1989
DOI: 10.1016/0024-3205(89)90045-3
|View full text |Cite
|
Sign up to set email alerts
|

Blockade of “reverse tolerance” to cocaine and amphetamine by MK-801

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1
1

Citation Types

8
201
1
1

Year Published

1996
1996
2008
2008

Publication Types

Select...
9

Relationship

0
9

Authors

Journals

citations
Cited by 471 publications
(211 citation statements)
references
References 8 publications
8
201
1
1
Order By: Relevance
“…Most research has studied this process using locomotor sensitization as a model (Kilbey and Ellinwood, 1977;Karler et al, 1989Karler et al, , 1990Kalivas and Duffy, 1993a, b;Vanderschuren et al, 1999), and a number of labs are now examining the link between psychostimulantinduced locomotor activation and self-administration. For example, self-administration of cocaine produces sensitization to the locomotor-activating effects (Hooks et al, 1994;Phillips and Di Ciano, 1996;Zapata et al, 2003;Ben-Shahar et al, 2004).…”
Section: Discussionmentioning
confidence: 99%
“…Most research has studied this process using locomotor sensitization as a model (Kilbey and Ellinwood, 1977;Karler et al, 1989Karler et al, , 1990Kalivas and Duffy, 1993a, b;Vanderschuren et al, 1999), and a number of labs are now examining the link between psychostimulantinduced locomotor activation and self-administration. For example, self-administration of cocaine produces sensitization to the locomotor-activating effects (Hooks et al, 1994;Phillips and Di Ciano, 1996;Zapata et al, 2003;Ben-Shahar et al, 2004).…”
Section: Discussionmentioning
confidence: 99%
“…The systemic administration of either NMDA (Karler et al, 1989;Wolf et al, 1995) or AMPA/kainate (Karler et al, 1991a;Li et al, 1997;cf Akiyama et al, 1998) receptor antagonists as well as the application into the VTA of either NMDA (Cador et al, 1999;Vezina and Queen, 2000) or mGlu (Kim and Vezina, 1998) receptor antagonists has been shown to prevent the induction of AMPH-induced locomotor sensitization. Moreover, systemically administering NMDA receptor antagonists with AMPH during preexposure also prevents cellular correlates of locomotor Figure 6 Injection cannula tip placements in the VTA.…”
Section: Induction Of Sensitization By Amph Requires Activation Of Glmentioning
confidence: 99%
“…Indeed, induction of locomotor sensitization by AMPH has been shown to be dependent on activation of Nmethyl-D-aspartate (NMDA: Cador et al, 1999;Vezina and Queen, 2000) and metabotropic glutamate (mGlu: Kim and Vezina, 1998) receptors in the VTA. Systemic administration of NMDA (Karler et al, 1989;Wolf et al, 1995) or a-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA)/kainate receptor antagonists (Karler et al, 1991a;Li et al, 1997) also prevents the development of locomotor sensitization by systemic AMPH. Moreover, induction of locomotor sensitization by AMPH is blocked by lesions of the PFC, which provides major glutamatergic afferentation to the VTA Cador et al, 1999).…”
Section: Introductionmentioning
confidence: 99%
“…One interesting feature of sensitization is its long-lasting aspect (Robinson and Becker 1986;Woolverton and Johnson 1992) that is reminiscent of long-term potentiation (LTP) and other N-methyl-D-aspartate (NMDA) receptor-mediated events. Indeed, extracellular levels of glutamate increase in the ventral tegmental area (VTA) after cocaine administration in sensitized rats (Kalivas and Duffy 1998) and inhibition of the NMDA receptor has been shown to block sensitization induced by psychostimulants (Karler et al 1989, see also Vanderschuren and Kalivas 2000, for review). These data strongly suggest that hyperactivity of not only the dopaminergic but also the glutamatergic system is involved in cocaine-induced sensitization.…”
Section: Introductionmentioning
confidence: 99%