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1.
Biol Bull ; 201(3): 424-34, 2001 Dec.
Article in English | MEDLINE | ID: mdl-11751254

ABSTRACT

Changes in the heart rates of lobsters (Homarus americanus) were used as an indicator that the animals were capable of sensing a reduction in the salinity of the ambient seawater. The typical response to a gradual (1 to 2 ppt/min) reduction in salinity consisted of a rapid increase in heart rate at a mean threshold of 26.6 +/- 0.7 ppt, followed by a reduction in heart rate when the salinity reached 22.1 +/- 0.5 ppt. Animals with lesioned cardioregulatory nerves did not exhibit a cardiac response to changes in salinity. A cardiac response was elicited from lobsters exposed to isotonic chloride-free salines but not to isotonic sodium-, magnesium- or calcium-free salines. There was little change in the blood osmolarity of lobsters when bradycardia occurred, suggesting that the receptors involved are external. Furthermore, lobsters without antennae, antennules, or legs showed typical cardiac responses to low salinity, indicating the receptors are not located in these areas. Lobsters exposed to reductions in the salinity of the ambient seawater while both branchial chambers were perfused with full-strength seawater did not display a cardiac response until the external salinity reached 21.6 +/- 1.8 ppt. In contrast, when their branchial chambers were exposed to reductions in salinity while the external salinity was maintained at normal levels, changes in heart rate were rapidly elicited in response to very small reductions in salinity (down to 29.5 +/- 0.9 ppt in the branchial chamber and 31.5 +/- 0.3 ppt externally). We conclude that the primary receptors responsible for detecting reductions in salinity in H. americanus are located within or near the branchial chambers and are primarily sensitive to chloride ions.


Subject(s)
Heart Rate/drug effects , Nephropidae/physiology , Animals , Calcium/pharmacology , Chlorides/pharmacology , Female , Heart Rate/physiology , Magnesium/pharmacology , Male , Nephropidae/drug effects , New Hampshire , Osmolar Concentration , Seawater/chemistry , Sodium/pharmacology , Sodium Chloride/pharmacology
2.
J Comp Neurol ; 423(1): 132-9, 2000 Jul 17.
Article in English | MEDLINE | ID: mdl-10861542

ABSTRACT

It has been hypothesized that normal pruning of exuberant branching of afferent neurons in the developing cochlea is caused by the arrival of the olivocochlear efferent neurons and the resulting competition for synaptic sites on hair cells. This hypothesis was supported by a report that afferent innervation density on mature outer hair cells (OHCs) is elevated in animals deefferented at birth, before the olivocochlear system reaches the outer hair cell area (Pujol and Carlier [1982] Dev. Brain Res. 3:151-154). In the current study, this claim was evaluated quantitatively at the electron microscopic level in four cats that were de-efferented at birth and allowed to survive for 6-11 months. A semiserial section analysis of 156 OHCs from de-efferented and normal ears showed that, although de-efferentation essentially was complete in all four cases, the number and distribution of afferent terminals on OHCs was indistinguishable from normal, and the morphology of afferent synapses was normal in both the inner hair cell area and the OHC area. Thus, the postnatal presence of an efferent system is not required for the normal development of cochlear afferent innervation, and the synaptic competition hypothesis is not supported.


Subject(s)
Afferent Pathways/growth & development , Afferent Pathways/ultrastructure , Axotomy/adverse effects , Denervation/adverse effects , Hair Cells, Auditory, Inner/growth & development , Hair Cells, Auditory, Inner/ultrastructure , Hair Cells, Auditory, Outer/growth & development , Hair Cells, Auditory, Outer/ultrastructure , Vestibulocochlear Nerve Injuries , Afferent Pathways/physiology , Age Factors , Animals , Animals, Newborn , Cats , Cell Count , Cell Size , Hair Cells, Auditory, Inner/physiology , Hair Cells, Auditory, Outer/physiology , Microscopy, Electron , Nerve Degeneration/pathology , Nerve Degeneration/physiopathology , Presynaptic Terminals/pathology , Presynaptic Terminals/physiology , Presynaptic Terminals/ultrastructure , Vestibulocochlear Nerve/pathology , Vestibulocochlear Nerve/physiopathology
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