PubMed Health⌕ Search

Biomedical subjects

M C Brown

Publications and source records attributed to M C Brown.

At least 19 recordsLinked to original sources
PubMed1995

Cell body response to injury in motoneurons and primary sensory neurons of a mutant mouse, Ola (Wld), in which Wallerian degeneration is delayed.

We examined the response to axon injury in the facial motoneurons and dorsal root ganglion (DRG) neurons of C57BL/Ola (Wld) mice, compared with the responses of C57BL/6J mice. The peripheral nerves of Ola mutants undergo remarkably slowed and muted Wallerian degeneration after injury. The increase in GAP-43 mRNA levels in facial motoneurons and DRG neurons was similar in both strains of mice, as was the initial decrease in medium-weight neurofilament (NFM) mRNA in facial motoneurons, and the increase in JUN immunoreactivity in both types of neurons. However, the subsequent recovery to normal low levels of JUN and GAP-43 mRNA expression and high levels of NFM mRNA was delayed in Ola motoneurons. We ascribe this delay to the slow regeneration and target reinnervation of facial axons in the Ola mice. These results show that absence of rapid Wallerian degeneration does not affect the initial cell body response to axonal injury. They also provide further evidence that restoration of normal levels of expression of GAP-43 and NFM mRNAs is dependent on target reinnervation and/or trophic factors provided by the distal nerve. Impaired regeneration in the Ola mouse does not seem to be a consequence of a defective cell body response to injury, and our results illustrate the general principle that, even if there is a vigorous cell body response to injury, normal axonal regeneration requires the additional provision of a favorable environment for growth.

Animals↗
PubMed1995

The rate of Wallerian degeneration in cultured neurons from wild type and C57BL/WldS mice depends on time in culture and may be extended in the presence of elevated K+ levels.

Wallerian degeneration of severed axons is delayed in C57BL/WldS mice. We have examined this further in cultured sympathetic, sensory and CNS neurons using superior cervical ganglion (SCG), dorsal root ganglion (DRG) and cerebellar granule neurons respectively from neonatal mice. We found that the time taken for the neurites to degenerate depends upon the length of time in culture before cutting, reaching a maximum by approximately 7 days when C57BL/WldS neurites survive for > 6 days after axotomy. The onset of degeneration could also be extended in SCG and DRG neurites from wild type C57BL/6J mice. After 7 days in culture these neurites normally degenerate within approximately 12-16 h of axotomy, but in the presence of raised K+ (50 mM) degeneration often did not begin until a further 2 days had lapsed. Under similar conditions degeneration of neurites from C57BL/WldS mice was also found to be further delayed, extending survival from approximately 5-6 days to > 7 days. The L-type Ca2+ channel blockers nifedipine (5 microM) and verapamil (10 microM) both blocked the effect of raised [K+], although not completely. Thapsigargin, which raises cytoplasmic [Ca2+], and the cAMP analogue 8-(4-chlorophenyl-thio)cAMP were also able to delay degeneration, but only when added 24 h prior to axotomy. These results show that it is possible to influence the course of Wallerian degeneration and that increases in levels of cytoplasmic Ca2+ can protect neurites from its onset.

Animals↗
PubMed1995

Persistence of neuromuscular junctions after axotomy in mice with slow Wallerian degeneration (C57BL/WldS).

The present study was undertaken to examine the fate of neuromuscular junctions in C57BL/WldS mice (formerly known as OLA mice) after nerve injury. When a peripheral nerve is injured, the distal axons normally degenerate within 1-3 days. For motor axons, an early event is deterioration of motor nerve terminals at neuromuscular junctions. Previously, the vulnerability of motor terminals has been attributed either to a 'signal' originating at the site of nerve injury and transported rapidly to the terminals or to their continual requirement for essential maintenance factors synthesized in the motor neuron cell body and supplied to the terminals by fast axonal transport. Mice of the WldS strain have normal axoplasmic transport but show an abnormally slow rate of axon and myelin degeneration. Structure and function are retained in the axons of distal nerve stumps for several days or even weeks after nerve injury in these mice. The results of the present study show that WldS neuromuscular junctions are also preserved and continue to release neurotransmitter and recycle synaptic vesicle membrane for at least 3 days and in some cases up to 2 weeks after nerve injury. Varying the site of the nerve lesion delayed degeneration by approximately 1-2 days per centimetre of distal nerve remaining. These findings suggest that the mechanisms of nerve terminal degeneration after injury are more complex than can be accounted for simply by the failure of motor neuron cell bodies to supply their terminals with essential maintenance factors. Rather, the data support the view that nerve section normally activates cellular components or processes already present, but latent, in motor nerve endings, and that in WldS mice either the trigger or the cellular response is abnormal.

