Search PubMed⌕ Search

Biomedical subjects

S F Maier

Publications and source records attributed to S F Maier.

At least 145 records · Page 8Linked to original sources
PubMed1986

Stressor controllability and the pituitary-adrenal system.

Stressor controllability can alter both behavior and pituitary-adrenal activity. Potential mediation of these behavioral effects by differential pituitary-adrenal output requires that the precise conditions that lead to differential behavioral consequences also produce differential pituitary-adrenal activity. Both plasma ACTH and corticosterone levels were measured at various times following escapable and yoked inescapable electric shock conditions known to produce differential behavioral outcomes. The escapable and inescapable shock procedures did not produce a detectable differential effect. Both shock conditions produced equivalent elevation of ACTH and corticosterone. Neither decay rates nor the ACTH and corticosterone response to shock reexposure differed among shocked groups.

Adrenocorticotropic Hormone↗
PubMed1985

Coping and seizure susceptibility: control over shock protects against bicuculline-induced seizures.

Rats were either given 80 escapable shocks, yoked inescapable shocks, restraint or given no treatment. Two hours later all subjects received i.p. injection of bicuculline (4, 6 or 8 mg/kg) and were immediately tested for latency to initial myoclonic jerk and clonus. The latency to clonic convulsion was dramatically affected by prior shock treatment, and the direction of this change depended upon the escapability/inescapability of the shock. Subjects that were given escapable shock showed a delay of onset to seizure, while subjects inescapably shocked demonstrated a decreased latency to clonus in comparison to restrained and naive controls. It was also demonstrated that if the subjects were tested immediately following a stress experience, both the 80 escapable and inescapable shock condition protected against bicuculline-induced seizures in comparison to the control condition. Finally Experiment 2 confirmed a previous finding that less stress, i.e., 20 inescapable shocks, protects against seizures when the animals are challenged with bicuculline either immediately or 2 h later. Our suggestion is that control over stress may facilitate GABAergic transmission, and this may be the mechanism whereby coping protects against the behavioral and physiological disruption produced by exposure to a stressor.

Adaptation, Psychological↗
PubMed1985

An anxiogenic benzodiazepine receptor ligand induces learned helplessness.

Rats treated with the anxiogenic beta-carboline, N-methyl-beta-carboline-3-carboxamide (FG-7142), failed to acquire an escape response 24 h after treatment. Administration of FG-7142 resulted in a behavioral effect equivalent to a session of inescapable tailshock in this paradigm of learned helplessness. Pretreatment of rats with the selective benzodiazepine receptor antagonist Ro15-1788 blocked the development of learned helplessness elicited by FG-7142. These findings suggest that 'anxiety' may be a major factor in the development of learned helplessness.

Animals↗
PubMed1985

Spinal pain suppression mechanisms may differ for phasic and tonic pain.

The dorsolateral funiculus (DLF) spinal pathway has previously been identified as a major pathway involved in descending modulation of pain. While bilateral lesions of the DLF attenuated systemic morphine analgesia as measured by the tail-flick test, they failed to attenuate analgesia as measured by the formalin test. These results suggest that phasic and tonic pain, modeled by the tail-flick and formalin tests, respectively, may utilize different pain suppression mechanisms.

Animals↗
PubMed1985

Shock controllability and the nature of stress-induced analgesia.

Three experiments were conducted to examine the impact of the escapability of shock on the nature of the analgesia produced by shock. In Experiment 1, rats were exposed to 0, 20, 40, or 80 escapable or yoked inescapable shocks. Tail-flick testing revealed a "double-peak" pattern in which analgesia was present after 20 and 80 shocks. This was true for both escapable and inescapable shock. Analgesia after 20 escapable or inescapable shocks was insensitive to naltrexone, as was the analgesia after 80 escapable shocks. However, the analgesia after 80 inescapable shocks was completely blocked by naltrexone. Moreover, in Experiment 2 the analgesia following 80 inescapable shocks persisted for at least 2 hr, whereas it dissipated rapidly following 80 escapable shocks. Further, the analgesia produced by escapable shock even dissipated with the continued occurrence of escapable shock. Finally, shock controllability was shown to alter the analgesia produced by subsequent exposure to shock. Prior experience with controllable shock completely blocked the late-appearing naltrexone reversible analgesia; prior experience with uncontrollable shock led it to appear sooner.

Animals↗
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

Librium prevents the analgesia and shuttlebox escape deficit typically observed following inescapable shock.

Administration of a benzodiazepine, chlordiazepoxide (CDP), prior to exposure to inescapable shock prevented both the long-term analgesia and the shuttle-escape deficit typically observed following inescapable shock. If given only prior to testing, CDP had little effect. The protective effects of CDP were determined not to be a result of state dependency or a general facilitatory effect of the drug on escape performance. It is suggested that the induction of anxiety or fear by inescapable shock is critical in mobilizing endogenous changes such as transmitter depletion which are thought to be responsible for the deficits observed.

Analgesia↗
PubMed1984

The formalin test and the opioid nature of stress-induced analgesia.

