ABSTRACT
Cross-fostering studies suggest cocaine-induced deficits in maternal behavior could be associated with altered behavior of offspring following prenatal cocaine-exposure. Neonatal vocalizations are an important offspring cue facilitating early interactions between dam and rodent pup offspring and have been shown to be altered following prenatal cocaine-exposure. It is unclear how variations in acoustic parameters of USVs impact maternal behavior and the mechanism(s) underlying these processes. The present study examined differences in cocaine-exposed and control rodent dam maternal preference of cocaine-exposed or untreated pups in a dual choice apparatus. Relationship of preference-like behavior with pup USVs and dam oxytocin expression was explored. Gestational cocaine-exposure interfered with preference-like behavior of dams on postpartum day 1 with cocaine-exposure associated with decreased time spent on the cocaine-exposed pup side compared to the control pup side, and decreases in preference-like behavior associated in part with decreased number of USVs being emitted by cocaine-exposed pups. On postpartum day 5, decreased oxytocin expression in the medial preoptic area was associated with altered preference-like behavior in cocaine-exposed dams, including frequency and latency to touch/sniff pups. Results indicate cocaine's effects on the mother-infant relationship is likely synergistic, in that cocaine influences mother and offspring both independently and concertedly and that variations within pup vocalizations and the oxytocin system may be potential mechanism(s) underlying this synergistic relationship during the postpartum period.
Subject(s)
Cocaine/toxicity , Cues , Dopamine Uptake Inhibitors/toxicity , Maternal Behavior/drug effects , Oxytocin/metabolism , Prenatal Exposure Delayed Effects , Preoptic Area/metabolism , Age Factors , Analysis of Variance , Animals , Animals, Newborn , Female , Gestational Age , Postpartum Period/drug effects , Pregnancy , Prenatal Exposure Delayed Effects/chemically induced , Prenatal Exposure Delayed Effects/metabolism , Prenatal Exposure Delayed Effects/pathology , Preoptic Area/drug effects , Rats , Rats, Sprague-Dawley , Vocalization, Animal/drug effectsABSTRACT
The purpose of this study was to evaluate healthy geriatric dogs for the presence of systemic hypertension. Thirty-three geriatric dogs (i.e., dogs exceeding the geriatric age range for their weight group) and 22 control dogs (i.e., dogs less than six years of age) were evaluated by measuring blood pressure with an oscillometric monitor. Five consecutive blood pressure measurements were taken in each dog, averaged, and compared. Diastolic and mean blood pressure measurements were significantly lower in the geriatric group as compared to the control group. Systolic blood pressure measurements were not significantly different between the two groups. Systemic hypertension does not appear to be a common clinical problem in the healthy geriatric dog.
Subject(s)
Aging/physiology , Blood Pressure , Dog Diseases/physiopathology , Dogs/physiology , Hypertension/veterinary , Animals , Blood Pressure Determination/methods , Blood Pressure Determination/veterinary , Case-Control Studies , Dog Diseases/diagnosis , Dog Diseases/epidemiology , Female , Hypertension/diagnosis , Hypertension/epidemiology , Hypertension/physiopathology , Male , PrevalenceABSTRACT
The initiation of Wallerian degeneration in the severed optic nerve of the newt (Triturus viridescens) was very rapid and intense. Significant degeneration of nonmyelinated axons was observed as early as six hours after lesion (h.a.l.) and was almost complete by 48 h.a.l. Initial degeneration of non-myelinated axons began in "extracellular digestion chambers" formed between burgeoning ependymoglial processes. The remaining fragments and debris were later phagocytized by surrounding ependymoglial processes. Many axons of myelinated fibers have degenerated as early as 6 h.a.l. However, the overall population of myelinated axons degenerates at a much slower rate than nonmyelinated ones, for many of them appear intact as late as 48 h.a.l. Some myelin sheaths show significant signs of degeneration by 6 h.a.l. Indeed, by this time a number of myelinated fibers have completely degenerated leaving only large vacuolated spaces in the nerve parenchyma. Swelling and vacuolization of the sheath are among the earliest signs of myelin degeneration. The ependymoglial cell response to optic nerve lesion is manyfold and dramatic. By 6 h.a.l. there are signs of burgeoning ependymoglial processes which begin to resemble scar formation (gliosis) by 48 h.a.l. The morphological evidence is consistent with the concept of an important phagocytic role of ependymoglial cells during the early stages of optic nerve degeneration.