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R L Hyson

Publications and source records attributed to R L Hyson.

28 records · Page 2Linked to original sources
PubMed1987

Ontogenetic change in the analysis of sound frequency in the infant rat.

Previous research has shown that there is an ontogenetic shift in the spatial code of sound frequency in the cochlea and central auditory nuclei. During ontogenesis, a given area of the basilar membrane or central auditory nuclei is maximally stimulated by sounds of progressively higher frequencies. Here, a similar ontogenetic shift in the rat's "perception" of sound frequency is reported. Animals were trained with a tone (CS) paired with footshock (US) and generalization of their conditioned response (CR) to different frequencies was assessed either 0.5 or 72 hr later. When 15-day-old animals were trained with an 8-kHz tone and tested 0.5 hr later, greater suppression of activity (CR) was evoked by the 8-kHz tone than by either a 12-kHz or a 6-kHz tone. When tested 72 hr after training, however, greater suppression of activity was evoked by a 12-kHz tone than by the 8-kHz training stimulus or by a 24-kHz tone. This shift in the peak of the generalization gradient could not be accounted for by changes in unconditioned responses to the test stimuli. Additionally, the observed shift in the generalization gradient was age-dependent. It was not observed when pups were trained at 18 days old and tested 72 hr later. The implications of these data for studies of the ontogenesis of learning and memory are discussed.

Age Factors↗
PubMed1984

Opiate and non-opiate analgesia induced by inescapable tail-shock: effects of dorsolateral funiculus lesions and decerebration.

Previous studies have demonstrated that inescapable tail-shock can produce either non-opiate or opiate short-term analgesia, dependent on the number of shocks delivered. Additionally, extended exposure to inescapable tail shock can produce long-term, opiate analgesic effects. Several lines of investigation suggest that the psychological dimension of perceived controllability may powerfully influence these phenomena in that each form of opiate analgesia can only be produced following exposure to inescapable, rather than equal amounts and distribution of escapable, shock. This has suggested that these opiate analgesias result from the organism's learning that it has no control over shock. Although it has been assumed that the opiate and non-opiate analgesias induced by tail shock may be subserved by neural circuitry similar to that mediating morphine analgesia and other forms of environmentally induced analgesia, no direct evidence exists to support this assumption. The present study sought to provide an initial attempt at defining the neural circuitry involved in these phenomena by examining the effect of bilateral dorsolateral funiculus (DLF) lesions and decerebration. These experiments revealed that pathways within the spinal cord DLF are critical for the production of short-term non-opiate analgesia, short-term opiate analgesia, and long-term opiate analgesia since bilateral DLF lesions abolished all three pain inhibitory effects. Additionally, it was found that decerebration did not attenuate either the short-term non-opiate or short-term opiate analgesia induced by inescapable tail shock. Combining the observations that these non-opiate and opiate short-term effects are not reduced by decerebration yet are abolished by DLF lesions clearly delimits the source of descending pain inhibition as being within the caudal brainstem.

Animals↗
PubMed1984

Ontogenesis of learning: II. Variation in the rat's reflexive and learned responses to acoustic stimulation.

The ontogenesis of the rat's reflexive and simple learned reactions to acoustic stimulation was investigated in five experiments. The pattern of results suggests that (a) reflexive reactions to tonal stimulation emerge earlier in ontogenesis than the capacity to learn about these stimuli, and (b) the age at which simple Pavlovian conditioning is first observed depends on the nature of the acoustic conditioned stimulus (CS). Specifically, these data suggest that pups are not capable of simple Pavlovian conditioning to a 2000-Hz tone (CS) paired with an oral infusion of sucrose (US) until they are 14-15 days old. The same acoustic stimulus will, however, evoke reflexive reactions (startle inspiration) in pups as young as 10-12 days old. Additionally, when a different auditory stimulus (an intermittent train of clicks) serves as the CS, there is evidence of conditioning in pups only 12-13 days old. It is suggested that these age-related dissociations in the emergence of reflexive and simple learned responses to sound reflect a caudal-to-rostral maturational sequence of the components of the ascending auditory system.

Acoustic Stimulation↗
PubMed1984

Ontogenesis of learning: III. Variation in the rat's differential reflexive and learned responses to sound frequencies.

