Increased polysialic acid neural cell adhesion molecule expression in human hippocampus of heroin addicts

Exploring the Neuroimmunopharmacology of Opioids: An Integrative Review of Mechanisms of Central Immune Signaling and Their Implications for Opioid Analgesia

“…These opioid-induced adaptations in CNS-immune cell receptor expression are accompanied by profound changes in astrocyte and microglial cellular morphology (Holdridge et al, 2007), with the total length of NEUROIMMUNOPHARMACOLOGIC IMPLICATIONS FOR OPIOID ANALGESIA astrocytes altered in a regional specific fashion (Lazriev et al, 2001). Moreover, these preclinical data are confirmed by postmortem clinical evidence of opioid-induced microglial cell surface marker expression phenotypic reactivity (Weber et al, 2006). Such changes in cell morphology are also accompanied by alterations in the blood-brain barrier permeability and hence tight gap junction protein expression and function (Weber et al, 2006).…”

“…Moreover, these preclinical data are confirmed by postmortem clinical evidence of opioid-induced microglial cell surface marker expression phenotypic reactivity (Weber et al, 2006). Such changes in cell morphology are also accompanied by alterations in the blood-brain barrier permeability and hence tight gap junction protein expression and function (Weber et al, 2006). These macrostructural changes have clear implications for drug and metabolite access into the CNS, as well as peripheral cell migration.…”

Gene expression changes in a zebrafish model of drug dependency suggest conservation of neuro-adaptation pathways

“…5B). References: (1) (Mead and Stephens, 2003), (2) (Sanchis-Segura et al, 2006), (3) (Kalivas, 2004), (4) (Follesa and Ticku, 1995), (5) (Noda and Nabeshima, 2004), (6) (Ahmed et al, 2005), (7) (Boutrel, 2005), (8) (Borgland et al, 2006), (9) (Biala et al, 2005), (10) , (11) (Raghavendra and Kulkarni, 1999), (12) (Weber et al, 2006), (13) (Miller et al, 2006), (14) (Abrous et al, 2002), (15) (Alonso et al, 2007), (16) (Bermak et al, 2002).…”

“…Several of these shared genes are components of pathways that also show lasting adaptation in the brains of mammalian models of dependence. These include glutamate receptors [AMPA and NMDAR1 (N-methyl-D-aspartate receptor 1) (Kalivas, 2004;Noda and Nabeshima, 2004;SanchisSegura et al, 2006)] and the peripheral BDZR , and molecules associated with synaptic plasticity such as NCAM (Abrous et al, 2002;Miller et al, 2006;Weber et al, 2006). Although neuro-adaptations related directly to dopamine stimulation are thought to be critical for the development of addiction, alterations in glutamatergic neurotransmission are thought to be key to the relapsing nature of drug addiction (Chao et al, 2002;Gao et al, 2006;Kalivas, 2004).…”

The Genetic Basis Of The Comorbidity Between Cannabis Use And Major Depression

“…NCAM1 encodes a brain-expressed cell adhesion protein [50], known to be involved in the development of the nervous system and neuroplasticity (important in learning and memory, as reviewed by [51]). This is pertinent for addiction, as it is posited to involve the subversion of reward-related learning and there is also evidence that addiction phenotypes alter expression levels of polysialylated NCAM in the brain [52][53][54]. Similarly, depressive episodes have been linked to neuronal atrophy, whilst efficacious antidepressant treatment increases neurogenesis and enhances neural plasticity [55,56] and there is evidence that NCAM levels may be associated with MDD (and related behaviors) [57][58][59].…”