Aging↗
PubMed1995

Fos-like immunoreactivity in central auditory neurons of the mouse.

Fos-like immunoreactivity was used to study sound-induced activation of neurons in the auditory brainstem. Immunoreactivity was assayed with a polyclonal antibody to Fos. In response to 6-kHz tone bursts, the pattern of staining was a band of immunoreactive neurons positioned at the tonotopically appropriate position within the cochlear nucleus and the inferior colliculus. The band was narrow at low sound pressure levels but wider along the tonotopic axis at higher sound levels. In response to noise bursts, the pattern was broader and often extended throughout the auditory nuclei. Often within this broad pattern were "sub-bands" of immunostained neurons, interspersed with bands of unstained neurons. With increasing sound pressure levels above 35-55 dB, the number of Fos-like immunoreactive neurons increased for the cochlear nucleus, superior olivary complex, and inferior colliculus. In the cochlear nucleus and inferior colliculus, the stained cells were small, and hence their activity would be difficult to sample in electrophysiological studies. In the medial nucleus of the trapezoid body, the stained neurons had larger somata and other characteristics of principal cells. Anesthesia with Nembutal or Avertin, but not with ketamine or urethane, decreased the number of Fos-like immunoreactive neurons in the cochlear nucleus. The different anesthetics produced more variable results in the inferior colliculus. In anesthetized, monaurally stimulated animals, the presence of staining in the contralateral cochlear nucleus indicates that some Fos-like immunoreactivity may be mediated by descending or commissural systems. These observations indicate that Fos assays are useful for studying the pattern of neuronal activation in the auditory system and may also be useful in studying the descending auditory pathways.

Acoustic Stimulation↗
PubMed1995

Radiation-induced reductions in macrophage recruitment have only slight effects on myelin degeneration in sectioned peripheral nerves of mice.

Macrophage recruitment into the distal nerve stump of the cut or crushed sciatic or saphenous nerves of C57BL/6J mice was reduced by prior whole body irradiation. This procedure was successful in keeping the numbers of cells stained with the mouse macrophage-specific antibody F4/80 to the levels found in unsectioned nerves. Quantitative image analysis of immunostained sections showed that the rate of loss of myelin basic protein was identical in nerves from irradiated and unirradiated mice up to 5 days but thereafter was slower in macrophage-deprived nerves. Similar analysis of semithin sections stained with toluidine blue detected more undegenerated myelin in the nerves from irradiated mice 10 days after operation. Quantitative counts made from electron micrographs of the sectioned nerves at 7 days also showed slightly less extensive myelin breakdown in the nerves from irradiated mice. Complete removal of myelin from some Schwann cells can occur without macrophages, but macrophages accelerate the removal of myelin in the later stages of Wallerian degeneration. It is concluded that there are two phases to the breakdown of myelin in peripheral nerves undergoing Wallerian degeneration: an initial stage entirely dependent on the activity of Schwann cells and a later stage dependent on both Schwann cells and the presence of macrophages.

Animals↗
PubMed1995

Predictive ability of acute physiology and chronic health evaluation II scoring applied to human immunodeficiency virus-positive patients.

OBJECTIVE: To evaluate the predictive ability of the Acute Physiology and Chronic Health Evaluation II (APACHE II) prognostic scoring system when applied to human immunodeficiency virus (HIV) seropositive patients in the medical intensive care unit (ICU). DESIGN: A retrospective chart review. SETTING: An urban university hospital serving the local community population and also functioning as a tertiary care referral center. PATIENTS: All HIV-positive patients who were discharged from the Yale-New Haven Hospital medical ICU between October 1, 1986 and September 30, 1991. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: APACHE II scoring significantly underestimated the mortality rate in our patient population (n = 161) (35.5% estimated vs. 44.1% observed, p < .025). When patients were evaluated according to total lymphocyte count, APACHE II scores accurately predicted the mortality rate of all patients with a total lymphocyte count of > or = 201 cells/mm3 (n = 112) (32.6% estimated vs. 33.0% observed). However, APACHE II scoring significantly underestimated the mortality rate in the group of patients with a total lymphocyte count of < or = 200 cells/mm3 (n = 36) (44.2% expected vs. 61.1% observed, p < .05), particularly those patients with pneumonia or sepsis (n = 14) (50.5% expected vs. 85.7% observed, p < .01). CONCLUSION: APACHE II scoring significantly underestimates mortality risk in HIV-positive patients admitted to the medical ICU with a total lymphocyte count of < or = 200 cells/mm3. This finding is particularly true regarding patients admitted due to pneumonia or sepsis.

