that produced by thiazide diuretics. Blood pressure changed in relation to body weight in individual patients, and appeared to correlate with their sodium balance. The more a patient was depleted of sodium, the lower was the blood pressure. The serum potassium level fell with the use of thiazide diuretics, but in this group of patients there was little change in total body potassium content. The fall in serum potassium level appeared to relate to a shift into the cells due to the accompanying alkalosis. Potassium supplementation appeared to have had little effect and was unnecessary for most patients who were given diuretics for hypertension. Amiloride corrected the alkalosis and restored the serum potassium level to normal.

Amiloride↗

PubMed1975

Objective measurement of human motor activity: a preliminary normative study.

Motor activity values have been generated for a population of young adult subjects in order to develop normative values for motor activity levels. Using the large-scale-integrated (LSI) motor activity monitor, day and night motor activity have been continuously and noninvasively monitored for approximately 1 month on 13 normal subjects. Comparisons between measured and self-rated motor activity tend to validate this technique. The results are discussed in relation to ongoing motor activity studies showing definite changes in activity associated with fluctuations in mood and anxiety.

Adult↗

PubMed1973