In prepulse inhibition (PPI), startle responses to sudden, unexpected stimuli are markedly attenuated if immediately preceded by a weak stimulus of almost any modality. This experimental paradigm exposes a potent inhibitory process, present in nervous systems from invertebrates to humans, that is widely considered to play an important role in reducing distraction during the processing of sensory input. The neural mechanisms mediating PPI are of considerable interest given evidence linking PPI deficits with some of the cognitive disorders of schizophrenia. Here, in the marine mollusk Tritonia diomedea, we describe a detailed cellular mechanism for PPI--a combination of presynaptic inhibition of startle afferent neurons together with distributed postsynaptic inhibition of several downstream interneuronal sites in the startle circuit.

In vitro slice preparations of CNS tissue are invaluable for studying neuronal function. However, up to now, slice protocols for adult mammal spinal motoneurons--the final common pathway for motor behaviors--have been available for only limited portions of the spinal cord. In most cases, these preparations have not been productive due to the poor viability of motoneurons in vitro. This report describes and validates a new slice protocol that for the first time provides reliable intracellular recordings from lumbar motoneurons of adult rats. The key features of this protocol are: preexposure to 100% oxygen; laminectomy prior to perfusion; anesthesia with ketamine/xylazine; embedding the spinal cord in agar prior to slicing; and, most important, brief incubation of spinal cord slices in a 30% solution of polyethylene glycol to promote resealing of the many motoneuron dendrites cut during sectioning. Together, these new features produce successful recordings in 76% of the experiments and an average action potential amplitude of 76 mV. Motoneuron properties measured in this new slice preparation (i.e., voltage and current thresholds for action potential initiation, input resistance, afterhyperpolarization size and duration, and onset and offset firing rates during current ramps) are comparable to those recorded in vivo. Given the mechanical stability and precise control over the extracellular environment afforded by an in vitro preparation, this new protocol can greatly facilitate electrophysiological and pharmacological study of these uniquely important neurons and other delicate neuronal populations in adult mammals.

When repeatedly elicited, the oscillatory escape swim of the marine mollusc Tritonia diomedea undergoes habituation of the number of cycles per swim. Although similar in most respects to habituation observed in vertebrates and other invertebrates, one key feature, dishabituation, has been surprisingly difficult to demonstrate. Here we evaluate the hypothesis that this is due to interference from short-term sensitization, which is manifested as a reduction in swim onset latency, that occurs simultaneously during habituation training. Robust dishabituation was obtained using a multisession habituation protocol designed to allow this sensitization to dissipate before the dishabituatory stimulus was applied. These results extend the similarity of habituation in Tritonia to that described in other species, strengthening the usefulness of this preparation as a model system for studies of the cellular basis of habituation.

Previous studies in our laboratory have shown that a single exposure to 100% carbon dioxide (CO2) can serve as an effective unconditioned stimulus (US) in a Pavlovian aversive-context conditioning paradigm in rats. Although the US exposure parameters employed in the initial studies were sufficient for producing a context-specific enhancement of behavioral freezing and analgesia, it had yet to be determined whether variations of these CO2 conditioning procedures would produce other conditioning effects. Thus, the purpose of the following experiment was to investigate the intensity of the US on the conditioned response (CR). The findings confirm that variations in CO2 concentrations produce changes in the CR that are consistent with principles of Pavlovian conditioning. The findings lend additional support to the tenability of a dyspneic suffocation fear theory of panic disorder, a theory that postulates that at least one type of panic attack could be a consequence of Pavlovian conditioning.