AIDS-Related Complex↗
PubMed1995

Induction of pseudoseizures with intravenous saline placebo.

For a 2-year period, all patients admitted to the inpatient adult EEG videotelemetry unit of the University of Miami School of Medicine underwent attempted event induction with intravenous normal saline placebo. Of 175 patients monitored during that period, 101 underwent attempted placebo saline induction, whereas 58 patients were either in the pediatric age group, were undergoing a repeat hospitalization (i.e., depth electrode monitoring), or refused induction. The final diagnosis in each patient was established after review of the history; physical, interictal, and ictal EEG findings; brain imaging studies; interictal and postictal brain single photon emission computed tomography (SPECT) and serum prolactin levels; psychiatric and psychological evaluations; and detailed neuropsychological testing. Final diagnoses were separated into epilepsy alone, pseudoseizures, epilepsy and pseudoseizures, and other (neither epilepsy nor pseudoseizures). No patient with an eventual diagnosis of epilepsy alone was inducible. Forty-one patients with a diagnosis of epilepsy were not inducible. Of 32 patients with an eventual diagnosis of pseudoseizures, 29 were inducible. One of these 29 was also diagnosed with epilepsy. Three patients with an eventual diagnosis of pseudoseizures were not inducible; 90.6% of patients with an eventual diagnosis of pseudoseizures were inducible, i.e., had events identical to those reported by history, after injection of saline placebo. Placebo saline injection is a safe and effective means of distinguishing epilepsy from pseudoseizures.

Adult↗
PubMed1995

Lipoarabinomannans derived from different strains of Mycobacterium tuberculosis differentially stimulate the activation of NF-kappa B and KBF1 in murine macrophages.

The inflammatory cytokine tumor necrosis factor alpha (TNF-alpha) is rapidly induced in macrophages after exposure to Mycobacterium tuberculosis. Recently it was shown that lipoarabinomannan (LAM) derived from an attenuated (H37Ra) strain of M. tuberculosis (AraLAM) was capable of macrophage activation and induction of TNF-alpha production, whereas LAM derived from the virulent Erdman strain (ManLAM) was considerably reduced in this activity. A critical component in the regulation of many genes central to immune function is the transcription factor NF-kappa B. Lipopolysaccharide (LPS)-mediated induction of TNF-alpha expression in murine macrophages has been demonstrated to be regulated in part by NF-kappa B. In this study, we demonstrate that AraLAM is capable of rapid activation of NF-kappa B- and KBF1-binding activities in C3H/HeN bone marrow-derived macrophages and the J774.A and RAW264.7 murine macrophagelike cell lines, whereas ManLAM is considerably less potent at stimulating NF-kappa B. Treatment of RAW264.7 cells with AraLAM or LPS results in the stimulation of DNA binding of both forms within 7.5 min, which peaks within 30 min and 1 h, respectively. Interestingly, treatment of RAW264.7 macrophage-like cells with AraLAM, LPS, or ManLAM for greater than 2 h resulted in significant accumulation of KBF1. Inhibition of protein synthesis blocked the transient nature of NF-kappa B activation as well as the accumulation of KBF1. Using Western immunodetection of the NF kappa B1 p50 subunit, we also show that AraLAM and LPS stimulate the loss of the NF kappa B1 p105 precursor. These results demonstrate that NF-kappa B and KBF1 are rapidly induced in response to AraLAM and may play a role in avirulent M. tuberculosis activation of TNF-alpha expression in macrophages. The differential temporal regulation of kappa B element DNA-binding activities and the transient stimulation of NF kappa B followed by the sustained accumulation of KBF1 may serve as a feedback switch ensuring transient induction of TNF-alpha transcription.

