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Jacqueline F. Mcginty - One of the best experts on this subject based on the ideXlab platform.
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Local μ and δ opioid receptors regulate amphetamine-induced behavior and neuropeptide mRNA in the striatum
Neuroscience, 2003Co-Authors: M.v Gonzalez-nicolini, W.j. Berglind, K.s Cole, C.l Keogh, Jacqueline F. McgintyAbstract:The purpose of this study was to investigate the role that mu and delta opioid receptor blockade has upon stimulant-induced behavior and neuropeptide gene expression in the striatum. Acute administration of amphetamine (2.5 mg/kg i.p.) caused an increase in behavioral activity and Preprodynorphin, substance P, and preproenkephalin mRNA expression. Intrastriatal infusion of the mu opioid antagonist, H-D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH(2) (CTAP), or the delta opioid antagonist, H-Tyr-Tic[CH(2)NH]-Phe-Phe-OH (TIPPpsi), significantly decreased amphetamine-induced vertical activity. However, only CTAP reduced amphetamine-induced distance traveled. Quantitative in situ hybridization histochemistry revealed that CTAP blocked amphetamine-induced Preprodynorphin and substance P mRNA. However, preproenkephalin mRNA levels in the dorsal striatum were increased to the same extent by CTAP, amphetamine, or a combination of the two drugs. In contrast, TIPPpsi significantly decreased amphetamine-induced mRNA expression of all three neuropeptides. These data indicate that both mu and delta receptor subtypes differentially regulate amphetamine-induced behavior and neuropeptide gene expression in the rat striatum.
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Opioid peptide messenger RNA expression is increased at spinal and supraspinal levels following excitotoxic spinal cord injury.
Neuroscience, 2000Co-Authors: K.e Abraham, Kori L. Brewer, Jacqueline F. McgintyAbstract:Spinal cord injury in rats is known to cause anatomical, physiological and molecular changes within the spinal cord. These changes may account for behavioral syndromes that appear following spinal cord injury, syndromes believed to be related to the clinical condition of chronic pain. Intraspinal injection of quisqualic acid produces an excitotoxic injury with pathological characteristics similar to those associated with ischemic and traumatic spinal cord injury. In addition, recent studies have demonstrated changes in blood flow, neuronal excitability and gene expression in the brain following excitotoxic injury, indicating that behavioral changes may result from modification of neuronal substrates at supraspinal levels of the neuraxis. Because changes in spinal opioid peptide expression have been demonstrated in models of traumatic spinal cord injury and chronic pain, the present study investigated messenger RNA expression of the opioid peptides, preproenkephalin and Preprodynorphin, at spinal and supraspinal levels following excitotoxic spinal cord injury. Male, Long-Evans rats were given three intraspinal injections of quisqualic acid (total 1.2 microl, 125mM). After one, three, five, seven or 10days, animals were killed and quantitative in situ hybridization performed on regions of the spinal cord surrounding the lesion site, as well as whole-brain sections through various levels of the thalamus. Preproenkephalin and Preprodynorphin expression was increased in spinal cord areas adjacent to the site of quisqualic injection and in cortical regions associated with nociceptive function, preproenkephalin in the cingulate cortex and Preprodynorphin in the parietal cortex, both ipsilaterally and contralaterally at various time-points following injury. These results further our knowledge of the secondary events that occur following spinal cord injury, specifically implicating supraspinal opioid systems in the CNS response to spinal cord injury.
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The muscarinic toxin 3 augments neuropeptide mRNA in rat striatum in vivo.
European journal of pharmacology, 1997Co-Authors: John Q. Wang, Mikael Jolkkonen, Jacqueline F. McgintyAbstract:Abstract The selective M 4 muscarinic receptor toxin, MT3, was used in vivo to evaluate the role of M 4 receptors in cholinergic inhibition of neuropeptide mRNA expression in striatonigral neurons. Unilateral injection of the muscarinic toxin 3 (0.04–4 nmol) into the dorsal striatum of chronically-cannulated rats elevated basal levels of Preprodynorphin, substance P and preproenkephalin mRNAs in the ipsilateral dorsal striatum as revealed by quantitative in situ hybridization. Pretreatment with muscarinic toxin 3 also augmented amphetamine (2.5 mg/kg, i.p.)-stimulated Preprodynorphin and substance P expression in the dorsal striatum in a manner similar to that observed after the muscarinic antagonist, scopolamine. Since muscarinic toxin 3 has a much greater affinity for muscarinic M 4 receptors than for other subtypes, it is possible that muscarinic toxin 3, by interacting with the muscarinic M 4 subtype, regulates basal and/or dopamine-stimulated striatal neuropeptide gene expression.
