Elevation of striatal and accumbal preproenkephalin, preprotachykinin and preprodynorphin mRNA abundance subsequent to N-methyl-d-aspartate receptor blockade with MK-801

Angulo, Jesús A.; Williams, Anastasia; Ledoux, Marie; Watanabe, Yoshifumi; McEwen, Bruce S.

doi:10.1016/0169-328x(94)00223-2

Cited by 14 publications

(3 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It was unexpected that chronic METH exposure could have resulted in such differential responses in Tac1 and Pdyn mRNA levels since both of their promoters contain AP1/CRE sites that bind members of the AP1 family of IEGs (Calin-Jageman et al, 2006; Cole et al, 1995; Messersmith et al, 1994; 1996; 1998). We had predicted that both Tac1 and Pdyn would show similar changes in expression after chronic METH exposure because they are localized in the same striatal neurons (Angulo et al, 1995) and because previous data suggested that they are both induced by METH (Bannon et al, 1987; Wang et al, 1995). Our present findings, although unexpected, thus, point to the possible existence of factors, other than AP1 transcription factors (Bronstein et al, 1996), which might play more essential roles in regulating Pdyn expression.…”

Section: Discussionmentioning

confidence: 99%

Chronic methamphetamine exposure suppresses the striatal expression of members of multiple families of immediate early genes (IEGs) in the rat: normalization by an acute methamphetamine injection

et al. 2011

View full text Add to dashboard Cite

Rationale Repeated injections of cocaine cause blunted responses to acute cocaine challenge-induced increases in the expression of immediate early genes (IEGs). Objectives The aim of this study was to test if chronic methamphetamine (METH) exposure might cause similar blunting of acute METH-induced increases in IEG expression. Results Repeated saline or METH injections were given to rats over 14 days. After one day of withdrawal, they received a single injection of saline or METH (5 mg/kg). Acute injection of METH increased c-fos, fosB, fra2, junB, Egr1-3, Nr4a1 (Nur77), and Nr4a3 (Nor-1) mRNA levels in the striatum of saline-pretreated rats. Chronic METH treatment alone reduced the expression of AP1, Erg1-3, and Nr4a1 transcription factors below control levels. Acute METH challenge normalized these values in METH-pretreated rats. Unexpectedly, acute METH challenge to METH-pretreated animals caused further decreases in Nr4a2 (Nurr1) mRNA levels. In contrast, the METH challenge caused significant but blunted increases in Nr4a3 and Arc expression in METH-pretreated rats. There were also chronic METH-associated decreases in the expression of cAMP responsive element binding protein (CREB) which modulates IEG expression via activation of the cAMP/PKA/CREB signal transduction pathway. Chronic METH exposure also caused significant decreases in preprotachykinin, but not in prodynorphin, mRNA levels. Conclusions These results support the accumulated evidence that chronic administration of psychostimulants is associated with blunting of their acute stimulatory effects on IEG expression. The METH-induced renormalization of the expression of several IEGs in rats chronically exposed to METH hints to a potential molecular explanation for the recurrent self-administration of the drug by human addicts.

show abstract

Section: Discussionmentioning

confidence: 99%

Chronic methamphetamine exposure suppresses the striatal expression of members of multiple families of immediate early genes (IEGs) in the rat: normalization by an acute methamphetamine injection

et al. 2011

View full text Add to dashboard Cite

show abstract

“…1996). Receptors of the NMDA type have also been shown to be involved in the regulation of neuropeptide and receptor gene expression in the neostriatum (Lannes & Micheletti 1993;Angulo et al . 1995;Beckstead 1995;Laprade & Soghomonian 1995) and immediate‐early gene expression following activation of the cortex (Liste et al .…”

Section: Discussionmentioning

confidence: 99%

Subcellular and subsynaptic distribution of the NR1 subunit of the NMDA receptor in the neostriatum and globus pallidus of the rat: co‐localization at synapses with the GluR2/3 subunit of the AMPA receptor