Animals↗
PubMed1995

Antiemetic efficacy and pharmacokinetics of intravenous ondansetron infusion during chemotherapy conditioning for bone marrow transplant.

We investigated the antiemetic efficacy and safety of intravenous ondansetron infusion in the BMT setting. We conducted prospective randomized comparison trials between ondansetron at 2 dose levels and metoclopramide (MCP) plus droperidol for the prevention of chemotherapy-induced nausea and vomiting in 2 patient populations scheduled to undergo BMT. One patient population (n = 30) received CY alone, the other population (n = 30) received combination chemotherapy of Bu and CY. The CY alone group received ondansetron for 3 days, and the Bu/CY group received ondansetron for 7 days. The primary endpoints were emesis control and nausea. Secondary endpoints included acute (headache, diarrhea and sedation) and delayed (engraftment and regimen-related) side-effects. In both trials, ondansetron provided better emesis control than did MCP plus droperidol during CY administration (P = 0.009, 3-day trial; P = 0.0022, 7-day trial). There was a wide interpatient variation in serum ondansetron levels, although group averages were proportional to the dose administered. Intrapatient day-to-day variation was 10-30% and did not change significantly with concurrent CY administration. Antiemetic efficacy did not correlate with ondansetron serum levels at the doses tested. Headache incidence was similar in all groups. Sedation was highest in the MCP plus droperidol group (P = 0.048, 3-day trial; P = 0.016, 7-day trial). No statistically significant differences in engraftment or regimen-related toxicities were observed between groups in either trial. Ondansetron appears to be a safe and efficacious antiemetic during conditioning for BMT.

Aged↗
PubMed1995

A novel cholinergic "slow effect" of efferent stimulation on cochlear potentials in the guinea pig.

This report documents slow changes in cochlear responses produced by electrical stimulation of the olivocochlear bundle (OCB), which provides efferent innervation to the hair cells of the cochlea. These slow changes have time constants of 25-50 sec, three orders of magnitude slower than those reported previously. Such "slow effects" are similar to classically described "fast effects" in that (1) they comprise a suppression of the compound action potential (CAP) of the auditory nerve mirrored by an enhancement of the cochlear microphonic potential (CM) generated largely by the outer hair cells; (2) the magnitude of suppression decreases as the intensity of the acoustic stimulus increases; (3) they share the same dependence on OCB stimulation rate; (4) both are extinguished upon cutting the OCB; and (5) both are blocked with similar concentrations of a variety of cholinergic antagonists as well as with strychnine and bicuculline. These observations suggest that both fast and slow effects are mediated by the same receptor and are produced by conductance changes in outer hair cells. Slow effects differ from fast effects in that (1) fast effects are greatest for acoustic stimulus frequencies between 6 and 10 kHz, whereas slow effects peak for frequencies from 12 to 16 kHz, and (2) fast effects persist over long periods of OCB stimulation, whereas slow effects diminish after 60 sec of stimulation. The time course of the slow effects can be described mathematically by assuming that each shock-burst produces, in addition to a fast effect, a small decrease in CAP amplitude that decays exponentially with a time constant that is long relative to the intershock interval. The long time constant of the slow effect compared to the fast effect suggests that it may arise from a distinct intracellular mechanism, possibly mediated by second-messenger systems.

Acoustic Stimulation↗
PubMed1994

Loss of the compound action potential: an electrophysiological, biochemical and morphological study of early events in axonal degeneration in the C57BL/Ola mouse.