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intrastriatal injection of the metabotropic glutamate receptor antagonist mcpg attenuates acute amphetamine stimulated neuropeptide mrna expression in rat striatum
Neuroscience Letters, 1996Co-Authors: John Q. Wang, Jacqueline F. McgintyAbstract:Abstract In chronically cannulated rats, microinjection of a competitive metabotropic glutamate receptor (mGluR) antagonist, (+)-α-methyl-4-carboxyphenylglycine (MCPG), into the dorsal striatum at doses of 0.4, 2 and 10 μg/1 μl did not affect basal levels of Preprodynorphin, substance P and preproenkephalin mRNAs in the dorsal striatum as revealed by quantitative in situ hybridization. However, intrastriatal MCPG (0.08, 0.4 and 2 μg/l μl) dose-dependently attenuated increases in the three mRNA expression induced by acute amphetamine injection (2 mg/kg, i.p.). MCPG had no significant effect on spontaneous, and amphetamine-stimulated, behavioral activities. These data indicate that activation of MCPG-sensitive mGluRs is necessary for upregulation of striatal neuropeptide mRNA expression in response to amphetamine exposure. However, the mGluR activity is not implicated in maintaining basal levels of the peptide gene expression in the striatum.
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Acute methamphetamine-induced zif/268, Preprodynorphin, and preproenkephalin mRNA expression in rat striatum depends on activation of NMDA and kainate/AMPA receptors
Brain research bulletin, 1996Co-Authors: John Q. Wang, Jacqueline F. McgintyAbstract:Abstract This study tested the role of N-methyl- d -aspartate and kainate/AMPA receptors in mediating mRNA expression of the immediate early gene zif/268 and the opioid peptide genes Preprodynorphin and preproenkephalin in rat forebrain following a single injection of methamphetamin. At 3 h after acute methamphetamine [4 mg/kg, intraperitoneally (IP)], quantitative in situ hybridization histochemistry revealed that zif/268 mRNA expression was increased in the dorsal striatum (caudoputamen) and in the sensory cortex. Preprodynorphin was increased in both dorsal and ventral striatum (nucleus accumbens) and preproenkephalin was increased in the dorsal striatum. Pretreatment with (±)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP) (10 mg/kg, IP), an N-methyl- d -aspartate receptor antagonist, blocked the methamphetamine-induced zif/268 mRNA expression in the striatum and in the region of sensory cortex representing the upper limb and nose. 6,7-Dinitro-quinoxaline-2,3-dione (DNQX) (100 mg/kg, IP), a kainate/AMPA receptor antagonist, did not reduce the ability of methamphetamine to induce zif/268 mRNA in striatal and cortical neurons. Furthermore, both antagonists caused a parallel blockade of methamphetamine-stimulated preproenkephalin mRNA expression in the dorsal and ventral striatum but did not significantly affect methamphetamine-stimulated preproenkephalin mRNA expression. CPP and DNQX reduced basal levels of zif/268 mRNA in cortical and striatal neurons but did not affect the constitutive expression of the two opioid mRNAs in the striatum. Neither antagonist had a significant effect on methamphetamine-induced demonstrate that both N-methyl- d -aspartate and kainate/AMPA receptor-mediated glutamatergic transmission is linked to modulation of the methamphetamine-stimulated opioid peptide gene expression in rat forebrain. Furthermore, N-methyl- d -aspartate receptors participate in methamphetamine-stimulated zif/268 expression.
John Q. Wang - One of the best experts on this subject based on the ideXlab platform.
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Intrastriatal GABAA receptor blockade does not alter dopamine D1/D2 receptor interactions in the intact rat striatum
Neuroscience, 2001Co-Authors: E.a Jones, John Q. Wang, J.f. McgintyAbstract:The purpose of this study was to investigate the effects of intrastriatal blockade of GABA(A) receptors on dopamine D(1)/D(2) receptor interactions in the intact rat striatum. Muscarinic receptors mediate the ability of the D(2) receptor antagonist, eticlopride, to block an increase in striatonigral neuropeptide messenger RNA stimulated by the full D(1) agonist, SKF-82958. However, because D(2) receptor antagonists activate striatopallidal neurons, it is possible that increased GABA release from local medium spiny axon collaterals also contributes to the ability of eticlopride to block the effects of SKF-82958. This hypothesis was addressed by infusing the GABA(A) receptor antagonist, bicuculline, into the dorsal striatum in rats treated with eticlopride and SKF-82958. In contrast to the actions of the muscarinic antagonist, scopolamine, bicuculline did not affect the increase in behaviors induced by SKF-82958 or the ability of eticlopride to block them. Quantitative in situ hybridization demonstrated that bicuculline did not significantly affect basal Preprodynorphin messenger RNA, nor did it affect the ability of eticlopride to decrease SKF-82958-induced Preprodynorphin messenger RNA. However, the level of the Preprodynorphin hybridization signal in bicuculline plus SKF-82958-treated rats was significantly lower than in saline plus SKF-82958-treated rats. In contrast, bicuculline, eticlopride or SKF-82958 by themselves increased basal preproenkephalin messenger RNA. However, there was no significant interaction among bicuculline, eticlopride and SKF-82958 on preproenkephalin messenger RNA levels.These data indicate that blockade of striatal GABA(A) receptors has only a subtle effect on acute dopamine agonist-induced changes in gene expression. These results are discussed in the context of local intrastriatal interactions.
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The muscarinic toxin 3 augments neuropeptide mRNA in rat striatum in vivo.
