AN ANALOGUE EVALUATION OF ENVIRONMENTAL ENRICHMENT: THE ROLE OF STIMULUS PREFERENCE

To evaluate the effects of environmental enrichment on stereotypic self-injurious behavior (SIB), we conducted an assessment of preference for manipulating alternative stimuli rather than engaging in SIB. First, for each of 3 participants, a functional analysis of SIB was conducted in Phase 1. Participants were selected for Phase 2 if the functional analysis showed that SIB persisted in the absence of social consequences. In Phase 2, a preference assessment was conducted in which participants were observed manipulating preferred stimuli in a free-operant format. A measure was taken of time spent manipulating each stimulus and time spent engaging in SIB. In Phase 3, environmental enrichment was evaluated using stimuli that were preferred over the target response, and alternative treatments were evaluated in the event of environmental enrichment failure. Results suggested that the free-operant preference assessment (a) predicted the efficacy or inefficacy of an environmental enrichment procedure and (b) suggested possible treatment alternatives when environmental enrichment was ineffective. Collectively, the results may provide a basis for interpreting the idiosyncratic effects of environmental enrichment and a rationale for treatment selection when behavioral function is unknown.     

Distinguishing “slit” and “split”—an invariant timing cue in speech perception

The effect of speech rate on the distinction between “slit” and “split” was investigated. This distinction may be cued solely by a silent interval (SI) of sufficient duration between the [s] and the [1], and the boundary SI, at which “slit” and “plit” are perceived with equal probability, determined. In this experiment, although subjects showed good identification of the stimulus categories within the range of silent intervals used, no shift in the boundary SI was found for a twofold increase in speech rate. This finding is contrasted with most recent experiments which demonstrate “compensation” for changes in speaker characteristics, such as speech rate. Implications for models of speech perception are discussed.     

A microcomputer-controlled complex reaction time instrument

An inexpensive microcomputer system that measures complex reaction time to a visual stimulus is described. This system can determine the rate of gain of information by utilizing a two-, four-, or eight-choice reaction time task encompassed within the same unit. The system turns on randomly chosen lights and monitors the time required for the subject to depress a corresponding switch. Information describing the stimulus and the subject’s response are printed on a Teletype after each response.     

Gabaergic mechanisms of hypothalamic nuclei in the expression of conditioned fear

The amygdala, the dorsal periaqueductal gray (dPAG), and the medial hypothalamus have long been recognized to be a neural system responsible for the generation and elaboration of unconditioned fear in the brain. It is also well known that this neural substrate is under a tonic inhibitory control exerted by GABA mechanisms. However, whereas there is a growing body of evidence to suggest that the amygdala and dPAG are also able to integrate conditioned fear, it is still unclear, however, how the distinct hypothalamic nuclei participate in fear conditioning. In this work we aimed to examine the extent to which the gabaergic mechanisms of this brain region are involved in conditioned fear using the fear-potentiated startle (FPS). Muscimol, a GABA-A receptor agonist, and semicarbazide, an inhibitor of the GABA synthesizing enzyme glutamic acid decarboxylase (GAD), were used as an enhancer and inhibitor of the GABA mechanisms, respectively. Muscimol and semicarbazide were injected into the anterior hypothalamus (AHN), the dorsomedial part of the ventromedial nucleus (VMHDM), the dorsomedial (DMH) or the dorsal premammillary (PMD) nuclei of male Wistar rats before test sessions of the fear conditioning paradigm. The injections into the DMH and PMD did not produce any significant effects on FPS. On the other hand, muscimol injections into the AHN and VMHDM caused significant reduction in FPS. These results indicate that injections of muscimol and semicarbazide into the DMH and PMD fail to change the FPS, whereas the enhancement of the GABA transmission in the AHN and VMHDM produces a reduction of the conditioned fear responses. On the other hand, the inhibition of this transmission led to an increase of this conditioned response in the AHN. Thus, whereas DMH and PMD are known to be part of the caudal-most region of the medial hypothalamic defensive system, which integrates unconditioned fear, systems mediating conditioned fear select the AHN and VMHDM nuclei that belong to the rostral-most portion of the hypothalamic defense area. Thus, distinct subsets of neurons in the hypothalamus could mediate different aspects of the defensive responses.