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R C Carlsen

Publications and source records attributed to R C Carlsen.

50 records · Page 3Linked to original sources
PubMed1985

A rapid startle response in larval lampreys.

Electromyography (EMG) and cinematography revealed a rapid, vibration-evoked startle response in intact larval lampreys. Vibratory stimuli produce simultaneous contraction of both sides of the body, and the response is lost after labyrinthectomy. Midbody EMGs exhibit a stimulus-response latency of 26.5 +/- 4.2 ms. Direct stimulation of the otic capsules, using an electrically driven probe applied to a semi-intact preparation, first evokes a volley of giant axon spikes in the spinal cord followed by the bilateral trunk response.

Animals↗
PubMed1985

Infusion of very hypertonic saline to bled rats: membrane potentials and fluid shifts.

Anesthetized rats were subjected to a moderate degree of hemorrhagic shock, lowering their mean arterial pressure to approximately 50 mm Hg for approximately 100 min. At the end of the shock period, resting skeletal muscle transmembrane potentials had depolarized from a baseline value of -82 mV to -65 mV; intracellular water had increased by 13%; and intracellular sodium and chloride contents had doubled. Eight rats were then given an infusion of very hypertonic saline (2400 mOsmole/kg, calculated osmolality) in a volume equal to only 10% of the volume of shed blood; another eight rats were given the equivalent amount of sodium and chloride in an isotonic solution (volume equal to 80% of shed blood). The mean arterial pressure in the rats that were given the very hypertonic saline returned to 81 mm Hg, compared to 55 mm Hg in the animals given normal saline. The membrane potentials in the hypertonic group polarized back to near normal- -78 mv--compared to no changes in the normal saline group. Intracellular water returned to preshock values in the hypertonic group as did intracellular sodium and chloride contents. Cellular contents in the normal saline group remained at shock levels. It was concluded that, in rats, infusion of small amounts of hypertonic saline can reverse some of the cellular abnormalities induced by hemorrhagic shock.

Animals↗
PubMed1985

A fast-twitch oxidative-glycolytic muscle with a robust inward calcium current.

This report describes the histochemical and physiological properties of a rat skeletal muscle with a robust activity-dependent slow inward Ca2+ current. The muscle, the flexor digitorum brevis (FDB), is a small plantar flexor from the hindfoot. It is a homogeneous muscle consisting of approximately 90% fast-twitch oxidative-glycolytic (type IIA) fibers. Stimulation of the FDB with repetitive stimulus trains (30 or 50 Hz for 330 ms, 1 train/s for 2-5 min) produced a slow increase in the base-line or resting tension of the muscle between trains. This progressive increase in resting tension appears to be due to the activation of voltage-dependent slow Ca2+ channels, since it could be eliminated (i) by stimulating the muscle in a medium containing 2 mM EGTA and without Ca2+, and (ii) by the addition of either Co2+ or verapamil. The presence of a slow current may be associated with an increase in K+ efflux as stimulation continues, and with a prolongation of relaxation time. We also propose that the slow Ca2+ current may contribute to the allosteric activation of phosphorylase kinase during muscle activity. The FDB provides an excellent preparation to investigate the regulation of muscle metabolism by intra- and extra-cellular Ca2+ during exercise.

Action Potentials↗
PubMed1983

Delayed induction of the cell body response and enhancement of regeneration following a condition/test lesion of frog peripheral nerve at 15 degrees C.

Axons subjected to a prior injury exhibit an enhanced regenerative capability following a subsequent lesion. This phenomenon, known as the 'conditioning effect' has been demonstrated in both central and peripheral axons from a variety of species, but the locus of enhancement has remained in doubt. Several reports have tentatively concluded that the effect involves processes located in the cell body of the injured axon, while other investigators have implicated local processes at the site of the injury. The present experiments made use of a previous observation, the apparent suppression of the cell body response in injured frog neurons when the animals are housed at 15 degrees C, to investigate the location of the conditioning effect. The effect occurred in frog neurons from animals at 25 degrees C in the presence of a cell body response. The prior (conditioning) lesion produced a significant increase in regeneration rate (12-17%) and a significant decrease in the latency to the onset of regenerative outgrowth (12%). In contrast, regeneration was initially unaffected by the earlier conditioning lesion when the frogs were kept at 15 degrees C. After a 26-30 day interval, however, the rate of regeneration increased by 27%, coincident with the appearance of chromatolysis in the injured cell bodies. The 'conditioned' axons also continued to elongate, in contrast to singly-lesioned axons at 15 degrees C, and eventually reinnervated their target muscles. The cell body appeared to be the primary locus of the 'conditioning effect' in these experiments. This conclusion was further examined by measuring regenerative outgrowth in 15 degrees C neurons in which a cell body response had been induced prior to the test lesion. This was accomplished by maintaining frogs at 25 degrees C for 7 days after the conditioning lesion. The animals were then returned to the 15 degrees C environment for an additional 7 days before producing the test lesion. With this paradigm, regenerative outgrowth was enhanced without the 26-30 day delay interval. These results also suggest that the conditioning effect stimulates processes in the cell body of the injured axon, but the experiments do not indicate which processes were affected.