Exposure to electric shock produces an analgesic reaction (SIA) that is reversed by opiate antagonists ("opioid" SIA) under some conditions but not under other conditions ("nonopioid" SIA). A number of studies using tail-flick to radiant heat as the measure of pain sensitivity have found that a small number of shocks lead to nonopioid SIA, while a large number of shocks produce opioid SIA. In contrast, a small number of shocks have been reported to produce opioid SIA when the Formalin test was used to measure pain reactivity. However, the Formalin test involves administering a chronic pain stimulus (injection of Formalin into the paw) for an extended period before the shocks. Here it is reported that this "preexperimental" stress is sufficient to convert the SIA after a small number of shocks measured by tail-flick to the opioid form.

Afferent Pathways↗
PubMed1984

Exposure to uncontrollable stress alters withdrawal from morphine.

Prior exposure to uncontrollable stress potentiates morphine analgesia. This study was designed to examine the influence of the controllability/uncontrollability of shock as a stressor on the severity of subsequent morphine withdrawal. In Experiment 1, rats that received two daily sessions of 80 yoked-inescapable shocks, in contrast to those given 80 escapable shocks or restrained without shock, showed an enhanced series of correlated withdrawal behaviors (i.e., mouthing, teeth chattering, and head/body shakes) 24 hr later when injected with morphine (5 mg/kg) followed by a naloxone (5 mg/kg) challenge. In Experiment 2, this finding was replicated with escape-yoked-restrained groups of rats given saline injections during the pretreatment phase, but the impact that only inescapable shock had on later precipitated withdrawal was completely blocked when subjects were administered naltrexone (14 mg/kg) before each shock session. These findings are discussed in terms of the capability of inescapable shock to activate an endogenous opiate system(s) and thereby lead to a sensitization of release or receptor processes which could potentiate later morphine withdrawal.

Animals↗
PubMed1984

Learned helplessness and animal models of depression.

The degree to which organisms can exert control over events to which they are exposed has a strong impact on behavior and physiological functioning. Effects caused by the uncontrollability of events that are beyond the organism's control rather than by the events per se have been called learned helplessness effects. The present paper reviews such learned helplessness effects. At a behavioral level, uncontrollable aversive events result in associative, motivational, and emotional deficits. At a neurochemical level, uncontrollable but not controllable aversive events have been reported to lead to disturbances in cholinergic, noradrenergic, dopaminergic, serotonergic, and GABAergic systems. However, there are interpretive difficulties in this literature, and these are discussed. The controllability/uncontrollability of aversive events has a role in producing stress-induced analgesia and the activation of endogenous opiate systems. These relationships are reviewed. It is proposed that the learning that aversive events cannot be controlled activates an opiate system. The research reviewed is related to depression, and the general issue of animal models of depression is discussed. It is concluded that no experimental paradigm can be a model of depression in some general sense, but can only model a particular aspect. Learned helplessness may model "stress and coping".

Affect↗
PubMed1984

Effects of task-irrelevant cues and reinforcement delay on choice-escape learning following inescapable shock: evidence for a deficit in selective attention.

Prior exposure to inescapable shock has been reported to interfere with choice-escape learning, but several investigators have failed to obtain this effect. A series of five experiments examined the conditions under which choice-escape learning in an automated Y-maze is impaired by pretreatment with inescapable shock. Inescapably shocked rats made more errors and responded more slowly than did controls only when shock termination was delayed and task-irrelevant cues were present during choice-escape training. These findings are discussed in terms of information processing and neurochemical consequences of exposure to inescapable shock.

Animals↗
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↗
PubMed1983

Coping and the stress-induced potentiation of stimulant stereotypy in the rat.

It has been shown that stressed rats display increased stereotypy in response to a subsequent amphetamine challenge. Evidence is presented showing that stress potentiates cocaine stereotypy as well. These effects of stress were found to be particular to stress that could not be controlled in that rats receiving an identical amount of stress from footshock, but allowed to control its duration, displayed no more stereotypy than did nonstressed rats. These findings have implications for the role of stress and coping in amphetamine and cocaine psychoses, endogenous psychoses, and some forms of schizophrenia.

Animals↗
PubMed1983

Long-term stress-induced analgesia blocked by scopolamine.

An 'opioid' form of analgesia ('long-term analgesia') was completely blocked by scopolamine. This effect of a muscarinic antagonist suggests that muscarinic cholinergic processes may play an important role in this analgesia and in other types of endogenous pain control.

Animals↗
PubMed1983

The opioid/nonopioid nature of stress-induced analgesia and learned helplessness.

Exposure to a variety of stressors produces a subsequent analgesic reaction. This stress-induced analgesia (SIA) is sometimes opioid in nature (reversed by opiate antagonists and cross-tolerant with morphine) and sometimes nonopioid. Both 30 min of intermittent footshock and 60-80 five-sec tailshocks have been shown to produce opioid SIA, whereas 3 min of continuous footshock and 5-40 tailshocks produce nonopioid SIA. We report that both of the opioid SIA procedures produce a learned helplessness effect as assessed by shuttlebox escape acquisition and an analgesia that is reinstatable 24 hr. later. The nonopioid procedures produce neither a learned helplessness effect nor a reinstatable analgesia. It is argued that these data implicate the learning of uncontrollability in the activation of opioid systems.

Analgesia↗
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↗