European journal of pharmacology, 1997Co-Authors: John Q. Wang, Mikael Jolkkonen, Jacqueline F. McgintyAbstract:Abstract The selective M 4 muscarinic receptor toxin, MT3, was used in vivo to evaluate the role of M 4 receptors in cholinergic inhibition of neuropeptide mRNA expression in striatonigral neurons. Unilateral injection of the muscarinic toxin 3 (0.04–4 nmol) into the dorsal striatum of chronically-cannulated rats elevated basal levels of Preprodynorphin, substance P and preproenkephalin mRNAs in the ipsilateral dorsal striatum as revealed by quantitative in situ hybridization. Pretreatment with muscarinic toxin 3 also augmented amphetamine (2.5 mg/kg, i.p.)-stimulated Preprodynorphin and substance P expression in the dorsal striatum in a manner similar to that observed after the muscarinic antagonist, scopolamine. Since muscarinic toxin 3 has a much greater affinity for muscarinic M 4 receptors than for other subtypes, it is possible that muscarinic toxin 3, by interacting with the muscarinic M 4 subtype, regulates basal and/or dopamine-stimulated striatal neuropeptide gene expression.
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intrastriatal injection of the metabotropic glutamate receptor antagonist mcpg attenuates acute amphetamine stimulated neuropeptide mrna expression in rat striatum
Neuroscience Letters, 1996Co-Authors: John Q. Wang, Jacqueline F. McgintyAbstract:Abstract In chronically cannulated rats, microinjection of a competitive metabotropic glutamate receptor (mGluR) antagonist, (+)-α-methyl-4-carboxyphenylglycine (MCPG), into the dorsal striatum at doses of 0.4, 2 and 10 μg/1 μl did not affect basal levels of Preprodynorphin, substance P and preproenkephalin mRNAs in the dorsal striatum as revealed by quantitative in situ hybridization. However, intrastriatal MCPG (0.08, 0.4 and 2 μg/l μl) dose-dependently attenuated increases in the three mRNA expression induced by acute amphetamine injection (2 mg/kg, i.p.). MCPG had no significant effect on spontaneous, and amphetamine-stimulated, behavioral activities. These data indicate that activation of MCPG-sensitive mGluRs is necessary for upregulation of striatal neuropeptide mRNA expression in response to amphetamine exposure. However, the mGluR activity is not implicated in maintaining basal levels of the peptide gene expression in the striatum.
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Acute methamphetamine-induced zif/268, Preprodynorphin, and preproenkephalin mRNA expression in rat striatum depends on activation of NMDA and kainate/AMPA receptors
Brain research bulletin, 1996Co-Authors: John Q. Wang, Jacqueline F. McgintyAbstract:Abstract This study tested the role of N-methyl- d -aspartate and kainate/AMPA receptors in mediating mRNA expression of the immediate early gene zif/268 and the opioid peptide genes Preprodynorphin and preproenkephalin in rat forebrain following a single injection of methamphetamin. At 3 h after acute methamphetamine [4 mg/kg, intraperitoneally (IP)], quantitative in situ hybridization histochemistry revealed that zif/268 mRNA expression was increased in the dorsal striatum (caudoputamen) and in the sensory cortex. Preprodynorphin was increased in both dorsal and ventral striatum (nucleus accumbens) and preproenkephalin was increased in the dorsal striatum. Pretreatment with (±)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP) (10 mg/kg, IP), an N-methyl- d -aspartate receptor antagonist, blocked the methamphetamine-induced zif/268 mRNA expression in the striatum and in the region of sensory cortex representing the upper limb and nose. 6,7-Dinitro-quinoxaline-2,3-dione (DNQX) (100 mg/kg, IP), a kainate/AMPA receptor antagonist, did not reduce the ability of methamphetamine to induce zif/268 mRNA in striatal and cortical neurons. Furthermore, both antagonists caused a parallel blockade of methamphetamine-stimulated preproenkephalin mRNA expression in the dorsal and ventral striatum but did not significantly affect methamphetamine-stimulated preproenkephalin mRNA expression. CPP and DNQX reduced basal levels of zif/268 mRNA in cortical and striatal neurons but did not affect the constitutive expression of the two opioid mRNAs in the striatum. Neither antagonist had a significant effect on methamphetamine-induced demonstrate that both N-methyl- d -aspartate and kainate/AMPA receptor-mediated glutamatergic transmission is linked to modulation of the methamphetamine-stimulated opioid peptide gene expression in rat forebrain. Furthermore, N-methyl- d -aspartate receptors participate in methamphetamine-stimulated zif/268 expression.