Animals↗
PubMed1983

Regeneration of sciatic nerve in frogs maintained at 15 degrees C: failure to sustain regeneration after initiation.

Peripheral nerve regeneration proceeds through a series of phases which include axonal sprouting, elongation, and maturation. Each phase requires interaction between intrinsic properties of the injured neuron and nonneural elements in the environment into which the nerve grows. It has been difficult, however, to separate processes which depend on the induction of a cell body response from those which may depend on local factors at the site of injury. Recently, we found that frog peripheral nerves, in animals housed at 15 degrees C, were able to initiate regeneration in the absence of an apparent cell body response. Subsequently, we found that these nerves did not continue to regenerate normally. I investigated the ultrastructure of regenerating nerves from frogs kept at 15 degrees C for 92 days after a freeze-lesion. Injured sciatic nerves showed extensive axonal sprouting at the lesion site but little continued growth distal to the injury, indicating an impairment in elongation and maturation. Nonneural cells in the local environment showed extensive distributions of rough endoplasmic reticulum and free ribosomes near the regenerative sprouts but the type and quantity of protein actually being synthesized was not determined. The basis for the suppression of axonal growth remains unknown but in the absence of an apparent cell body response it appears probable that a necessary cell body contribution to regeneration was also absent. That contribution could provide direct support to axonal growth or could trigger periaxonal support of regeneration. This experimental preparation offers a means of investigating those alternatives and the opportunity to determine the origin of the various processes responsible for nerve regeneration.

Animals↗
PubMed1982

Suppression of the cell body response in axotomized frog spinal neurons does not prevent initiation of nerve regeneration.

Frog spinal neurons, in animals maintained at environmental temperatures above 20 degree C, show the classic features of the cell body response following peripheral axotomy. In contrast, axotomized spinal neurons in frogs held at an ambient temperature of 15 degree C showed no apparent cell body response. The 15 degree C neurons retained normal morphology, continued to synthesize and transport normal levels of acetylcholinesterase activity, and sustained normal reflex connections. Despite the apparent absence of a cell body response, the proximal nerve stump began to regenerate. The apparent latency to the initiation of axonal growth was increased at 15 degree C; regeneration began 3.8 days after axotomy at 25 degree C, but 4.5 days following nerve section at 15 degree C. The rate of axon regeneration was also considerably slower at 15 degree C: 0.6 mm/day compared to 2.4 mm/day at 25 degree C. Nonetheless, these data imply that initiation of axonal sprouting and regeneration may not depend on alterations in the cell body. Additional data indicated that the appearance of the cell body response may not be linked to the elimination of a normal, peripherally-derived, constituent of the retrograde transport system. Injured motor axons at 15 degree C were able to acquire and transport horseradish peroxidase from the point of transection to the cell body. Material normally in transit to the cell body should also be drained from the injured axons over time. Yet, the elimination of this "trophic' supply did not induce the appearance of the cell body response.

Acetylcholinesterase↗
PubMed1982

Axonal transport of adenylate cyclase activity in normal and axotomized frog sciatic nerve.

