Abstract
The striatum is the main input structure of the basal ganglia. It is a centrally located region where afferents from the cerebral cortex, thalamus, and substantia nigra converge and interact. Glutamate is released from cortical and, to a lesser extent, thalamic terminals (1,2). Dopamine (DA) is released from nigrostriatal terminals (3). Because glutamate and DA inputs terminate on the same spines of striatal medium-sized spiny neurons (MSSNs), these sites offer the potential for physiological interactions between the glutamate and DA transmitter systems (4).
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Fonnum F, Storm-Mathisen J, Divac I. Biochemical evidence for glutamate as neurotransmitter in corticostriatal and corticothalamic fibres in rat brain. Neuroscience 1981; 6:863–873.
McGeer PL, McGeer EG, Scherer U, Singh K. A glutamatergic corticostriatal path? Brain Res 1977; 128:369–373.
Lindvall O, Bjorklund A, Skagerberg G. Selective histochemical demonstration of dopamine terminal systems in rat di-and telencephalon: new evidence for dopaminergic innervation of hypothalamic neurosecretory nuclei. Brain Res 1984; 306:19–30.
Freund TF, Powell JF, Smith AD. Tyrosine hydroxylase-immunoreactive boutons in synaptic contact with identified striatonigral neurons, with particular reference to dendritic spines. Neuroscience 1984; 13:1189–1215.
Calabresi P, Centonze D, Gubellini P, et al. Synaptic transmission in the striatum: from plasticity to neurodegeneration. Prog Neurobiol 2000; 61:231–265.
Chesselet MF, Delfs JM. Basal ganglia and movement disorders: an update. Trends Neurosci 1996; 19:417–422.
Graybiel AM. Building action repertoires: memory and learning functions of the basal ganglia. Curr Opin Neurobiol 1995; 5:733–741.
Rolls ET. Neurophysiology and cognitive functions of the striatum. Rev Neurol (Paris) 1994; 150:648–660.
Schultz W. Dopamine neurons and their role in reward mechanisms. Curr Opin Neurobiol 1997; 7:191–197.
Graveland GA, Williams RS, DiFiglia M. Evidence for degenerative and regenerative changes in neostriatal spiny neurons in Huntington’s disease. Science 1985; 227:770–773.
DiFiglia M. Excitotoxic injury of the neostriatum: a model for Huntington’s disease. Trends Neurosci 1990; 13:286–289.
Sapp E, Penney J, Young A, Aronin N, Vonsattel JP, DiFiglia M. Axonal transport of Nterminal huntingtin suggests early pathology of corticostriatal projections in Huntington disease. J Neuropathol Exp Neurol 1999; 58:165–173.
MacDonald V, Halliday G. Pyramidal cell loss in motor cortices in Huntington’s disease. Neurobiol Dis 2002; 10:378–386.
Rosas HD, Liu AK, Hersch S, et al. Regional and progressive thinning of the cortical ribbon in Huntington’s disease. Neurology 2002; 58:695–701.
Vonsattel JP, DiFiglia M. Huntington disease. J Neuropathol Exp Neurol 1998; 57:369–384.
Huntington’s Disease Collaborative Research G. A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington’s disease chromosomes. Cell 1993; 72:971–983.
Rasmussen A, Macias R, Yescas P, Ochoa A, Davila G, Alonso E. Huntington disease in children: genotype-phenotype correlation. Neuropediatrics 2000; 31:190–194.
Gencik M, Hammans C, Strehl H, Wagner N, Epplen JT. Chorea Huntington: a rare case with childhood onset. Neuropediatrics 2002; 33:90–92.
Strong TV, Tagle DA, Valdes JM, et al. Widespread expression of the human and rat Huntington’s disease gene in brain and nonneural tissues. Nat Genet 1993; 5:259–265.
Landwehrmeyer GB, McNeil SM, Dure LSt, et al. Huntington’s disease gene: regional and cellular expression in brain of normal and affected individuals. Ann Neurol 1995; 37: 218–230.
