Conditioned stereotypy: Behavioral specification of the UCS and pharmacological investigation of the neural change

Hiroi, Noboru; White, Norman M.

doi:10.1016/0091-3057(89)90241-4

Cited by 33 publications

(15 citation statements)

References 22 publications

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“…As pointed out by Schiff (1982), since the original observation of Pavlov (1927) that some symptoms seen with an acute morphine injection could be elicited by preinjection procedure alone, numerous investigators demonstrated the classical conditioning of morphine responses (see Lynch et al 1976). In this respect, hyperactivity and stereotyped behaviors induced by dopamine agonists such as apomorphine, amphetamine and L-DOPA have also been conditioned in rodents (Pickens and Crowder 1967;Tilson and Rech 1973;Schiff et al 1980;Schiff 1982;Hiroi and White 1989;Carey 1992). However, in all of these studies the conditioned stimulus was an injection procedure with signals such as tone and/or specific environments.…”

Section: Discussionmentioning

confidence: 99%

Conditioning to Injection Procedures and Repeated Testing Increase SCH 23390-Induced Catalepsy in Mice

Chinen

Frussa‐Filho

1999

Neuropsychopharmacology

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The cataleptic behavior induced by the dopamine D 1 antagonist SCH 23390 (SCH) has proven to be a useful assay for investigating the sensitivity of D 1 -like dopamine receptor-mediated effects during chronic drug administration. A fundamental flaw in most of these studies may be the involvement of the "repeated measures effect," a behavioral phenomenon well demonstrated for neurolepticinduced catalepsy but not yet investigated for dopamineThe ability of chronic neuroleptic treatment to produce increasing or decreasing degrees of both Parkinsonism in humans (see Hansen and Hoffman 1997) and catalepsy in laboratory animals (Barnes et al. 1990) over time remains controversial. Specifically, concerning the evolution of catalepsy during chronic haloperidol treatment, tolerance (Asper et al. 1973;Ezrin-Waters and Seeman 1977;Campbell and Baldessarini 1981), sensitization (Antelman et al. 1986;Kinon and Kane 1989;Barnes et al. 1990), or no effects (György et al. 1969;Moller Nielsen et al. 1974;Frussa-Filho et al. 1992) have been reported. Although the patterns of change in catalepsy responses to chronic neuroleptic treatment are influenced by multiple determinants (Barnes et al. 1990), two specific biological mechanisms seem to be of particular importance in determining the development of tolerance or sensitization: dopamine receptor supersensitivity (Ezrin-Waters and Seeman 1977;Hoffman and Beninger 1988) and a learning process due to repeated testing in the catalepsy apparatus (Iwata et al. 1989;Ferré et al. 1990), respectively. In regards to the learning process, both repeated measures in a single session after acute haloperidol administration (Stanley and Glick 1976;Hillegaart et al. 1987 Received October 12, 1998; revised April 30, 1999; accepted May 17, 1999. N EUROPSYCHOPHARMACOLOGY 1999 -VOL . 21 , NO . 5 Conditioning and SCH 23390-Induced Catalepsy 671 et al. 1990) have been reported to markedly enhance the cataleptic behavior presented by rodents.For many years, dopamine D 2 -like receptors were implicated as the only site mediating the cataleptic behavior of neuroleptics (Seeman 1980). However, in 1984, Christensen et al. (1984 first reported the cataleptogenic properties of SCH 23390, a selective antagonist of D 1 -like dopamine receptors (Hyttel 1983). Thus, besides providing a functional correlate of dopamine D 1 receptor antagonism (Mizuki et al. 1996), SCH 23390-induced catalepsy has proven to be a useful assay for investigating the functional interactions between D 1 -and D 2 -like dopamine receptors (see Klemm 1993). Catalepsy has also been used to investigate the sensitivity of D 1 -like dopamine receptor-mediated effects during chronic drug administration. In two landmark investigations, Hess et al. (1986Hess et al. ( , 1988 reported that although chronic treatment of rats with SCH 23390 resulted in an increase in D 1 -like striatal dopamine receptors as well as in spontaneous locomotion and D 1 -like and D 2 -like dopamine agonist-induced stereotypy, no tolerance to the cataleptic effect ...

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Section: Discussionmentioning

confidence: 99%

Conditioning to Injection Procedures and Repeated Testing Increase SCH 23390-Induced Catalepsy in Mice

Chinen

Frussa‐Filho

1999

Neuropsychopharmacology

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“…Finally, we recently reported that signaling drug administration in the HOME environment using discrete stimuli (lights, tones, vibrations, and odors) is not sufficient to promote robust sensitization, even though such stimuli acquire CS properties (Crombag et al 2000). We conclude, therefore, that the ability of environmental context to act as a traditional excitor (CSϩ) does not account for its ability to promote sensitization (Carey and Gui 1998;Hiroi and White 1989;Martin-Iverson and Fawcett 1996).…”

Section: Effect Of Environmental Novelty On the Induction Of Psychomomentioning

confidence: 97%

The Ability of Environmental Context to Facilitate Psychomotor Sensitization to Amphetamine Can Be Dissociated from Its Effect on Acute Drug Responsiveness and on Conditioned Responding