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acute methamphetamine induced zif 268 Preprodynorphin and preproenkephalin mrna expression in rat striatum depends on activation of nmda and kainate ampa receptors
Brain Research Bulletin, 1996Co-Authors: John Q. Wang, Jacqueline F. McgintyAbstract:Abstract This study tested the role of N-methyl- d -aspartate and kainate/AMPA receptors in mediating mRNA expression of the immediate early gene zif/268 and the opioid peptide genes Preprodynorphin and preproenkephalin in rat forebrain following a single injection of methamphetamin. At 3 h after acute methamphetamine [4 mg/kg, intraperitoneally (IP)], quantitative in situ hybridization histochemistry revealed that zif/268 mRNA expression was increased in the dorsal striatum (caudoputamen) and in the sensory cortex. Preprodynorphin was increased in both dorsal and ventral striatum (nucleus accumbens) and preproenkephalin was increased in the dorsal striatum. Pretreatment with (±)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP) (10 mg/kg, IP), an N-methyl- d -aspartate receptor antagonist, blocked the methamphetamine-induced zif/268 mRNA expression in the striatum and in the region of sensory cortex representing the upper limb and nose. 6,7-Dinitro-quinoxaline-2,3-dione (DNQX) (100 mg/kg, IP), a kainate/AMPA receptor antagonist, did not reduce the ability of methamphetamine to induce zif/268 mRNA in striatal and cortical neurons. Furthermore, both antagonists caused a parallel blockade of methamphetamine-stimulated preproenkephalin mRNA expression in the dorsal and ventral striatum but did not significantly affect methamphetamine-stimulated preproenkephalin mRNA expression. CPP and DNQX reduced basal levels of zif/268 mRNA in cortical and striatal neurons but did not affect the constitutive expression of the two opioid mRNAs in the striatum. Neither antagonist had a significant effect on methamphetamine-induced demonstrate that both N-methyl- d -aspartate and kainate/AMPA receptor-mediated glutamatergic transmission is linked to modulation of the methamphetamine-stimulated opioid peptide gene expression in rat forebrain. Furthermore, N-methyl- d -aspartate receptors participate in methamphetamine-stimulated zif/268 expression.
Kristen A. Keefe - One of the best experts on this subject based on the ideXlab platform.
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regulation of psychostimulant induced Preprodynorphin c fos and zif 268 messenger rna expression in the rat dorsal striatum by mu opioid receptor blockade
European Journal of Pharmacology, 2006Co-Authors: Kristen A. Horner, Kristen A. KeefeAbstract:Several studies have shown that psychostimulants can induce differential immediate early gene and neuropeptide expression in the patch versus matrix compartments of dorsal striatum. The patch compartment contains a high density of mu opioid receptors and activation of these receptors may contribute to psychostimulant-induced gene expression in the patch versus matrix compartments of dorsal striatum. However, the contribution of mu opioid receptor activation to psychostimulant-induced changes in gene expression in the patch compartment of dorsal striatum has not been examined. The current study examined the role of mu opioid receptors in psychostimulant induction of Preprodynorphin, c-fos and zif/268 messenger RNA expression in the patch versus matrix compartments of dorsal striatum. Male Sprague-Dawley rats were treated with the mu opioid receptor antagonist, clocinnamox (1 mg/kg, s.c.), 24 h prior to treatment with cocaine (30 mg/kg, i.p.) or methamphetamine (15 mg/kg, s.c.) and sacrificed 45 min or 3 h later. Mu opioid receptor antagonism blocked psychostimulant-induced Preprodynorphin messenger RNA expression only in the rostral patch compartment, whereas psychostimulant-induced zif/268 messenger RNA expression in the patch and matrix compartments was attenuated throughout the dorsal striatum. Clocinnamox pretreatment had no effect on stimulant-induced increases in c-fos expression. These data suggest that mu opioid receptor activation plays a specific role in psychostimulant-induced Preprodynorphin messenger RNA expression in the rostral patch compartment and zif/268 messenger RNA expression throughout dorsal striatum.
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Regulation of psychostimulant-induced Preprodynorphin, c-fos and zif/268 messenger RNA expression in the rat dorsal striatum by mu opioid receptor blockade
European Journal of Pharmacology, 2006Co-Authors: Kristen A. Horner, Kristen A. KeefeAbstract:Several studies have shown that psychostimulants can induce differential immediate early gene and neuropeptide expression in the patch versus matrix compartments of dorsal striatum. The patch compartment contains a high density of mu opioid receptors and activation of these receptors may contribute to psychostimulant-induced gene expression in the patch versus matrix compartments of dorsal striatum. However, the contribution of mu opioid receptor activation to psychostimulant-induced changes in gene expression in the patch compartment of dorsal striatum has not been examined. The current study examined the role of mu opioid receptors in psychostimulant induction of Preprodynorphin, c-fos and zif/268 messenger RNA expression in the patch versus matrix compartments of dorsal striatum. Male Sprague-Dawley rats were treated with the mu opioid receptor antagonist, clocinnamox (1 mg/kg, s.c.), 24 h prior to treatment with cocaine (30 mg/kg, i.p.) or methamphetamine (15 mg/kg, s.c.) and sacrificed 45 min or 3 h later. Mu opioid receptor antagonism blocked psychostimulant-induced Preprodynorphin messenger RNA expression only in the rostral patch compartment, whereas psychostimulant-induced zif/268 messenger RNA expression in the patch and matrix compartments was attenuated throughout the dorsal striatum. Clocinnamox pretreatment had no effect on stimulant-induced increases in c-fos expression. These data suggest that mu opioid receptor activation plays a specific role in psychostimulant-induced Preprodynorphin messenger RNA expression in the rostral patch compartment and zif/268 messenger RNA expression throughout dorsal striatum.
