Eben J. Carey

Morphologic Effects of Poliomyelitis Virus upon Motor End Plates in the Monkey.

Summary Coincident with and shortly following paralysis by poliomyelitis virus with following morphologic changes occur in the motor and plates: 1, disappearance of many endplates resulting in denervation at the myoneural junction; 2, ephemeral appearance of masses of inclusion of bodies, some of which are cross striated, within and near the degenerating motor end plates; 3, differential rates of motor nerve degeneration; 4, degeneration beginning in the motor and plates and proceeding in a centripetal direction in the axis-cylinders of many motor nerves.

Morphologic Effects of DDT on Nerve Endings, Neurosomes, and Fiber Types in Voluntary Muscles.∗:

Summary The limited experimental evidence presented in this paper tends to support the statement that DDT increases the discharge of auriphilic neurogenic substances from some motor end plates into the myoplasm of some of the voluntary muscle fibers. These neurogenic substances form massive aggregates of neurosomes in parts of some voluntary muscle fibers. This results in a partial or complete dissociation of the neurogenic from the myogenic substances in the muscle fiber. Auriphilic granules are likewise found at the 2 poles of the elongated nuclei in the dark muscle fibers. The supporting evidence that some of the auriphilic granules and masses found after DDT toxicity are neurogenic in origin follows : (1) anatomical continuity of the auriphilic bodies in muscle with the auriphilic hypolemmal axons of the motor end plates; (2) similarity of staining reaction of the masses in muscle and axons of nerve endings with gold impregnation; (3) massive aggregation of auriphilic bodies in some muscle fibers contemporaneous with the centrifugal depletion of the related nerve axons and endings of their auriphilic substances. Presumptive evidence is presented that the normal fiber types in voluntary muscle are dependent, in part, upon the periodic alternation of the discharge and disappearance, by chemical action, of the neurogenic granules in the same muscle fiber at different time periods. The limited evidence also indicates that DDT poisoning may be produced in normal rats by feeding, and in chameleons by the intraperitoneal injection of the previously perfused, dehydrated, and emulsified muscles of rats manifesting toxicity with DDT.

Microincineration of Active Smooth, Transitional and Skeletal Muscles.

The distribution of inorganic salts in the active and inactive smooth muscle of the intestine and the transitional muscle of the gizzard of birds and skeletal muscle is revealed by the technic of microincineration perfected by Scott. 1 He emphasized the distribution of ash in relatively inactive smooth and skeletal muscle by this method. He did not report in detail on the ash distribution in the active smooth, transitional, and skeletal muscles. This method of incinerating microscopic sections of tissue without disturbing the relationship of the mineral components was suggested by Liesegang 2 and developed by Policard. 3 The recent studies of Kruszynski 4 are on the topography of the mineral content in relatively resting muscle after microincineration. The muscle is fixed for 24 hours in 9 parts of absolute alcohol and 1 part of neutral formalin. The mineral salts are neither increased nor decreased by this fixative. The tissue is completely dehydrated by several changes in absolute alcohol. The mineral salts remain intact by this method. It is then cleared in xylol, embedded in paraffin, and cut serially at 4 to 6 microns. Alternate sections are mounted by the usual method, and stained with hematoxylin and erythrosin, whereas, the intervening sections are mounted with liquid petrolatum to spread the tissue evenly. After the section is flat the excess liquid petrolatum is removed carefully by smooth blotting paper. The intervening sections are incinerated in a closed electric furnace at varying temperatures from 400° to 650°C. The temperature is raised 50°C every 10 minutes until the highest temperature is reached. Sudden elevation of temperature with an excess of liquid petrolatum underlying the paraffin section results in explosive distortions due to sudden thermal agitation. The slide is cooled slowly over a period of 8 to 12 hours and the incinerated section is then covered with a number 0 cover glass around the edges of which melted paraffin is applied.

Effects of use and disuse on nerve endings, neurosomes, and fiber types in skeletal muscle.

