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  • Cocaine  (2)
  • 3-Methoxy-4-hydroxyphenylglycol (MHPG)  (1)
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  • 1
    Electronic Resource
    Electronic Resource
    Clonidine infusions into the locus coeruleus attenuate behavioral and neurochemical changes associated with naloxone-precipitated withdrawal (1988)
    Springer
    Psychopharmacology 96 (1988), S. 121-134 
    Details
    ISSN: 1432-2072
    Keywords: Clonidine ; Locus coeruleus ; Intracerebral infusion ; Withdrawal ; Naloxone ; Morphine ; 3-Methoxy-4-hydroxyphenylglycol (MHPG) ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Clonidine, an alpha-2-adrenergic agonist, suppresses signs of opiate withdrawal in animals and in man. Electrical or chemical stimulation of the nucleus locus coeruleus (LC) increases noradrenergic activity and brain concentration of the noradrenergic metabolite MHPG, and produces many signs of opiate withdrawal. Thus, clonidine's ability to attenuate withdrawal might be due to the reduction of noradrenergic neuronal activity originating in the LC, but additional alpha-2-adrenergic receptors throughout the body and other mechanisms may also play a role. The present study explored the neuroanatomical and pharmacological selectivity of alpha-2-adrenergic receptors of the LC in the anti-withdrawal action of clonidine. Experiment 1 tested the hypothesis that behavioral and biochemical measures of naloxone-precipitated withdrawal from morphine would be blocked by infusions of clonidine (0.6 or 2.4 μg/μl) into the LC. Significant reductions were observed in the occurrence of diarrhea, ptosis, weight loss and wet-dog shakes. Clonidine also reversed the naloxone-precipitated increase in hippocampus MHPG concentration. In experiment 2 subjects received an LC infusion or IP injection of a non-lipophilic alpha-2-agonist (ST-91), which does not penetrate the blood-brain barrier, or of clonidine into the dorsal parabrachial nucleus (DPB) to test the selectivity of the effects of clonidine infusions into the LC. ST-91 infusions into the LC reduced several of the observed withdrawal signs and increased others (e.g., jumping). Although peripheral injections of ST-91 attenuated some of the checked signs associated with naloxone-precipitated withdrawal, the frequency of wet-dog shakes was not reduced. ST-91 infusions into the LC, but not systemic ST-91 administration, prevented the withdrawal-induced increase in hippocampus MHPG concentration. Clonidine infused lateral to the LC into the DPB did not significantly attenuate withdrawal or reduce hippocampus MHPG levels. These results provide behavioral and biochemical evidence to support the suggestion that clonidine significantly attenuates naloxone-precipitated withdrawal through an interaction with noradrenergic neurons located in the vicinity of the LC.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02431544
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Impulsivity resulting from frontostriatal dysfunction in drug abuse: implications for the control of behavior by reward-related stimuli (1999)
    Springer
    Psychopharmacology 146 (1999), S. 373-390 
    Details
    ISSN: 1432-2072
    Keywords: Key words Compulsion ; Addiction ; Cocaine ; Amphetamine ; Cannabis ; Phencyclidine ; Nucleus accumbens ; Amygdala ; Frontal cortex ; Limbic ; Stimulus-reward association ; Conditioned reward ; Sensitization ; Drug-seeking ; Inhibitory control ; Cognition ; Conditioned stimulus ; Incentive motivational ; Dopamine ; Rat ; Monkey
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Drug abuse and dependence define behavioral states involving increased allocation of behavior towards drug seeking and taking at the expense of more appropriate behavioral patterns. As such, addiction can be viewed as increased control of behavior by the desired drug (due to its unconditioned, rewarding properties). It is also clear that drug-associated (conditioned) stimuli acquire heightened abilities to control behaviors. These phenomena have been linked with dopamine function within the ventral striatum and amygdala and have been described specifically in terms of motivational and incentive learning processes. New data are emerging that suggest that regions of the frontal cortex involved in inhibitory response control are directly affected by long-term exposure to drugs of abuse. The result of chronic drug use may be frontal cortical cognitive dysfunction, resulting in an inability to inhibit inappropriate unconditioned or conditioned responses elicited by drugs, by related stimuli or by internal drive states. Drug-seeking behavior may thus be due to two related phenomena: (1) augmented incentive motivational qualities of the drug and associated stimuli (due to limbic/amygdalar dysfunction) and (2) impaired inhibitory control (due to frontal cortical dysfunction). In this review, we consider the neuro-anatomical and neurochemical substrates subserving inhibitory control and motivational processes in the rodent and primate brain and their putative impact on drug seeking. The evidence for cognitive impulsivity in drug abuse associated with dysfunction of the frontostriatal system will be discussed, and an integrative hypothesis for compulsive reward-seeking in drug abuse will be presented.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00005483
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Enhanced responding for conditioned reward produced by intra-accumbens amphetamine is potentiated after cocaine sensitization (1999)
    Springer
    Psychopharmacology 142 (1999), S. 31-40 
    Details
    ISSN: 1432-2072
    Keywords: Key words Locomotor activity ; Nucleus accumbens ; d-Amphetamine ; Cocaine ; Sensitization ; Conditioned reward
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The mesolimbic dopamine (DA) system has been implicated in conditioned reward (CR), locomotor sensitization, and the reinforcing properties of psychomotor stimulants. Stimuli with formerly motivationally neutral properties that gain incentive properties by their predictive association with primary reinforcers are termed conditioned, or secondary, reinforcers. In these experiments, we investigated whether cocaine sensitization could potentiate augmented responding for CR produced by intra-accumbens amphetamine. After subjects were trained on the CR paradigm for 14 days, they received a regimen of cocaine sensitization or saline injections. On 2 test days, 8–10 days later, subjects were given amphetamine (6 µg/0.5 µl) or saline infusions into the nucleus accumbens (NAc) and responding for CR was measured using the ”acquisition of a new response” paradigm. Responding on one novel lever resulted in the delivery of the conditioned stimulus (conditioned reinforcer, or CR lever), whereas responding on the other lever resulted in no CR stimulus presentation (NCR lever). Animals sensitized to cocaine showed increased responding on the CR lever after intra-NAc saline and potentiated CR lever responding after intra-NAc amphetamine. No differences in responding between the cocaine- and saline-treated groups on the NCR lever after the challenge were found. Locomotor sensitization under these conditions was confirmed in a separate group of subjects. These findings show that prior exposures to cocaine results in changes that potentiate the ability of intra-NAc amphetamine to enhance CR. Repeated stimulant drug use may induce long-term neuronal adaptations that result in increased sensitivity to the behavioral, or incentive motivational, effects of stimulant drugs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002130050859
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    Paper (German National Licenses)
    Fulltext
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