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3,4-Methylenedioxymethamphetamine increases neuropeptide messenger RNA expression in rat striatum.
Brain research. Molecular brain research, 2005Co-Authors: David H. Adams, Glen R. Hanson, Kristen A. KeefeAbstract:The amphetamine analog 3,4-methylenedioxymethamphetamine (MDMA) is also known as the recreational drug of abuse, Ecstasy. Several neuropeptides are found in striatal neurons postsynaptic to dopamine and serotonin nerve terminals, and changes in neuropeptide neurotransmission may be important for behavioral effects of 3,4-methylenedioxymethamphetamine. This study used in situ hybridization to characterize the effects of 3,4-methylenedioxymethamphetamine on four neuropeptide mRNAs: Preprodynorphin, preprotachykinin, neurotensin/neuromedin N, and preproenkephalin. Male, Sprague-Dawley rats received a single administration of 10 mg/kg 3,4-methylenedioxymethamphetamine and were sacrificed 30 min or 3 h later. Three hours after administration, 3,4-methylenedioxymethamphetamine increased Preprodynorphin, preprotachykinin, and neurotensin/neuromedin N mRNAs. These increases were most prominent in ventral and medial aspects of the rostral-middle striatum, and then became more dorsally restricted in the caudal striatum. At the 30-minute time point, MDMA significantly decreased the signal for preproenkephalin mRNA in a general manner but did not affect the signal for the other neuropeptide precursors. These data suggest that 3,4-methylenedioxymethamphetamine has a generalized, transient, inhibitory effect on striatopallidal neuron gene expression, and then preferentially influences striatonigral neuropeptide systems at the later time point in a regionally selective manner.
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Blockade of stimulant-induced Preprodynorphin mRNA expression in the striatal matrix by serotonin depletion.
Neuroscience, 2005Co-Authors: Kristen A. Horner, David H. Adams, Glen R. Hanson, Kristen A. KeefeAbstract:Cocaine and methamphetamine (METH) induce Preprodynorphin (PPD) mRNA expression in the striatum. Cocaine induces PPD expression in both the patch and matrix compartments of the rostral striatum, whereas METH induces PPD expression in the patch compartment of the rostral striatum. In middle striatum, both stimulants increase PPD expression in the patch and matrix compartments. METH and cocaine treatment also increase extracellular serotonin (5-HT). Several studies have shown that 5-HT receptors are present on striatonigral neurons that express PPD mRNA, and that 5-HT is a positive regulator of striatal neuropeptide expression. The current study examined whether 5-HT plays a role in the patch/matrix expression of PPD mRNA induced by cocaine and METH in striatum. Male Sprague-Dawley rats were treated with p-chloroamphetamine (PCA; 8 mg/kg, i.p), a serotonin neurotoxin, 1 week prior to cocaine (30 mg/kg, i.p) and METH (15 mg/kg, s.c.) treatment. The 80% loss of 5-HT induced by PCA-pretreatment blocked cocaine-induced PPD expression in the rostral matrix compartment. Cocaine- and METH-induced PPD expression in the rostral patch compartment was unaffected by PCA-pretreatment. PCA-pretreatment also decreased both cocaine- and METH-induced PPD expression in the matrix, but not patch of middle striatum. PCA-induced 5-HT depletion did not affect stimulant-induced increases in PPT mRNA expression in the striatum. These data suggest that 5-HT plays a role in stimulant-induced PPD expression in the matrix compartment of rostral and middle striatum. Thus, 5-HT innervation may play a critical role in basal ganglia function.
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Distinct effects of methamphetamine and cocaine on Preprodynorphin messenger RNA in rat striatal patch and matrix.
Journal of neurochemistry, 2002Co-Authors: David H. Adams, Glen R. Hanson, Kristen A. KeefeAbstract:We and others previously reported that equimolar doses of methamphetamine and cocaine differentially increase Preprodynorphin mRNA in striatum: methamphetamine causes a patchy increase, whereas cocaine produces a more homogenous one. The current study directly examined whether this effect reflects differential induction in the patch–matrix division of striatum, as identified by µ opioid receptor immunohistochemistry. In addition, we determined whether doses of cocaine (30 mg/kg) and methamphetamine (2 mg/kg) that produced equivalent increases in extracellular dopamine differentially affected Preprodynorphin mRNA expression in striatum of male, Sprague–Dawley rats. In both experiments, methamphetamine and cocaine differentially affected Preprodynorphin mRNA in striatum after 3 h. The high, equimolar dose of methamphetamine selectively increased Preprodynorphin mRNA in the patch division of rostral striatum, whereas cocaine increased Preprodynorphin mRNA throughout patch and matrix divisions of striatum. In contrast, a dose of methamphetamine (2.0 mg/kg) that caused an increase in extracellular dopamine similar to that produced by 30 mg/kg cocaine did not significantly affect Preprodynorphin mRNA in any region of striatum. These data provide further evidence that cocaine and amphetamines exert distinct effects on the patch–matrix division of striatum and suggest further that the post-synaptic consequences of elevated extracellular dopamine produced by methamphetamine and cocaine are distinct.