In the C57BL/Ola (Ola) mouse strain there is a marked slowing of axonal disintegration during Wallerian degeneration. The locus of the mutation controlling this phenomenon (slow Wallerian degeneration--Wlds) has been mapped to chromosome 4, and its protective effect decreases with advancing age. Using biochemical, electrophysiological and histological techniques, the present study was undertaken to determine whether neurofilament phosphorylation and stability are altered or whether calcium-activated proteases are absent in the sciatic nerves of Ola mice. A compound action potential was detectable only when neurofilaments were present and normal axonal architecture was seen. In 1-month-old Ola mice, compound action potentials and neurofilaments were still detectable at 21 days post-transection, whereas both were undetectable by 2 days in BALB/c and C57BL/6J (6J) mice of the same age. Neurofilament levels declined faster with advancing Ola age, confirming previous results, whereas degeneration slowed in ageing BALB/c and 6J mice. In vitro and in vivo degeneration rates were comparable in BALB/c and 6J nerves. Ola nerves, however, showed more rapid decline in vitro than in vivo. Ola and BALB/c nerves frozen and then thawed and incubated in the presence of calcium ions and the ionophore A23187 were not resistant to degradation by intrinsic proteases. Even when a compound action potential could no longer be elicited, however, a majority of nerves still had > 50% of myelinated and unmyelinated axons whose electron microscopic profiles appeared normal. Thus, it appears that the first event in Wallerian degeneration in the Ola mouse is a change at the plasma membrane--a transected nerve becomes unable to conduct a compound action potential.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1994

Further studies on motor and sensory nerve regeneration in mice with delayed Wallerian degeneration.

The axons of both peripheral and central neurons in C57BL/Wlds (C57BL/Ola) mice are unique among mammals in degenerating extremely slowly after axotomy. Motor and sensory axons attempting to regenerate are thus confronted with an intact distal nerve stump rather than axon- and myelin-free Schwann cell-filled endoneurial tubes. Surprisingly, however, motor axons in the sciatic nerve innervating the soleus muscle regenerate rapidly, and there is evidence that they may use Schwann cells associated with unmyelinated fibres as a pathway. If this is so, motor axon regeneration might be impaired in C57BL/Wlds mice in the phrenic nerve, which has very few unmyelinated fibres. We found that as long as the myelinated axons in the distal stump of the phrenic nerve remained intact (up to 10 days), regeneration of motor axons did not occur, in spite of vigorous production of sprouts at the crush site. In contrast to motor axons, myelinated sensory axons regenerate very poorly in C57BL/Wlds mice, even in the presence of unmyelinated axons. We showed that this was also due to adverse local conditions confronting nerve sprouts, for the dorsal root ganglion cell bodies responded normally to injury with a rapid induction of Jun protein-like immunoreactivity and when the saphenous nerve was forced to degenerate more rapidly by multiple crush lesions sensory axons regrew much more successfully. The findings show that motor and sensory axons in C57BL/Wlds mice, although very atypical in the way that they degenerate, are able to regenerate normally but only in an appropriate environment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Motor neuron death induced by axotomy in neonatal mice occurs more slowly in a mutant strain in which Wallerian degeneration is very slow.

In contrast to motor neurons of adults, motor neurons of neonatal mice die if their axons are cut. We have examined the extent, the time course and the loss of susceptibility with age to such induced death in C57BL/Wlds mice. This is a strain which has a dominant autosomal mutation which dramatically slows the rate of degeneration of axons separated from their cell bodies. Following axotomy in neonatal animals the total number of motor neurons killed is no less in C57BL/Wlds mice than in two other strains (C57BL/6J/Ola and BALB/c/Ola). Indeed, the susceptibility to axotomy persists to a later age in C57BL/Wlds mice. However, the rate of cell death is significantly slower than in the two other strains; in C57BL/Wlds mice under a week old at the time of sciatic nerve section only approximately 16% of motor neurons have been lost 3 days after axotomy, whereas in the other mice approximately 45-84% of the final loss has by then occurred. This result extends previous work which showed that retrograde degeneration of retinal ganglion cells of adult mice was slower in C57BL/Wlds mice (V. H. Perry et al., Eur. J. Neurosci., 2, 408-413, 1991). It is therefore possible that Wallerian degeneration of axons shares features in common with retrograde nerve cell death and that the Wlds mutation may throw light on aspects of this complex process.

Aging↗
PubMed1994

Melatonin replacement nullifies the effect of light-induced functional pinealectomy on nociceptive rhythm in the rat.

Rats maintained on a 12 h daily photoperiod (12:12 LD cycle), exhibited a diurnal variation in sensitivity to both heat-elicited and pressure-elicited pain, with low sensitivity at 2 h before the end of the scotophase and higher at 4 h after the onset of photophase. Functional pinealectomy induced by a single LL day effaced the baseline diurnal rhythm of sensitivity to pressure-elicited pain, and reversed that to heat-elicited pain. Oral administration of physiological doses of melatonin into functionally pinealectomized rats, nullified the effect of functional pinealectomy, restoring the normal baseline rhythms of both pressure-elicited and heat-elicited nociceptive responses. The role of melatonin in modulating nociception is discussed in light of an indoleaminergic-opioid system.