Adenylate cyclase activity accumulated proximal to a constriction placed around the frog sciatic nerve. The rate of accumulation was linear between 8 and 24 h following placement of the constriction; accumulation rate declined substantially after 24 h. Accumulation of activity distal to the constriction in normal nerve was not significantly different from control for the first 72 h, but increased at 5 days. These data are interpreted as indicating that adenylate cyclase is transported from the cell body to the nerve terminals in normal frog nerve, but not in the reverse direction. Following axon transection, anterograde transport of adenylate cyclase activity declined, but a transient retrograde transport of adenylate cyclase activity appeared. In addition, adenylate cyclase activity accumulated in the proximal transected nerve stump during the period when Schwann cell proliferation and the initiation of nerve regeneration both appear. The pattern of response of adenylate cyclase activity to nerve injury suggests that the adenylate cyclase: cAMP system could play some role in peripheral nerve regeneration.

Adenylyl Cyclases↗
PubMed1977

A comparison of the reflex organization of thoracic and lumbar segments in the frog spinal cord.

Both lumbar dorsal root (DR) primary afferents and descending fibers in the lateral column (LC) make monosynaptic connections with ipsilateral lumbar motoneurons in the frog spinal cord. We have determined that LC fibers also make monosynaptic connections with thoracic motoneurons, while thoracic primary afferents do not. The central reflex time (CRT) for the lumbar DR-VR pathway was 2.5 +/- 0.3 msec, but the CRT for the thoracic DR-VR pathway was 8.5 +/- 2.6 msec. By using a conditioning-test paradigm we have been able to determine that the earliest sign of segmental synaptic transmission in thoracic motoneurons occurs only after a delay of 6.1 +/- 0.9 msec. These results correlate very well with the different morphological characteristics of lumbar and thoracic segments. We have also investigated the central organization of lumbar and thoracic segments and found that the segmental polysynaptic input to motoneurons is more diffuse in thoracic than in lumbar segments. The intersegmental reflexes between thoracic and lumbar segments provide additional evidence for a more diffuse organization in thoracic segments.

Animals↗
PubMed1975

The possible role of cyclic AMP in the neurotrophic control of skeletal muscle.

1. Motoneurones provide trophic control of some of the functional characteristics of skeletal muscle fibres. This study has been designed to test whether the adenylate cyclase: cyclic AMP system may offer one potential mechanism for the mediation of neurotrophic regulation. 2. The concentration of cyclic AMP was measured at various intervals after muscle denervation. Muscle cyclic AMP concentration increases for the first 2 days after nerve section. It reaches a maximum value at 48 h and subsequently returns to the control value at 7 days. 3. Cyclic AMP concentration is unchanged by muscle disuse for the first 3 days following limb immobilization. Four days after immobilization, however, cyclic AMP increases in both the disused and contralateral control muscles. This phenomenon has been tentatively ascribed to some aspect of the inflammatory response. 4. Changing the level of nerve section, and therefore the length of the residual nerve stump, changes the temporal pattern of the increase in muscle cyclic AMP concentration. 5. Reinnervation of a denervated muscle produces a decrease in muscle cyclic AMP concentration. 6. It is concluded from the results that some aspect of nerve function provides trophic regulation of the muscle adenylate cyclase: cyclic AMP system. The mechanisms by which this regulation may be applied are considered in the Discussion.

Adenylyl Cyclases↗
PubMedDate not supplied

Forskolin activation of adenylate cyclase in vivo stimulates nerve regeneration.

The previous demonstration of an increase and redistribution of adenylate cyclase activity in injured peripheral nerve suggests that an increase in neuronal cyclic AMP concentration could play a role in peripheral nerve regeneration. We report our finding that accumulating adenylate cyclase activity was translated into a twofold increase in cyclic AMP concentration in the regenerating nerve stump, coincident with the initiation and elongation of regenerative nerve sprouts. We sought to magnify the role of cyclic AMP in regeneration by using forskolin, a robust activator of adenylate cyclase, to produce an additional increase in neuronal cyclic AMP in situ. Forskolin in vitro produced an approximately 40-fold greater elevation in neuronal cyclic AMP than an equimolar (10(-5] concentration of isoprenaline. Moreover, the elevated cyclic AMP concentration persisted for at least 60 min in the continued presence of forskolin. Daily injection of forskolin into the dorsal lymph sac of Rana pipiens, or delivery of forskolin through an implanted osmotic pump produced a sustained 40% increase in the rate of sensory nerve regeneration in freeze-lesioned sciatic nerves. We conclude that an increase in cyclic AMP concentration and, presumably, the activation of appropriate protein kinases stimulates regenerative nerve growth following trauma.

Adenylyl Cyclases↗