Reduction of distress vocalization in chicks by opiate-like peptides

Panksepp, Jaak; Vilberg, Tom; Bean, N. Jay; Coy, David H.; Kastin, Abba J.

doi:10.1016/0361-9230(78)90014-x

Cited by 150 publications

(46 citation statements)

References 10 publications

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“…A number of researchers have suggested that excessive brain opioid activity could explain the purported decreased pain sensitivity observed in autism, and contribute to or even determine the pathogenesis of autism (Frescka and Davis 1991;Panksepp 1979;Panksepp and Sahley 1987;Sher 1997). There are apparent symptom similarities (face validity) between autism and opiate addiction or behavioral states following administration of opiate and opioid agents in animals (Chamberlain and Herman 1990;Herman and Panksepp 1978;Kalat 1978;Panksepp et al 1978Panksepp et al , 1980aPanksepp et al , b, 1985Sahley and Panksepp 1987;Sandman 1992;Sandman et al 1979Sandman et al , 1991. Autistic children and opiate-addicted animals appear less sensitive to pain, less emotional and social.…”

Section: Predictive Modelsmentioning

confidence: 95%

“…Autistic children and opiate-addicted animals appear less sensitive to pain, less emotional and social. Additionally, stereotyped behaviors and social interaction impairments (which represent two main behavioral domains of autistic impairments) following administration of opioid agents in animals are reversed by naloxone (Herman and Panksepp 1978;Panksepp et al 1978;Van Wimersma et al 1988). However, the predictive validity of these animal models remain to be ascertained considering the inconsistent results of studies measuring opioid levels (Tordjman et al 1997) and the absence of clear benefits of opiate antagonist therapies (naloxone or naltrexone) in individuals with autism (Campbell et al 1990;Sandman 1992;Sandman et al 1991;Willemsen-Swinkels et al 1995).…”

Section: Predictive Modelsmentioning

confidence: 98%

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Animal Models Relevant to Schizophrenia and Autism: Validity and Limitations

et al. 2006

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Development of animal models is a crucial issue in biological psychiatry. Animal models provide the opportunity to decipher the relationships between the nervous system and behavior and they are an obligatory step for drug tests. Mouse models or rat models to a lesser extent could help to test for the implication of a gene using gene targeting or transfecting technologies. One of the main problem for the development of animal models is to define a marker of the psychiatric disorder. Several markers have been suggested for schizophrenia and autism, but for the moment no markers or etiopathogenic mechanisms have been identified for these disorders. We examined here animal models related to schizophrenia and autism and discussed their validity and limitations after first defining these two disorders and considering their similarities and differences. Animal models reviewed in this article test mainly behavioral dimensions or biological mechanisms related to autistic disorder or schizophrenia rather than providing specific categorical models of autism or schizophrenia. Furthermore, most of these studies focus on a behavioral dimension associated with an underlying biological mechanism, which does not correspond to the complexity of mental disorders. It could be useful to develop animal models relevant to schizophrenia or autism to test a behavioral profile associated with a biological profile. A multi-trait approach seems necessary to better understand multidimensional disorders such as schizophrenia and autism and their biological and clinical heterogeneity. Finally, animal models can help us to clarify complex mechanisms and to study relationships between biological and behavioral variables and their interactions with environmental factors. The main interest of animal models is to generate new pertinent hypotheses relevant to humans opening the path to innovative research.

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Section: Predictive Modelsmentioning

confidence: 95%

Section: Predictive Modelsmentioning

confidence: 98%

Animal Models Relevant to Schizophrenia and Autism: Validity and Limitations

et al. 2006

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“…Panksepp et al, 1980a, b;Rossi et al, 1983;Vilberg et al, 1984;Watson and Sufka, 1996;Warnick et al, 2005). This laboratory has utilized DVocs to index separation stress (Sufka and Weed, 1994), and developed a set of procedures (chick separation stress paradigm: Feltenstein et al, 2002Feltenstein et al, , 2003bFeltenstein et al, , 2004) that allows the model to be used as a high-utility, high-throughput, early preclinical in-vivo anxiolytic screening assay (Panksepp et al, 1978(Panksepp et al, , 1980bSmith et al, 2001;Sufka et al, 2001;Feltenstein et al, 2003a). The model possesses convergent validity as an anxiety-like model, in that separation stress reliably increases corticosterone levels (Feltenstein et al, 2002), a neuroendocrine marker of many stress responses.…”

Section: Introductionmentioning

confidence: 98%

Modeling anxiety-like states: pharmacological characterization of the chick separation stress paradigm