Animals↗
PubMed1994

Using Gini-style indices to evaluate the spatial patterns of health practitioners: theoretical considerations and an application based on Alberta data.

The paper analyzes how Gini-style indices are optimally used in the evaluation of economic spatial models designed to predict where health care practitioners are likely to locate under competitive market conditions. At a conceptual level, the analysis establishes that Gini-style indices can be brought to bear on economic models, only if the ordering of geographic areas required to give Gini-coefficient values internal technical coherence also has meaning in terms of the conceptual predictions of the modelling. This, in turn, implies that Gini-indices are most likely to prove useful for fairly aggregated forms of economic analysis, involving relatively few and large geographic divisions. At an applied level, the analysis establishes that one particular geographic distribution of health practitioners is empirically dominant, and that is the distribution which involves the lowest practitioner:population ratio in rural areas, and the highest ratio in large urban areas, with the ratio for small urban areas in between. The empirical evidence also suggests that the spatial practitioner distributions are highly stable for most kinds of health personnel, making it problematic whether these distributions can be changed through normal types of public policy interventions.

Alberta↗
PubMed1994

Central trajectories of type II spiral ganglion cells from various cochlear regions in mice.

Type II spiral ganglion cells provide the afferent pathway from outer hair cells in the mammalian cochlea to neurons in the cochlear nucleus. The present study compares the projection patterns of type II fibers originating from spiral ganglion cells of apical, middle and basal cochlear regions in mice. Fibers were labeled by extracellular injections of horseradish peroxidase into the spiral ganglion. Type II fibers from all regions displayed many 'en passant' swellings (mean = 95) and had very few terminal swellings (mean = 6); fibers from the base had significantly more swellings than those from the apex. Type II fibers traveled into the cochlear nucleus together with type I fibers labeled by the same injection, and both types bifurcated in a cochleotopic manner. The bifurcations formed ascending and descending branches that traveled initially with type I branches in the magnocellular regions of the cochlear nucleus. Type II fibers differed from type I branches in that many fibers subsequently distributed collaterals and terminals to granule cell regions and to the boundaries of these regions that typically do not receive type I input. This projection into the granule cell regions depended on cochlear origin: ascending branches of type II fibers from the cochlea apex did not usually terminate in granule cell regions, whereas those from the base often ended in these regions. Descending branches of type II fibers from all regions, however, projected to the granule cell regions, particularly the granule cell lamina between ventral and dorsal cochlear nucleus. These observations suggest that afferent information from outer hair cells reaches a wide area of the magnocellular parts of the cochlear nucleus in a cochleotopic fashion, and reaches granule cell regions with a less distinct cochleotopic mapping.

Animals↗
PubMed1994

Central trajectories of type II (thin) fibers of the auditory nerve in cats.

This paper describes the central projections of thin fibers of the auditory nerve in cats. Both thin (type II) and thick (type I) fibers are labeled by extracellular injections of horseradish peroxidase (HRP) into the auditory nerve. Type I and almost all type II fibers bifurcate upon reaching the auditory nerve root of the cochlear nucleus. For a given bundle of auditory nerve fibers labeled by a discrete injection of HRP, bifurcations of type II and type I fibers are restricted to a narrow region of the nerve root. After the bifurcation, the pathways of type II branches within the anteroventral cochlear nucleus (AVCN) and posteroventral cochlear nucleus (PVCN) are similar to those of type I branches. This similarity in bifurcation and course of type I and type II fibers was observed in the ventral as well as dorsal parts of the ventral cochlear nucleus. The complete axonal course of most type II fibers could not be reconstructed, however, due to fading of the reaction product. Type II fibers produce very few collaterals in the cochlear nucleus (CN), but possess many 'en passant' swellings along their main processes and collaterals. Compared with type II fibers previously studied in mice (Berglund and Brown, 1989; 1994; Brown and Ledwith, 1990), cat type II fibers are similar in their general projections within the main body of the nucleus and in the frequency of 'en passant' swellings per length of fiber, but cat fibers have a higher percentage of 'complex' or pedunculated 'en passant' swellings.

Animals↗