J.f. Mcginty - One of the best experts on this subject based on the ideXlab platform.
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Intrastriatal GABAA receptor blockade does not alter dopamine D1/D2 receptor interactions in the intact rat striatum
Neuroscience, 2001Co-Authors: E.a Jones, John Q. Wang, J.f. McgintyAbstract:The purpose of this study was to investigate the effects of intrastriatal blockade of GABA(A) receptors on dopamine D(1)/D(2) receptor interactions in the intact rat striatum. Muscarinic receptors mediate the ability of the D(2) receptor antagonist, eticlopride, to block an increase in striatonigral neuropeptide messenger RNA stimulated by the full D(1) agonist, SKF-82958. However, because D(2) receptor antagonists activate striatopallidal neurons, it is possible that increased GABA release from local medium spiny axon collaterals also contributes to the ability of eticlopride to block the effects of SKF-82958. This hypothesis was addressed by infusing the GABA(A) receptor antagonist, bicuculline, into the dorsal striatum in rats treated with eticlopride and SKF-82958. In contrast to the actions of the muscarinic antagonist, scopolamine, bicuculline did not affect the increase in behaviors induced by SKF-82958 or the ability of eticlopride to block them. Quantitative in situ hybridization demonstrated that bicuculline did not significantly affect basal Preprodynorphin messenger RNA, nor did it affect the ability of eticlopride to decrease SKF-82958-induced Preprodynorphin messenger RNA. However, the level of the Preprodynorphin hybridization signal in bicuculline plus SKF-82958-treated rats was significantly lower than in saline plus SKF-82958-treated rats. In contrast, bicuculline, eticlopride or SKF-82958 by themselves increased basal preproenkephalin messenger RNA. However, there was no significant interaction among bicuculline, eticlopride and SKF-82958 on preproenkephalin messenger RNA levels.These data indicate that blockade of striatal GABA(A) receptors has only a subtle effect on acute dopamine agonist-induced changes in gene expression. These results are discussed in the context of local intrastriatal interactions.
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The effects of D1 or D2 dopamine receptor blockade on zif/268 and Preprodynorphin gene expression in rat forebrain following a short-term cocaine binge.
Brain research. Molecular brain research, 1996Co-Authors: J B Daunais, J.f. McgintyAbstract:Selective D1 or D2 dopamine receptor antagonists were used to investigate the transynaptic regulation of mRNAs coding for the opioid peptide, Preprodynorphin, and the nuclear transcription factor, zif/268 after an acute cocaine binge. Rats were injected intraperitoneally with the D1 receptor antagonist, SCH 23390, or the D2 receptor antagonist, sulpiride, 30 min prior to 3 hourly injections of saline or 20 mg/kg cocaine and killed 1 h after the final injection. Behavioral ratings indicated that SCH 23390 blocked, whereas sulpiride augmented, cocaine-induced stereotypical behaviors. Striatal sections were hybridized with oligonucleotides coding for zif/268 and Preprodynorphin. Quantitative image analysis of autoradiograms revealed that (1) SCH 23390 completely suppressed basal and cocaine binge-induced zif/268 mRNA in the striatal and cerebral cortical areas examined; (2) sulpiride enhanced basal levels of zif/268 mRNA in the medial caudate and dorsomedial shell of the nucleus accumbens; (3) sulpiride partially blocked cocaine binge-induced levels of zif/268 mRNA in the dorsal striatum but had no effect in sensory cortex; (4) SCH 23390, but not sulpiride, significantly reduced the constitutive expression of Preprodynorphin mRNA; and (5) SCH 23390 and sulpiride blocked cocaine binge-induced expression of Preprodynorphin mRNA in the dorsal striatum.
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dose dependent alteration in zif 268 and Preprodynorphin mrna expression induced by amphetamine or methamphetamine in rat forebrain
Journal of Pharmacology and Experimental Therapeutics, 1995Co-Authors: John Q. Wang, J.f. McgintyAbstract:The dose-related effects of a single injection of D-amphetamine (AMPH) or methamphetamine (METH) on the mRNA expression of the immediate early gene zif/268 and the opioid peptide Preprodynorphin, in rat forebrain, were investigated with quantitative in situ hybridization histochemistry 3 h after injection. Both drugs at equimolar doses (3.75, 7.5, 15 and 30 mumol/kg) up-regulated zif/268 mRNA expression in cerebral cortex in a dose-dependent fashion. In the "nose" area of the sensory cortex, all doses of METH, but not AMPH, induced a substantial, dose-dependent increase in zif/268 mRNA. Dose-dependent induction of zif/268 mRNA also occurred in caudoputamen after injection of AMPH at all doses. However, dose-dependent increases in zif/268 mRNA in caudoputamen in METH-treated rats and in nucleus accumbens in AMPH-treated and METH-treated rats were seen only after the three lower doses. Injection of 30 mumol/kg actually decreased zif/268 mRNA induction in these areas to or below that detected after 3.75 mumol/kg. Preprodynorphin mRNA expression in the striatum was dose-dependently increased by either drug at all doses. These results demonstrate a clear dose-related responsiveness of zif/268 and Preprodynorphin gene expression in cortical and/or striatal neurons that is positively correlated with a dose-dependent motor-stimulating effect of AMPH and METH. METH is a more potent psychostimulant than AMPH in eliciting behavioral and genomic activity at equimolar doses, and METH elicits a qualitatively different pattern of genomic activity in some forebrain regions, especially in the higher dose range.