Warnick¹,

Wicks²,

Sufka³

2006

Behavioural Pharmacology

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While previous research has sought to validate the chick separation stress paradigm as an anxiolytic screening assay, it is unknown whether the paradigm better models a nonspecific anxiety-like state or something similar to panic disorder or generalized anxiety disorder. To characterize the anxiety model pharmacologically, cockerels were administered drug probes that were either: (1) only effective for treating panic disorder (phenelzine 3.125-25.0 mg/kg), (2) effective for treating both panic disorder and generalized anxiety disorder (alprazolam 0.065-0.5 mg/kg; clonidine 0.1-0.25 mg/kg; imipramine 1.0-15.0 mg/kg), (3) only effective for treating generalized anxiety disorder (buspirone 2.5-10.0 mg/kg; trazodone 0.1-3.0 mg/kg) or (4) capable of exacerbating symptoms of panic disorder in humans (yohimbine 0.1-3.0 mg/kg). At 7 days after hatch, chicks received either vehicle or drug probe intramuscularly 15 min prior to social separation under a mirror (low-stress) or no-mirror (high-stress) condition for a 180-s observation period. Dependent measures were distress vocalizations to index separation stress and sleep-onset latency to index sedation. Phenelzine, alprazolam, imipramine and clonidine were able to attenuate distress vocalizations (at doses without significant sedation) whereas buspirone and trazodone did not. Paradoxically, yohimbine modestly attenuated distress vocalizations. These results suggest that the chick separation stress paradigm better models panic disorder than generalized anxiety disorder as an anxiolytic screen.

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“…Most of the research on opioids and social behavior has focused on the μ opioid receptor (MOR) and its role in offspring-mother relationships, as well as adult relationships in non-monogamous primates. MOR manipulation affects the separation distress response between infant and mothers (Herman and Panksepp, 1978, Panksepp et al, 1978a, Panksepp et al, 1978b, Panksepp et al, 1980, Kalin et al, 1988), as well as physical contact (Fabre-Nys et al, 1982, Keverne et al, 1989, Kalin et al, 1995, Martel et al, 1995). There is also evidence that the κ opioid receptor (KOR) regulates separation related ultrasonic vocalizations in rat pups, in that KOR activation results in an increase in ultrasonic vocalizations (Carden et al, 1991, Carden et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

μ and κ opioid receptor distribution in the monogamous titi monkey (Callicebus cupreus): Implications for social behavior and endocrine functioning

Ragen

Freeman²,

Laredo

et al. 2015

Neuroscience

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The opioid system is involved in infant-mother bonds and adult-adult bonds in many species. We have previously shown that μ opioid receptors (MOR) and κ opioid receptors (KOR) are involved in regulating the adult attachment of the monogamous titi monkey. The present study sought to determine the distribution of MOR and KOR in the titi monkey brain using receptor autoradiography. We used [3H]DAMGO to label MORs and [3H]U69,593 to label KORs. MOR binding was heterogeneous throughout the titi monkey brain. Specifically, MOR binding was observed in the cingulate gyrus, striatum, septal regions, diagonal band, amygdala, hypothalamus, hippocampus, and thalamus. Binding was particularly dense in the septum, medial amygdala, paraventricular nucleus of the hypothalamus, mediodorsal thalamus with moderate binding in the nucleus accumbens. Consistent with other primate species, MOR were also observed in “neurochemically unique domains of the accumbens and putamen” (NUDAPs). In general KOR binding was more homogenous. KORs were primarily found in the cingulate gyrus, striatum, amygdala and hippocampus. Dense KOR binding was observed in the claustrum. Relative MOR and KOR binding in the titi monkey striatum was similar to other humans and primates, but was much lower compared to rodents. Relative MOR binding in the titi monkey hypothalamus was much greater than that found in rodents. This study was the first to examine MOR and KOR binding in a monogamous primate. The location of these receptors gives insight into where ligands may be acting to regulate social behavior and endocrine function.

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Reduction of distress vocalization in chicks by opiate-like peptides

Cited by 150 publications

References 10 publications

Animal Models Relevant to Schizophrenia and Autism: Validity and Limitations

Animal Models Relevant to Schizophrenia and Autism: Validity and Limitations

Modeling anxiety-like states: pharmacological characterization of the chick separation stress paradigm

μ and κ opioid receptor distribution in the monogamous titi monkey (Callicebus cupreus): Implications for social behavior and endocrine functioning

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