Cocaine Addiction as a Neurological Disorder: Implications for Treatment

Majewska, Maria Dorota

doi:10.1037/e495672006-002

Cited by 35 publications

(33 citation statements)

References 101 publications

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“…Although this appears to be inconsistent with reports that cocaine abuse is associated with psychiatric impairments (e.g., Brady et al 1991;Majewska 1996), the majority of such reports concern dependent cocaine users in treatment, whereas the present study investigated recreational users who were not in treatment. There were also no group differences in performance of the "eyes task" (Baron-Cohen et al 2001).…”

Section: Discussioncontrasting

confidence: 62%

“…For example, 5-HT 1A receptors are downregulated in rat amygdala after chronic cocaine administration (Cunningham et al 1992). There is also clinical evidence that cocaine abuse is associated with: persistent neurological and psychiatric impairments (e.g., Brady et al 1991;Majewska 1996), and decreased absolute amygdala volume (Makris et al 2004). Thus, chronic cocaine-induced, serotonin-mediated, and amygdala dysfunction might manifest as an inability to recognize fear.…”

Section: Introductionmentioning

confidence: 98%

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Impaired fear recognition in regular recreational cocaine users

et al. 2007

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There were no group differences in psychopathology or "eyes task" performance, but the RC group, who otherwise had similar illicit substance use histories to the OC group, exhibited impaired fear recognition accuracy compared to the OC and CN groups. The RC group also correctly identified anger, fear, happiness, and surprise, more slowly than CN, but not OC participants. The OC group was slower than CN when correctly identifying disgust. The selective deficit in fear recognition accuracy manifested by the RC group cannot be explained by the subacute effects of cocaine, or ecstasy, because recent and less recent users of these drugs within this group were similarly impaired. Possible parallels between RC users and psychopaths with respect to impaired fear recognition, amygdala dysfunction, and etiology are discussed.

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Section: Discussioncontrasting

confidence: 62%

Section: Introductionmentioning

confidence: 98%

Impaired fear recognition in regular recreational cocaine users

et al. 2007

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“…Cocaine abusers may suffer from seizures (Koppel et al, 1996), cerebral ischaemia, cerebral hemorrhages, infarction, optic neuropathy, cerebral atrophy, cognitive impairment, and mood and movement disorders (Majewska, 1996). Brain lesions and cerebral atrophy are mainly observed in the prefrontal cortex and basal ganglia of human cocaine abusers (Bartzokis et al, 1996;Langendorf et al, 1996).…”

Section: Neurological Impairmentsmentioning

confidence: 99%

Cellular and molecular mechanisms involved in the neurotoxicity of opioid and psychostimulant drugs

Cunha‐Oliveira

Rego

Oliveira

2008

Brain Research Reviews

193

136

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Opiates such as heroin and morphine remain widely abused drugs with a high physical dependence liability (Pouletty, 2002).

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confidence: 99%

Markers in Morphine- and Cocaine-Addicted Animals

Hu¹,

Park²,

Han³

et al. 2011

Biomolecules and Therapeutics

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Addiction is a chronic relapsing disease, often accompanied by several neurological impairments such as defi cits in cognition, motivation, insight and attention, behavioral disinhibition, emotional instability, depression, anhedonia, impulsiveness, aggressiveness and movement disorders (Morley et al., 1980;Majewska, 1996;Leshner, 1997;Kalivas, 2007). Opiates and psychostimulants produce addictions after repeated administrations in animals and human (Heyne and Wolffgramm, 1998;Sevarino et al., 2000).Opiates such as heroin and morphine remain widely abused drugs with a high physical dependence liability (Pouletty, 2002). Opiates, acting on opioid receptors via Gi/Go classes of the G proteins, inhibit cyclic AMP (cAMP) formation (ColThese experiments were designed to use typical makers from behaviors and molecular basis in addicted animals of morphine and cocaine. Morphine has been widely abused with a high physical dependence liability. Morphine withdrawal activates the intracellular cAMP signaling pathway and further leads to changes in the expression of the cAMP response element binding protein (CREB), which may be important to the development and expression of morphine dependence. From these experiments, repeated morphine (10 mg/kg, twice per day for 7 days) developed physical dependence. Withdrawal signs were precipitated by naloxone and also increased the expression of the CREB. In addition, repeated exposure of cocaine (15 mg/kg) to mice develops locomotor sensitization and produced lasting behavioral sensitivity. Cocaine-and amphetamine-regulated transcript peptide (CART) peptide was up-regulated by repeated administration of cocaine in the striatum. Therefore, repeated morphine induced the development of physical dependence and increased pCREB. In addition, repeated cocaine induced locomotor sensitization and over-expressed CART peptide. In conclusion, the development of physical dependence and pCREB for morphine, and locomotor sensitization and CART peptide over-expression for cocaine would be useful markers to predict the abuse potential of opioid analgesics and pychostimulant drugs in animals, respectively. lier and Francis, 1975). These results in inhibition of neuronal excitability and synaptic transmission are mediated via cAMP and represent a classic cellular mechanism of opioid action. With continuing opioid exposure, activity of cAMP signaling gradually is recovered and is increased (up-regulation) above control level. Thus, prolonged exposure to opioids leads to tolerance of cAMP transmission at the single cell level. Abrupt removal of opioids after chronic exposure to these drugs induces subsequent adaptation that, at the cellular level, is manifested by an increase in cAMP levels and was suggested to represent a cellular model of tolerance and dependence (Nestler et al., 1993). Essentially similar regulation of the cAMP pathways was also demonstrated in vivo in certain brain structures. Opiates given acutely slightly inhibited the adenylyl cyclase, while this inhibition was gradually reversed...

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Cocaine Addiction as a Neurological Disorder: Implications for Treatment

Cited by 35 publications

References 101 publications

Impaired fear recognition in regular recreational cocaine users

Impaired fear recognition in regular recreational cocaine users

Cellular and molecular mechanisms involved in the neurotoxicity of opioid and psychostimulant drugs

Markers in Morphine- and Cocaine-Addicted Animals

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