Crombag

Badiani

Chan

et al. 2001

Neuropsychopharmacology

112

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Doses of amphetamine or cocaine that fail to induce psychomotor sensitization when given to a rat in its home NO . 6 Psychomotor Sensitization to Amphetamine 681 increasing attention because the neural changes underlying sensitization to drugs of abuse may contribute to addiction (Lett 1989;Piazza et al. 1989;Robinson and Berridge 1993). In studying the conditions that facilitate or retard sensitization we have found that the context in which drugs are administered has a large effect on their ability to induce psychomotor sensitization (Badiani et al. 1995a(Badiani et al. , 1995bRobinson et al. 1998, for review). For example, doses of amphetamine, cocaine, or morphine that fail to induce psychomotor sensitization when given in the home cage, induce robust sensitization when given in a distinct and relatively novel environment (Badiani et al. 2000b;Browman et al. 1998aBrowman et al. , 1998bCrombag et al. 1996). The mechanisms responsible for the facilitation of sensitization by a distinct environment are not known, but it is tempting to relate them to associative learning processes (Badiani et al. 1995a(Badiani et al. , 1995b. Indeed, it has been suggested that sensitization may be the result of a progressive increase in the ability of treatment-related stimuli to elicit a conditioned response (CR), which adds to the unconditioned drug response (UR) (Hinson and Poulos 1981;Pert et al. 1990;Tilson and Rech 1973). If this hypothesis is correct, manipulations that degrade the ability of contextual stimuli to acquire conditioned stimulus (CS) properties should attenuate the facilitation of sensitization that occurs when drugs are administered in a distinct environment. Increasing the interval between presentation of the would-be CS and the unconditioned stimulus (US) is known to impair conditioning (Kimble 1947;Pickens and Crowder 1967). Therefore, in the present experiment we studied the effect of increasing the CS-US interval on the development of sensitization produced by amphetamine, by habituating rats to the test environment prior to drug administration. The psychomotor stimulant effects of repeated intravenous (i.v.) injections of amphetamine were assessed by quantifying rotational behavior in rats with a unilateral 6-OHDA lesion. Injections were given (1) in the absence of any environmental stimuli predictive of drug administration (HOME groups); (2) immediately after rats were placed into a distinct environment (NOVEL groups); or (3) in a distinct environment, but after either 1 or 6-8 hr of habituation to that environment (1 hr and 6-8 hr HABITUA-TION groups). Intravenous injections of amphetamine were given using remote-controlled syringe pumps. Thus, amphetamine was administered in the absence of the aversive stimuli associated with other routes of experimental drug administration (e.g., appearance of an experimenter, handling, needle jab). MATERIALS AND METHODS Subjects and Behavioral MeasureMale Sprague-Dawley rats (Harlan Sprague Dawley, Indianapolis, IN), weighing 200-225 g on arrival were individu...

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“…Therefore, to maximize the intensity of locomotor activity and the temporal correlation between locomotor activation and the exposure to the test chamber, mice were placed in the test chambers for only 10 min. This procedure has been shown to optimize conditioning effects in rats (22), and pilot studies showed that this procedure established more reliable and robust locomotor sensitization and conditioned locomotor activity than longer exposure time (30 min) in mice at the dose of cocaine used. Locomotor activity predominates in this procedure, and focused stereotypy (which was rated blindly) was not observed over the six cocaine sessions in either the wild-type or mutant mice.…”

Section: Methodsmentioning

confidence: 99%

Fos B mutant mice: Loss of chronic cocaine induction of Fos-related proteins and heightened sensitivity to cocaine’s psychomotor and rewarding effects

Hiroi

Brown

Haile

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

262

190

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Chronic exposure to cocaine leads to prominent, long-lasting changes in behavior that characterize a state of addiction. The striatum, including the nucleus accumbens and caudoputamen, is an important substrate for these actions. We previously have shown that long-lasting Fos-related proteins of 35-37 kDa are induced in the striatum by chronic cocaine administration. In the present study, the identity and functional role of these Fos-related proteins were examined using fosB mutant mice. The striatum of these mice completely lacked basal levels of the 35-to 37-kDa Fos-related proteins as well as their induction by chronic cocaine administration. This deficiency was associated with enhanced behavioral responses to cocaine: fosB mutant mice showed exaggerated locomotor activation in response to initial cocaine exposures as well as robust conditioned place preference to a lower dose of cocaine, compared with wild-type littermates. These results establish the long-lasting Fos-related proteins as products of the fosB gene (specifically ⌬FosB isoforms) and suggest that transcriptional regulation by fosB gene products plays a critical role in cocaine-induced behavioral responses. This finding demonstrates that a Fos family member protein plays a functional role in behavioral responses to drugs of abuse and implicates fosB gene products as important determinants of cocaine abuse.

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Conditioned stereotypy: Behavioral specification of the UCS and pharmacological investigation of the neural change

Cited by 33 publications

References 22 publications

Conditioning to Injection Procedures and Repeated Testing Increase SCH 23390-Induced Catalepsy in Mice

Conditioning to Injection Procedures and Repeated Testing Increase SCH 23390-Induced Catalepsy in Mice

The Ability of Environmental Context to Facilitate Psychomotor Sensitization to Amphetamine Can Be Dissociated from Its Effect on Acute Drug Responsiveness and on Conditioned Responding

Fos B mutant mice: Loss of chronic cocaine induction of Fos-related proteins and heightened sensitivity to cocaine’s psychomotor and rewarding effects

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