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Dose-dependent alteration in zif/268 and Preprodynorphin mRNA expression induced by amphetamine or methamphetamine in rat forebrain.
The Journal of pharmacology and experimental therapeutics, 1995Co-Authors: John Q. Wang, J.f. McgintyAbstract:The dose-related effects of a single injection of D-amphetamine (AMPH) or methamphetamine (METH) on the mRNA expression of the immediate early gene zif/268 and the opioid peptide Preprodynorphin, in rat forebrain, were investigated with quantitative in situ hybridization histochemistry 3 h after injection. Both drugs at equimolar doses (3.75, 7.5, 15 and 30 mumol/kg) up-regulated zif/268 mRNA expression in cerebral cortex in a dose-dependent fashion. In the "nose" area of the sensory cortex, all doses of METH, but not AMPH, induced a substantial, dose-dependent increase in zif/268 mRNA. Dose-dependent induction of zif/268 mRNA also occurred in caudoputamen after injection of AMPH at all doses. However, dose-dependent increases in zif/268 mRNA in caudoputamen in METH-treated rats and in nucleus accumbens in AMPH-treated and METH-treated rats were seen only after the three lower doses. Injection of 30 mumol/kg actually decreased zif/268 mRNA induction in these areas to or below that detected after 3.75 mumol/kg. Preprodynorphin mRNA expression in the striatum was dose-dependently increased by either drug at all doses. These results demonstrate a clear dose-related responsiveness of zif/268 and Preprodynorphin gene expression in cortical and/or striatal neurons that is positively correlated with a dose-dependent motor-stimulating effect of AMPH and METH. METH is a more potent psychostimulant than AMPH in eliciting behavioral and genomic activity at equimolar doses, and METH elicits a qualitatively different pattern of genomic activity in some forebrain regions, especially in the higher dose range.
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Acute amphetamine or methamphetamine alters opioid peptide mRNA expression in rat striatum.
Brain research. Molecular brain research, 1994Co-Authors: A J Smith, J.f. McgintyAbstract:The effects of a single dose of amphetamine or methamphetamine on opioid peptide gene expression in the dorsal and ventral striatum of rats were investigated by quantitative in situ hybridization 3, 6, or 18 h after injection. Although amphetamine-treated rats exhibited significantly different behaviors than those treated with methamphetamine, both drugs caused a patchy increase in Preprodynorphin, but not preproenkephalin, mRNA in the caudate at all 3 time points. No changes were detected in the nucleus accumbens. These data indicate that prolonged elevation of Preprodynorphin expression may alter the responsiveness of striatonigral neurons to subsequent amphetamine exposure.
J.q. Wang - One of the best experts on this subject based on the ideXlab platform.
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Muscarinic receptors regulate striatal neuropeptide gene expression in normal and amphetamine-treated rats.
Neuroscience, 1996Co-Authors: J.q. Wang, Jacqueline F. McgintyAbstract:This study investigated the effects of pharmacological blockade or stimulation of muscarinic receptors on constitutive and amphetamine-stimulated Preprodynorphin, substance P and pre-proenkephalin gene expression in rat striatum. Acute administration of the non-selective muscarinic antagonist, scopolamine (2.5, 5 and 10 mg/kg, s.c.), caused a dose-dependent increase in Preprodynorphin and substance P, but not preproenkephalin, messenger RNA expression in the dorsal and ventral striatum as revealed by quantitative in situ hybridization. In contrast, acute injection of the non-selective muscarinic receptor agonist, oxotremorine (0.125, 0.25 and 0.5 mg/kg, s.c.), caused a dose-dependent increase in basal levels of preproenkephalin messenger RNA in the dorsal striatum, without causing a significant effect on constitutive striatal Preprodynorphin and substance P expression. Pretreatment with scopolamine (2.5 mg/kg, s.c.) significantly augmented striatal induction of Preprodynorphin and substance P messenger RNA induced by acute injection of amphetamine (1.25 and 2.5 mg/kg, i.p.), whereas scopolamine blocked amphetamine-stimulated striatal preproenkephalin expression. Pretreatment with oxotremorine (0.25 mg/kg, s.c.) significantly attenuated amphetamine (1.25 and 2.5 mg/kg, i.p.)-stimulated striatal Preprodynorphin and, to a lesser degree, substance P messenger RNA expression. Oxotremorine tended to increase amphetamine-stimulated preproenkephalin messenger RNA expression, but the effect did not reach statistical significance. In addition, scopolamine increased spontaneous, and enhanced amphetamine-stimulated, behavioral activity, whereas oxotremorine attenuated amphetamine-stimulated behaviors. These data support the concept that cholinergic transmission, via interaction with muscarinic receptors, inhibits basal and D1 receptor-stimulated striatonigral dynorphin/substance P gene expression and facilitates striatopallidal enkephalin gene expression.