Bernard

Bolam

1998

Eur J of Neuroscience

112

View full text Add to dashboard Cite

Glutamatergic neurotransmission in the neostriatum and the globus pallidus is mediated through NMDA-type as well as other glutamate receptors and is critical in the expression of basal ganglia function. In order to characterize the cellular, subcellular and subsynaptic localization of NMDA receptors in the neostriatum and globus pallidus, multiple immunocytochemical techniques were applied using antibodies that recognize the NR1 subunit of the NMDA receptor. In order to determine the spatial relationship between NMDA receptors and AMPA receptors, double labelling was performed with the NR1 antibodies and an antibody that recognizes the GluR2 and 3 subunits of the AMPA receptor. In the neostriatum all neurons with characteristics of spiny projection neurons, some interneurons and many dendrites and spines were immunoreactive for NR1. In the globus pallidus most perikarya and many dendritic processes were immunopositive. Immunogold methods revealed that most NR1 labelling is associated with asymmetrical synapses and, like the labelling for GluR2/3, is evenly spread across the synapse. Double immunolabelling revealed that in neostriatum, over 80% of NR1-positive axospinous synapses are also positive for GluR2/3. In the globus pallidus most NR1-positive synapses are positive for GluR2/3. In both regions many synapses labelled only for GluR2/3 were also detected. These results, together with previous data, suggest that NMDA and AMPA receptor subunits are expressed by the same neurons in the neostriatum and globus pallidus and that NMDA and AMPA receptors are, at least in part, colocalized at individual asymmetrical synapses. The synaptic responses to glutamate in these regions are thus likely be mediated by both AMPA and NMDA receptors at the level of individual synapses.

show abstract

“…Several lines of evidence suggest that striatal enkephalin and substance P expression is under the influence of corticostriatal glutamatergic afferents (Uhl et al, 1988;Somers and Beckstead, 1990;Salin and Chesselet, 1992). Based on the observation that systemic MK-801 administration, either acutely or once daily for 7 days, had no effect or increased striatal enkephalin and substance P mRNA levels according to the doses used (0.01-0.5 mg/kg), Angulo et al (1993Angulo et al ( , 1995 suggested that expression of these peptides undergoes tonic glutamate inhibitory influence through NMDA receptors. In this study, we report the opposite effect of chronic systemic treatment with MK-801 administered twice a day for 8 days at 0.2 mgikg.…”

Section: Role Of Nmda Receptors In the Regulation Of Striatal Substanmentioning

confidence: 99%

Chronic Dizocilpine Maleate (MK‐801) Treatment Suppresses the Effects of Nigrostriatal Dopamine Deafferentation on Enkephalin but not on Substance P Expression in the Rat Striatum

Hajji

Salin

Goff

1996

Eur J of Neuroscience

View full text Add to dashboard Cite

The present study examined the effects of chronic treatment with dizocilpine maleate (0.2 mg/kg i.p., twice a day for 8 days) alone or in combination with unilateral 6-hydroxydopamine-induced lesion of the nigrostriatal dopaminergic neurons on substance P and enkephalin expression in the rat striatum. This was done by means of quantitative in situ hybridization histochemistry and immunocytochemistry. As reported previously, the unilateral dopaminergic lesion resulted in marked decreases in substance P mRNA expression and immunoreactivity in the ipsilateral striatum while enkephalin mRNA expression and Met-enkephalin immunoreactivity were considerably increased in this structure. Blockade of NMDA receptors by chronic dizocilpine maleate treatment alone resulted in decreased levels of striatal substance P mRNA without significant change in substance P immunoreactivity versus controls. Enkephalin mRNA levels were also decreased in the striatum, matched by parallel reductions in Met-enkephalin immunoreactivity. These observations indicate that NMDA receptor activity may exert tonic excitatory effects on substance P and enkephalin expression in the striatum. The same chronic treatment with dizocilpine maleate started 12 days after the 6-hydroxydopamine injection suppressed the lesion-induced up-regulation of enkephalin expression without significantly affecting the down-regulation of substance P expression. These data provide evidence that NMDA receptor-mediated mechanisms contribute to the alteration of striatal enkephalin expression associated with dopaminergic depletion in hemiparkinsonian rat models.

show abstract

Elevation of striatal and accumbal preproenkephalin, preprotachykinin and preprodynorphin mRNA abundance subsequent to N-methyl-d-aspartate receptor blockade with MK-801

Cited by 14 publications

References 40 publications

Chronic methamphetamine exposure suppresses the striatal expression of members of multiple families of immediate early genes (IEGs) in the rat: normalization by an acute methamphetamine injection

Chronic methamphetamine exposure suppresses the striatal expression of members of multiple families of immediate early genes (IEGs) in the rat: normalization by an acute methamphetamine injection

Subcellular and subsynaptic distribution of the NR1 subunit of the NMDA receptor in the neostriatum and globus pallidus of the rat: co‐localization at synapses with the GluR2/3 subunit of the AMPA receptor

Chronic Dizocilpine Maleate (MK‐801) Treatment Suppresses the Effects of Nigrostriatal Dopamine Deafferentation on Enkephalin but not on Substance P Expression in the Rat Striatum

Contact Info

Product

Resources

About