Similarities of the cataleptic state induced by β-endorphin and morphine

Rondeau, D.B.; Turcotte, Maria C.; Young, Lis; Hébert, David

doi:10.1016/0091-3057(82)90350-1

Cited by 11 publications

(5 citation statements)

References 22 publications

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“…The rigid immobility state induced by high doses of systemically administered morphine is behaviorally similar to that observed when morphine or B-endorphin is microinjected into the ventricles (lateral, fourth) or into periventricular structures of the limbic forebrain (n. accumbens septi) or limbic midbrain (periaqueductal gray; Browne et al, 1979;Costall, Fortune, & Naylor, 1978a, 1978bDill & Costa, 1977;Pert, 1978;Rondeau et al, 1982;Segal, Browne, Bloom, Ling, & Guillemin, 1977). However, this opiate/opioid immobility state differs markedly from neuroleptic catalepsy (Costall & Naylor, 1974;De Ryck et al, 1980;Rondeau et al, 1982;Segal et al, 1977).…”

Section: Neural Mechanisms Of Morphine Catalepsymentioning

confidence: 70%

“…High doses of systematically administered morphine (e.g., 10-80 mg/kg ip) produce a specific immobility state, whose postural and locomotor subsystems differ from those underlying haloperidol-induced catalepsy (De Ryck et al, 1980;De Ryck & Teitelbaum, 1983). The behavioral profile of this opiate-induced state is similar to that induced by intracerebroventricular injection of the endogenous opioid B-endorphin (Browne, Derrington, & Segal, 1979;Rondeau, Turcotte, Young, & Hebert, 1982). Thus, the present morphine-induced behavioral and EEG effects, which are naloxone-sensitive, may be relevant to neurobehavioral mechanisms involving endogenous opioid systems.…”

Section: Discussionmentioning

confidence: 97%

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Morphine catalepsy as an adaptive reflex state in rats.

Ryck¹,

Teitelbaùm²

1984

Behavioral Neuroscience

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These experiments demonstrate that morphine-induced catalepsy consists of two complementary, but opposite, behavioral extremes (rigid immobility and sudden locomotor bursts), each of which can be controlled by distinct classes of external stimuli. When stimuli that involve pain and/or nonnociceptive skin pressure are tonic (continuous), morphine-induced electroencephalographic (EEG) deactivation and behavioral immobility are potentiated, even to the extent that a stimulation-bound reversible coma results. In contrast, phasic (discrete) stimulation produces behavioral and/or EEG activation. EEG and behavioral rebound effects are observed following stressful (intense, prolonged) stimuli. On the basis of the observed stimulus controls, sensorimotor characteristics, and EEG reactions, it is suggested that similarities may exist between morphine-induced catalepsy and defensive reactions of immobility and escape in drug-free animals (i.e., the adaptive death- feigning reflex).

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Section: Neural Mechanisms Of Morphine Catalepsymentioning

confidence: 70%

Section: Discussionmentioning

confidence: 97%

Morphine catalepsy as an adaptive reflex state in rats.

Ryck¹,

Teitelbaùm²

1984

Behavioral Neuroscience

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“…The cataleptic responses to either dopamine antagonist alone were relatively small, and morphine alone produced no catalepsy at the dose used (12 mg/kg). Although higher doses of morphine are reported to induce a cataleptic state, this catalepsy differs qualitatively from that induced by neuroleptic drugs (5,20). Nevertheless, it is thought that opioid systems in the striatum interact with dopaminergic nigrostriatal neurons to alter motor behavior.…”

Section: Discussionmentioning

confidence: 94%

Dopamine D-1 and D-2 receptor antagonists potentiate analgesic and motor effects of morphine

