A combination of anatomical and experimental preparations were used to explore the function of the venom delivery system in rattlesnakes (Crotalus). The distal end of the venom duct is compressed near the point where it empties into the venom chamber, a space surrounding the fang defined by the fang sheath. Within the venom chamber, the inner fang membrane lies obliquely over the base of the fang at least partially occluding the entrance orifice. When the fang is retracted the combination of the compressed venom duct and the spatial position of the inner fang membrane serve to inhibit or block venom flow. As the fang is erected beyond approximately 60°(relative to the roof of the mouth) localized compression of the fang sheath decreases the size of the venom chamber, relieves the compressive force from the venom duct, and displaces the inner fang membrane away from the entrance orifice of the fang. Pressure recordings taken at different locations along the venom delivery system demonstrate that the venom gland produces suction during relaxation of the extrinsic glandular musculature. These findings suggest that the venom delivery system of Crotalus is both more flexible and more regulated than previously assumed. Anat Rec 264: [415][416][417][418][419][420][421][422][423][424][425][426] 2001.
A combination of histology, whole muscle force physiology, glycogen depletion, and venom expulsion analyses using transonic probes to measure venom flow and fluid pressure transducers to measure venom pressure was performed on the m. compressor glandulae and m. pterygoideus glandulae. The m. pterygoideus glandulae has less than one‐third the cross‐sectional area of the m. compressor glandulae, and produces approximately one‐fifth the total twitch and tetanic force; however, in situ surface stimulation of the muscle produces venom flow and pressure levels that are similar to those produced by the m. compressor glandulae. The similarity in venom output following stimulation reflects in part the functional role of the larger m. compressor glandulae in jaw adduction, but also the functional subdivisions within this muscle. The m. compressor glandulae is divided into a series of columnar fascicles that run from the surface of the muscle to the venom gland. The combined results of clearing and staining and glycogen depletion studies suggest that these fascicles may represent functional compartments. Identical stimulations applied to different regions of the m. compressor glandulae result in up to a six‐fold difference in venom expulsion. This functional specialization may play a role in the regulation of venom flow during offensive and defensive strikes. J. Morphol. 246:249–259, 2000. © 2000 Wiley‐Liss, Inc.
Inherited ocular anomalies in chickens include several types of microphthalmia, retinal dysplasia, retinal degeneration, cataract, buphthalmos and pop-eye, or keratoconus in White Leghorns. [2][3][4][5]7,8,12,[15][16][17][18] In this report, a new ocular anomaly that appeared in pigmented White Leghorns homozygous for a mutation at the dominant white (I) locus is described with emphasis on clinical, gross, and histologic findings to aid in the diagnosis of the ocular lesions.An incompletely dominant mutation, called Smoky Joe (SJ), allows the production of feather pigment, which the I allele inhibits. The SJ mutation originally appeared in ADOL Line 0, a noninbred White Leghorn line maintained at the USDA Avian Disease and Oncology Laboratory (ADOL) in East Lansing, Michigan. Females homozygous for SJ have dark grey feathers with barring and homozygous males have much lighter colored plumage. This dimorphism in color is the result of the dilution that occurs with two copies of sexlinked barring in the males. The plumage of heterozygous birds (I, SJ) is intermediate in color compared to either parental type.Phthisis bulbi was noticed in adult females of the second generation of the homozygous SJ population. None of the parents of these females had apparent ocular lesions. Approximately 30% of the 85 surviving females had phthisis bulbi, while none of the 100 surviving males were affected. There was no clinical evidence of bacterial or viral infection, and the chickens were housed in pens isolated from chickens with experimental viral infections. Because the ocular anomaly appeared to be recessive and sex-linked, 4 test matings were designed to further study the inheritance.In matings 1 and 2, sighted SJ males, which were suspected of being carriers of the syndrome, were mated to either affected or sighted SJ females. These same male birds were then mated to either sighted females of Line 0 (II) (mating 3) or sighted females of ADOL Line 15I 5 (II) and Line 0 (II) (mating 4). All chicks had ophthalmic examinations at hatch and 2, 4, and 8 weeks of age.In mating 1,197 chicks were examined. Of the females, 62% were affected, and 10% of the males were affected. Received for publication January 12, 1997.Twenty-two progeny from mating 2 were examined, and 40% of the females and 8% of the males were affected. In both of these matings, approximately equal numbers of each sex were produced, and fertility and embryo viability were within a normal range. These data confirmed a much higher incidence of the ocular anomaly in females and therefore indicated a sex-influenced expression.In matings 3 and 4, when blind or carrier birds were mated to nonpigmented White Leghorns (II), only one affected chick was observed in 242 progeny. These data support the hypothesis that the anomaly is autosomal recessive. The affected chick in mating 4 was most likely the result of an error in the pedigree.Ophthalmic examinations of the newly hatched chicks were performed by using a slit lamp biomicroscope and an indirect ophthalmoscope. Affect...
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