Rapid acquisition of discrete-trial lever-press avoidance: effects of signal-shock interval

Acquisition of discrete-trial lever-press avoidance learning was studied in three experiments. Experiment I compared a new training procedure, which produces rates of lever-press avoidance learning comparable to those obtained in shuttle boxes, with a “conventional”, less efficient training procedure. A factorial design was used to compare continuous versus intermittent shock and a long-variable versus a short-fixed signal-shock interval. Learning was best in the groups trained with the long and variable interval and poorest in those trained with the short and fixed interval. Type of shock had no effect. Experiment II separated the effects of duration from those of variability of the signal-shock interval. Fixed and variable intervals of 10 and 60 sec were tested and duration was the only significant factor. Experiment III addressed the effect of the differential opportunity to avoid provided by long signal-shock intervals by varying this interval from 10 to 60 sec in 10-sec steps. Only the 10-sec group showed slow acquisition relative to the others. Analysis of avoidance response latencies showed that the distributions for all groups were positively skewed and that skewness increased with increasing duration of the signal-shock interval. At intervals longer than 20 sec, the animals made progressively less use of their increased opportunity to respond. The data do not support the opportunity-to-respond interpretation of the effects of duration of signal-shock interval and suggest that some type of inhibitory process may block lever-press avoidance learning at intervals as short as 10 sec. The significance of these findings for species-specific defense reaction and preparedness theories was emphasized.     

Analyzing mothers' speech to young autistic children: A methodological study

The development of a technique for analyzing mothers' speech to young children is described. The need for such a measure arose from two linked studies of autistic children, one comparing them with developmental dysphasic children and the other evaluating the results of a home-based approach to treatment. A 17-category system was developed which could encompass almost all the types of speech shown by mothers of young autistic and normal children and which differentiated between the speech used by different mothers in a way that was meaningfully related to the child's level of language development. The categories proved to be easily applicable and to show good inter-observer reliability. Tape-recordings made during home observations were found to be the best source of speech samples. The problems of time sampling, length and nature of speech sample, and observer effects are discussed.We are most grateful to our colleagues Dr. Lionel Hersov and Mr. William Yule for many helpful suggestions in developing the measures and for their comments on an earlier draft of the paper. The study is supported by a grant from the (British) Department of Health and Social Security.     

Differential effect of TEA on long-term synaptic modification in hippocampal CA1 and dentate gyrus in vitro.

The effectiveness of tetraethylammonium (TEA) and high-frequency stimulation (HFS) in inducing long-term synaptic modification is compared in CA1 and dentate gyrus (DG) in vitro. High-frequency stimulation induces long-term potentiation (LTP) at synapses of both perforant path-DG granule cell and Schaffer collateral-CA1 pyramidal cell pathways. By contrast, TEA (25 mM) induces long-term depression in DG while inducing LTP in CA1. The mechanisms underlying the differential effect of TEA in CA1 and DG were investigated. It was observed that T-type voltage-dependent calcium channel (VDCC) blocker, Ni2+ (50 microM), partially blocked TEA-induced LTP in CA1. A complete blockade of the TEA-induced LTP occurred when Ni2+ was applied together with the NMDA receptor antagonist, D-APV. The L-type VDCC blocker, nifidipine (20 microM), had no effect on CA1 TEA-induced LTP. In DG of the same slice, TEA actually induced long-term depression (LTD) instead of LTP, an effect that was blocked by D-APV. Neither T-type nor L-type VDCC blockade could prevent this LTD. When the calcium concentration in the perfusion medium was increased, TEA induced a weak LTP in DG that was blocked by Ni2+. During exposure to TEA, the magnitude of field EPSPs was increased in both CA1 and DG, but the increase was substantially greater in CA1. Tetraethylammonium application also was associated with a large, late EPSP component in CA1 that persisted even after severing the connections between CA3 and CA1. All of the TEA effects in CA1, however, were dramatically reduced by Ni2+. The results of this study indicate that TEA indirectly acts via both T-type VDCCs and NMDA receptors in CA1 and, as a consequence, induces LTP. By contrast, TEA indirectly acts via only NMDA receptors in DG and results in LTD. The results raise the possibility of a major synaptic difference in the density and/or distribution of T-type VDCCs and NMDA receptors in CA1 and DG of the rat hippocampus.     

Differential Effect of TEA on Long-Term Synaptic Modification in Hippocampal CA1 and Dentate Gyrus in vitro

The effectiveness of tetraethylammonium (TEA) and high-frequency stimulation (HFS) in inducing long-term synaptic modification is compared in CA1 and dentate gyrus (DG) in vitro. High-frequency stimulation induces long-term potentiation (LTP) at synapses of both perforant path-DG granule cell and Schaffer collateral-CA1 pyramidal cell pathways. By contrast, TEA (25 mM) induces long-term depression in DG while inducing LTP in CA1. The mechanisms underlying the differential effect of TEA in CA1 and DG were investigated. It was observed that T-type voltage-dependent calcium channel (VDCC) blocker, Ni²⁺ (50 μM), partially blocked TEA-induced LTP in CA1. A complete blockade of the TEA-induced LTP occurred when Ni²⁺ was applied together with the NMDA receptor antagonist, D-APV. The L-type VDCC blocker, nifidipine (20 μM), had no effect on CA1 TEA-induced LTP. In DG of the same slice, TEA actually induced long-term depression (LTD) instead of LTP, an effect that was blocked by D-APV. Neither T-type nor L-type VDCC blockade could prevent this LTD. When the calcium concentration in the perfusion medium was increased, TEA induced a weak LTP in DG that was blocked by Ni²⁺. During exposure to TEA, the magnitude of field EPSPs was increased in both CA1 and DG, but the increase was substantially greater in CA1. Tetraethylammonium application also was associated with a large, late EPSP component in CA1 that persisted even after severing the connections between CA3 and CA1. All of the TEA effects in CA1, however, were dramatically reduced by Ni²⁺. The results of this study indicate that TEA indirectly acts via both T-type VDCCs and NMDA receptors in CA1 and, as a consequence, induces LTP. By contrast, TEA indirectly acts via only NMDA receptors in DG and results in LTD. The results raise the possibility of a major synaptic difference in the density and/or distribution of T-type VDCCs and NMDA receptors in CA1 and DG of the rat hippocampus.