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a single injection of amphetamine or methamphetamine induces dynamic alterations in c fos zif 268 and Preprodynorphin messenger rna expression in rat forebrain
Neuroscience, 1995Co-Authors: J.q. Wang, A J Smith, Jacqueline F. McgintyAbstract:In this study, the effects of a single dose of the indirect dopamine agonists amphetamine and methamphetamine on behavior and messenger RNA expression were evaluated. Expression of c-fos, a member of the leucine zipper family, zif/268 (NGFI-A, egr1 and Krox-24), a member of the zinc finger family, and the opioid peptide, Preprodynorphin, was investigated in various regions of rat forebrain with quantitative in situ hybridization histochemistry 1, 2, 3, 6 or 30 h after injection. Behavioral observations indicated that a qualitatively different behavioral syndrome was induced following methamphetamine (15 mg/kg, i.p.) as compared with that observed after amphetamine (5 mg/kg, i.p.). Similarly, methamphetamine induced a different pattern of c-fos and zif/268 messenger RNA induction in sensory/motor cortex, dorsal striatum (caudatoputamen) and ventral striatum (nucleus accumbens) than did amphetamine. The increase in c-fos messenger RNA expression peaked at 1 h and returned to basal levels in all regions by 3 h. In contrast, the increase in zif/268 messenger RNA expression in the cortical regions was equally strong at 1 and 2 h, gradually returning to basal levels by 6 h after either drug. However, in the striatal regions, zif/268 messenger RNA levels peaked at 1 h and declined gradually to basal levels by 6 h. Interestingly, methamphetamine caused an actual suppression of zif/268 gene expression (> 50%) in both caudatoputamen and nucleus accumbens at 3 h. Preprodynorphin messenger RNA expression was increased in a patchy motif in the caudatoputamen and nucleus accumbens beginning at 2 h and returning to basal levels by 30 h after injection of either drug. This study, together with our recently published observation that Preprodynorphin messenger RNA is induced in the caudate 3, 6 and 18 h after amphetamine or methamphetamine injection, provides a detailed dynamic description of the differential modulation of c-fos, zif/268 and Preprodynorphin messenger RNA expression in the cerebral cortex and striatum by amphetamines over time. These data implicate immediate early gene and Preprodynorphin gene expression in the differential response of medium spiny striatal neurons to methamphetamine and amphetamine.
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A single injection of amphetamine or methamphetamine induces dynamic alterations in c-fos,zif/268 and Preprodynorphin messenger RNA expression in rat forebrain
Neuroscience, 1995Co-Authors: J.q. Wang, A J Smith, Jacqueline F. McgintyAbstract:In this study, the effects of a single dose of the indirect dopamine agonists amphetamine and methamphetamine on behavior and messenger RNA expression were evaluated. Expression of c-fos, a member of the leucine zipper family, zif/268 (NGFI-A, egr1 and Krox-24), a member of the zinc finger family, and the opioid peptide, Preprodynorphin, was investigated in various regions of rat forebrain with quantitative in situ hybridization histochemistry 1, 2, 3, 6 or 30 h after injection. Behavioral observations indicated that a qualitatively different behavioral syndrome was induced following methamphetamine (15 mg/kg, i.p.) as compared with that observed after amphetamine (5 mg/kg, i.p.). Similarly, methamphetamine induced a different pattern of c-fos and zif/268 messenger RNA induction in sensory/motor cortex, dorsal striatum (caudatoputamen) and ventral striatum (nucleus accumbens) than did amphetamine. The increase in c-fos messenger RNA expression peaked at 1 h and returned to basal levels in all regions by 3 h. In contrast, the increase in zif/268 messenger RNA expression in the cortical regions was equally strong at 1 and 2 h, gradually returning to basal levels by 6 h after either drug. However, in the striatal regions, zif/268 messenger RNA levels peaked at 1 h and declined gradually to basal levels by 6 h. Interestingly, methamphetamine caused an actual suppression of zif/268 gene expression (> 50%) in both caudatoputamen and nucleus accumbens at 3 h. Preprodynorphin messenger RNA expression was increased in a patchy motif in the caudatoputamen and nucleus accumbens beginning at 2 h and returning to basal levels by 30 h after injection of either drug. This study, together with our recently published observation that Preprodynorphin messenger RNA is induced in the caudate 3, 6 and 18 h after amphetamine or methamphetamine injection, provides a detailed dynamic description of the differential modulation of c-fos, zif/268 and Preprodynorphin messenger RNA expression in the cerebral cortex and striatum by amphetamines over time. These data implicate immediate early gene and Preprodynorphin gene expression in the differential response of medium spiny striatal neurons to methamphetamine and amphetamine.