Summary The limited experimental evidence presented in this paper tends to support the following statements: The normally used and innervated gastrocnemius muscle of the white rat is characterized histologically by dark, coarsely granular and light, finely granular and agranular muscle fibers. The nerve endings are usually retracted in the dark, coarsely granular fiber and expanded in the light, agranular fiber, as revealed by gold impregnation of teased whole muscle fibers. The atrophy of disuse following tenotomy of the gastrocnemius muscle with nerve supply intact, is accompanied, during the first month, by the progressive loss of the narrow and dark, coarsely granular muscle fiber, and by a depletion of its innervation. The dark, granular muscle fiber is determined by the reciprocal interaction of the normally intact and attached muscle fiber with its normally functioning innervation. During the process of atrophy of disuse after tenotomy, small and giant fusiform neurosomes are discharged from the altered nerve endings. It is assumed that these giant fusiform neurosomes are the product of a retardation in the rate of the discharge, diffusion, and disappearance by hydrolysis, following tenotomy and disuse atrophy of the innervated gastrocnemius muscle. There appears to be a parallelism between the atrophy by disuse of tenotomized muscle and the loss of the normal discharge of neurosomes from the altered and progressively depleted innervation of the muscle. One factor in the atrophy of disuse of muscle appeared, therefore, to be the substantial loss of the discharge of neurosomes into muscle as well as the quantitative decrease of the myoplasm. The giant fusiform neurosomes that appear during the early period following tenotomy disappear when the living muscle in situ is adequately restretched prior to excision and gold impregnation.

Acute Anatomic Breakdown of Motor End Plates in Hemorrhagic Shock.

Summary The limited evidence in this paper supports the claim that hemorrhagic shock profoundly alters the morphology of the motor end plates and finally produces loss of structural innervation of many muscle fibers in a single voluntary muscle. This histologic change is highly irregular in the different muscles of the rat, therefore large numbers of specimens from different muscles were teased. Gold staining masses of axonic materials drain out into and between the muscle fibers coincident in time with the loss of motor innervation due to the increased permeability of the end plates. The epilemmal axons, exhausted of their substances, are in many places likewise denuded of their hypolemmal end plates. There is therefore a real anatomic breakdown of many motor end plates and histologic alteration of certain skeletal muscles in hemorrhagic shock.

Effect of CO2 on Ameboid Changes in Motor Nerve Plates in Intercostal Muscle.

Summary The retracted motor nerve plates with wide, short projections were related to coarse, widely spaced cross striations, whereas expanded nerve plates with thin, elongated and moniliform processes were longer and separated by wider meshes than the retracted ones. 60% of the expanded motor nerve plates in the intercostal muscle accelerated in the transmission rate of the nervous impulses by carbon dioxide became twice the size of the relatively normal plates. Their processes were longer and separated by wider meshes than those of the normal controls. This morphologic expansion and extension of the processes of the plate by the proposed ameboid motion under the stimulus of the demand of increased functional activity evidently favors the transmission of the nerve impulse to the receptive muscle substance by increase of the surface area of the motor nerve plate. The differences in the histologic structure of motor nerve plates and muscle cross striations may be arranged in a graded series and are evidently determined by the active and inactive fibers in the fractional contraction of the same muscle. These structural changes favor the chemical theory of impulse transmission.

Sudden Destruction of Motor End Plates by Lactic Acid

Summary Lactic acid in concentrations of 0.05 to 0.3% injected into the exposed zone of innervation of the sternomastoid muscle in the white rat produced sudden destruction of most of the motor end plates within 30 seconds to 25 minutes dependent upon the concentration of the acid. This liquefaction of the hypolemmal axons of the end plates was preceded by a first phase of retraction and a second phase of expansion and fragmentation. Lactic acid caused a progressive depletion, in both the hypolemmal and the epilemma1 axons, of auriphilous substances. The blood vessels were enlarged, hyperemic, and contained clumps of agglutinated red blood cells in the rigorous muscle paralyzed by lactic acid. I t is suggested that the acid metabolites which accumulate during rigor mortis of muscle are responsible for the destruction of the end plates and that during life certain processes that result in the intramuscular accumulation of acid, such as vascular congestion and anoxia, likewise may result in the destruction of the motor end plates.

Exaggerated Discharge of Neurosomes into Spastic Muscle by Heat Reflex.

Summary The limited experimental evidence presented tends to support the statement that the reflex effects of heat applied to the skin are associated with the exaggerated discharge of ephemeral, pleomorphic, and lipoidal neurosomes from the motor end plates into spastic or cramp-like muscle. The neurosomes have a variable affinity for gold, silver, and lipoidal stains. There are characteristic instantaneous changes in the morphology of the motor end plates and myoplasm in response to the reflex effects of thermal trauma applied to the skin.

Morphologic Effects of Acute Inanition on Motor End Plates.

Summary Starvation of the albino rat is fatal within 8 to 15 days and produces a structural detachment of about 20% of the motor nerves in skeletal muscle, morphologically manifested by: (1) progressive retraction and eventual uprooting of the hypolemmal end plate from within the atrophic muscle fiber and loss of the granular sole plate of Kühne, and (2) enormous distention of the epilemmal axons which stain very intensely with gold chloride.