Kiritsy-Roy

Standish

Terry

1989

Pharmacology Biochemistry and Behavior

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To examine the role of dopamine receptor subtypes mediating analgesic and motor responses to opioids, rats were pretreated with either saline or a selective D-1 or D-2 dopamine receptor antagonist 10 min prior to morphine (12 mg/kg IP). Analgesic response latency was determined using the hot plate test (52.5 degrees C and 55 degrees C), and catalepsy was assessed using the abnormal posture test. Morphine increased analgesic response latency to 44.5 +/- 7.9% of the maximum possible response, but had no cataleptic effect in the abnormal posture test. Pretreatment with either the D-1 antagonist, SCH 23390 (50-100 micrograms/kg), or the D-2 antagonist, eticlopride (20-150 micrograms/kg), potently enhanced morphine analgesia as measured on the 52.5 degrees C hot plate. Peak analgesic responses to morphine increased to 100 +/- 0% and 91.9 +/- 7.5% of maximum with the highest doses of SCH 23390 and eticlopride, respectively. These treatments also produced catalepsy. Increasing the hot plate temperature to 55 degrees C reduced response latency in groups treated with either dopamine receptor antagonist plus morphine. This indicates that the animals were capable of responding at a shorter latency and demonstrates that motor impairment cannot account for potentiation of morphine analgesia by D-1 and D-2 antagonists at 52.5 degrees C. These results show that the relationship between dopamine and opioids with respect to analgesic and motor systems involves both dopamine receptor subtypes.

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“…82 Also in rats, etonitazene at a 2 μg intraventricular dose and morphine at a 20 mg/kg parenteral dose produced similar effects on motor behavior, including catalepsy, hyporeflexia, and muscle rigidity. 83…”

Section: > = >mentioning

confidence: 99%

“…An early study reported contrasting behavior in rats receiving intraventricular injection of these two drugs: etonitazene (9.2 μg total dose) produced extreme muscle rigidity, while morphine (160–385 μg dose range) induced explosive motor behavior . Also in rats, etonitazene at a 2 μg intraventricular dose and morphine at a 20 mg/kg parenteral dose produced similar effects on motor behavior, including catalepsy, hyporeflexia, and muscle rigidity …”

Section: Medicinal Chemistry and Structure–activity Relationshipmentioning

confidence: 99%

DARK Classics in Chemical Neuroscience: Etonitazene and Related Benzimidazoles

Ujváry¹,

Christie

Evans-Brown

et al. 2021

ACS Chem. Neurosci.

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Etonitazene and related 2-benzylbenzimidazoles are potent analgetics invented in the research laboratories of the Swiss pharmaceutical giant CIBA in the late 1950s. Though the unprecedented structure distinguishes this class of compounds from poppy-derived and other synthetic analgetics, a range of studies indicate that these drugs are selective μ opioid receptor agonists possessing morphine-like pharmacotoxicological properties in animals as well as humans. Several unscheduled members of this synthetically readily accessible class of opioids that are not controlled under the international and national drug control systems have recently emerged on the illicit drug market. Among them, isotonitazene has been implicated in at least 200 fatalities in Europe and North America. None of the 2-benzylbenzimidazole derivatives have been developed into medicines, but etonitazene and some of its derivatives have been used as receptor probes and in addiction behavior studies in animals. The unique structure has inspired research on such benzimidazoles and related benzimidazolones of which “brorphine” made its debut as one of the newest psychoactive substance to emerge on the illicit opioid drug market in mid-2019. This in-depth review provides a historical introduction, an overview on the chemistry, pharmacological profiles, adverse effects, addiction liability, regulatory status, and the impact on chemical neuroscience of the 2-benzylbenzimidazoles. Structurally related benzimidazoles with opioid and/or analgesic properties are also discussed briefly.

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Similarities of the cataleptic state induced by β-endorphin and morphine

Cited by 11 publications

References 22 publications

Morphine catalepsy as an adaptive reflex state in rats.

Morphine catalepsy as an adaptive reflex state in rats.

Dopamine D-1 and D-2 receptor antagonists potentiate analgesic and motor effects of morphine

DARK Classics in Chemical Neuroscience: Etonitazene and Related Benzimidazoles

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