PubMed · 4711964
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W D Trotter, F H Silverman. 1973. Experiments with the stutter-aid.. https://doi.org/10.2466/pms.1973.36.3c.1129
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In order to assess the role of L-type voltage-gated calcium channels in electrical stimulation-mediated neuroprotection in vivo, we assessed survival of primary auditory afferents (spiral ganglion cells) in systemically deafened guinea pigs following chronic electrical stimulation with or without intracochlear infusion of verapamil, an L-type voltage-gated calcium channel antagonist. Continuous intracochlear drug delivery (0.5 microl/h) was provided using a delivery system developed previously in our laboratory using Alzet mini-osmotic pumps. In the absence of chronic stimulation, spiral ganglion cell survival was relatively symmetric in animals treated unilaterally with either artificial perilymph or verapamil (50 microg/ml). In the presence of unilateral chronic electrical stimulation, spiral ganglion cell survival was significantly greater in stimulated, perilymph-infused ears, relative to the contralateral ear. In contrast, spiral ganglion cell survival was bilaterally symmetric in chronically stimulated, verapamil-infused animals. The difference in symmetry of spiral ganglion cell survival between the two groups was statistically significant. In vitro, passive depolarization has been demonstrated to enhance survival of cultured neurons via activation of L-type calcium channels. The results of this study indicate that, as suggested by in vitro depolarization models, in vivo electrical stimulation-mediated neuroprotection requires the activation of L-type voltage-gated calcium channels. Chronic electrical stimulation of the deaf ear is an ideal preparation for further studies in which to extrapolate findings from in vitro depolarization models.
Studies describing variations in fear-related memory in inbred mouse strains typically focus upon 24 h retention. As a consequence, little is known about strain differences in the establishment of longer lasting memories of aversive events. In the present study, male mice from the strains A/Ibg, AKR/J, BALB/cByJ, CBA/J, C3H/HeIbg, C57BL/6J, DBA/2J, LP/J, SJL/J and 129/SvevTac were tested 24 h, 14, or 60 days after contextual and auditory-cued fear conditioning. Consistent with previous data, 24 h after conditioning these strains exhibited substantial variation in levels of memory for the context and the auditory cue as measured by freezing scores. Sixty days after training, most strains exhibited some forgetting of the context and auditory cue, and again there was significant strain variation. Strain rankings at 60-day retention were similar to that at 24 h with a significant genetic correlation between freezing values for the two time periods. Fourteen days following training, nearly all strains exhibited generalized freezing, a behavioral phenotype originally observed in C57BL/6 but not DBA/2 mice. These data confirm that cognitive differences exist between several popular inbred mouse strains during 24 h contextual fear recall. In addition, they extend these differences into retention time frames longer than those typically used and reveal several unique learning profiles of mouse strains that may be useful in furthering our understanding of how memories are formed. Emotionally arousing situations are often recalled a great deal of time after an event. Therefore, a more complete picture of the biochemical and genetic underpinnings of learning and memory will benefit from studies using time points that assess time points beyond 24 h retention. The utility of the 14-day hyper responsiveness phenotype as a potential model for fear-related psychopathology is also discussed.
RATIONALE: The acoustic startle response is inhibited when the startling stimulus is preceded by a weaker non-startling acoustic stimulus. This phenomenon, termed prepulse inhibition of acoustic startle (PPI), is impaired in schizophrenics compared to normal controls. To date, there is conflicting evidence regarding whether PPI impairments improve with antipsychotic treatment. OBJECTIVES: To examine the effect of medication status on PPI in schizophrenic subjects. METHODS: First, we performed acoustic startle testing on 16 schizophrenic subjects when they were acutely decompensated off medication and later after they were stabilized on antipsychotic treatment. Second, in a between-group design, we tested 21 schizophrenic subjects off medication, 16 subjects on atypical neuroleptics, and 27 subjects on typical neuroleptics. RESULTS: In both the test-retest study and the between-group study, ANOVAs revealed no significant changes in startle to pulse alone stimuli, habituation of startle to pulse alone stimuli, PPI, latency to response onset, or latency to response peak between the treatment conditions. CONCLUSIONS: Our results do not support the hypothesis that impaired sensorimotor gating in schizophrenia improves with antipsychotic treatment. Rather, impaired gating persists despite symptomatic improvement on medication.