The ontogenesis of the rat's differential response to variation in sound frequency was investigated. Two behavioral procedures were employed: (a) a differential Pavlovian conditioning procedure that provided a means of inferring the pup's capacity to learn to respond differentially on the basis of sound frequency (e.g., 2000 Hz vs 900 Hz), and (b) a habituation-generalization task that indexed the capacity to discriminate different sound frequencies from the pup's reflexive behavior. Pups less than 17 days old failed to learn to respond differentially to a 2000-Hz vs 900-Hz tone (Experiment I, IIA, IIB, and III). In contrast, pups only 14 days old discriminated tones that differed by as little as 200 Hz when the reflex-habituation-generalization procedure was employed (Experiment IV). This suggests that the reflexive and learned behaviors, potentially controlled by sound frequency, are dissociated during ontogenesis, the former emerging prior to the latter. These data were interpreted within a neurobiological framework that related ontogenetic changes in behavioral capacity to a caudal-to-rostral maturational sequence in the ascending auditory system of the components that contribute to these capacities.

Acoustic Stimulation↗
PubMed1983

Coping and immunosuppression: inescapable but not escapable shock suppresses lymphocyte proliferation.

Rats were given series of escapable shocks, identical inescapable shocks, or no shock. The subjects were reexposed to a small amount of shock 24 hours later, after which an in vitro measure of the cellular immune response was examined. Lymphocyte proliferation in response to the mitogens phytohemagglutinin and concanavalin A was suppressed in the inescapable shock group but not in the escapable shock group. This suggests that the controllability of stressors is critical in modulating immune functioning.

Animals↗
PubMed1982

Corticosterone: a critical factor in an opioid form of stress-induced analgesia.

The finding that some opioid-mediated forms of stress-induced analgesia are antagonized by hypophysectomy and dexamethasone has led to the suggestion that beta-endorphin, released from the pituitary, may mediate these analgesic reactions. "Long-term analgesia" (an opioid-mediated form of stress-induced analgesia), which is blocked by dexamethasone and hypophysectomy, was also blocked by adrenalectomy and reinstated with corticosterone therapy. Corticosterone is proposed to play a permissive role in long-term analgesia and to be a critical hormone mediating this phenomenon.

Adrenalectomy↗
PubMed1982

Extent and control of shock affects naltrexone sensitivity of stress-induced analgesia and reactivity to morphine.

Opioid and nonopioid mediated changes in pain sensitivity have been observed after exposure to various stressful conditions. A series of inescapable shocks sequentially produces an early form of analgesia which is not affected by the opiate antagonist, naltrexone, and a late antinociceptive response which is sensitive to reversal by naltrexone. Here, this is shown to be true over a wide range of doses. In a further experiment subjects given either escapable or inescapable shock were analgesic immediately after the stress session. However, the analgesia of inescapably shocked subjects was more sensitive to reversal by naltrexone. A final experiment revealed that inescapably shocked subjects, but not escapably shocked subjects, were hyperreactive to the analgesic effects of morphine 24 hr after shock. These results suggest that activation of an opiate system occurs only after extended exposure to stress and that this activation is greater when the stress is inescapable. Implications for opioid versus nonopioid mechanisms of stress-induced analgesia are discussed.

Animals↗
PubMed1982

Dissociation of long-term analgesia and the shuttle box escape deficit caused by inescapable shock.

Inescapably shocked rats perform poorly on a two-way shuttle box escape task 24 hr after the shock. Because inescapably shocked rats become analgesic upon reexposure to a small amount of shock 24 hr after inescapable shock, they are likely to be analgesic during the shuttle box escape task. Subjects receiving an equivalent amount of escapable shock display neither the escape dificit nor the analgesia. Both the analgesia and the escape deficit respond in a similar fashion to the manipulation of a variety of other variables. These findings have led to the suggestion that the analgesia ("long-term analgesia") may cause the inescapable-shock-produced escape deficit. However, the present experiments demonstrated that two pituitary manipulations that completely eliminate the analgesia have no effect on the escape deficit. Both hypophysectomy and dexamethasone administration blocked the analgesic consequences of inescapable shock but did not reduce the magnitude of the escape deficit. Therefore, the long-term analgesia produced by inescapable shock does not cause the deficit in shuttle box escape performance displayed by inescapably shocked rats. Furthermore, these results indicate that the pituitary is not essential in the production of this escape deficit.

Analgesia↗