Young AB. Huntingtin in health and disease. J Clin Invest 2003; 111:299–302.
DiFiglia M, Sapp E, Chase K, et al. Huntingtin is a cytoplasmic protein associated with vesicles in human and rat brain neurons. Neuron 1995; 14:1075–1081.
Wood JD, MacMillan JC, Harper PS, Lowenstein PR, Jones AL. Partial characterisation of murine huntingtin and apparent variations in the subcellular localisation of huntingtin in human, mouse and rat brain. Hum Mol Genet 1996; 5:481–487.
Sun Y, Savanenin A, Reddy PH, Liu YF. Polyglutamine-expanded huntingtin promotes sensitization of N-methyl-d-aspartate receptors via post-synaptic density 95. J Biol Chem 2001; 276:24713–24718.
Perutz MF. Glutamine repeats and neurodegenerative diseases: molecular aspects. Trends Biochem Sci 1999; 24:58–63.
DiFiglia M, Sapp E, Chase KO, et al. Aggregation of huntingtin in neuronal intranuclear inclusions and dystrophic neurites in brain. Science 1997; 277:1990–1993.
Gutekunst CA, Li SH, Yi H, et al. Nuclear and neuropil aggregates in Huntington’s disease: relationship to neuropathology. J Neurosci 1999; 19:2522–2534.
Li H, Li SH, Cheng AL, Mangiarini L, Bates GP, Li XJ. Ultrastructural localization and progressive formation of neuropil aggregates in Huntington’s disease transgenic mice. Hum Mol Genet 1999; 8:1227–1236.
Kim M, Velier J, Chase K, et al. Forskolin and dopamine D1 receptor activation increase huntingtin’s association with endosomes in immortalized neuronal cells of striatal origin. Neuroscience 1999; 89:1159–1167.
Sapp E, Ge P, Aizawa H, et al. Evidence for a preferential loss of enkephalin immunoreactivity in the external globus pallidus in low grade Huntington’s disease using high resolution image analysis. Neuroscience 1995; 64:397–404.
Richfield EK, Maguire-Zeiss KA, Vonkeman HE, Voorn P. Preferential loss of preproenkephalin versus preprotachykinin neurons from the striatum of Huntington’s disease patients. Ann Neurol 1995; 38:852–861.
Monaghan DT, Bridges RJ, Cotman CW. The excitatory amino acid receptors: their classes, pharmacology, and distinct properties in the function of the central nervous system. Annu Rev Pharmacol Toxicol 1989; 29:365–402.
Hollmann M, Heinemann S. Cloned glutamate receptors. Annu Rev Neurosci 1994; 17:31–108.
Heuss C, Gerber U. G-protein-independent signaling by G-protein-coupled receptors. Trends Neurosci 2000; 23:469–475.
Watkins JC, Pook PC, Sunter DC, Davies J, Honore T. Experiments with kainate and quisqualate agonists and antagonists in relation to the sub-classification of “non-NMDA” receptors. Adv Exp Med Biol 1990; 268:49–55.
Nakanishi S. Metabotropic glutamate receptors: synaptic transmission, modulation, and plasticity. Neuron 1994; 13:1031–1037.
Conn PJ, Pin JP. Pharmacology and functions of metabotropic glutamate receptors. Annu Rev Pharmacol Toxicol 1997; 37:205–237.
Civelli O, Bunzow JR, Grandy DK. Molecular diversity of the dopamine receptors. Annu Rev Pharmacol Toxicol 1993; 33:281–307.
Sibley DR, Monsma FJ Jr. Molecular biology of dopamine receptors. Trends Pharmacol Sci 1992; 13:61–69.
Cepeda C, Hurst RS, Altemus KL, et al. Facilitated glutamatergic transmission in the striatum of D2 dopamine receptor-deficient mice. J Neurophysiol 2001; 85:659–670.
Konradi C, Cepeda C, Levine MS. Dopamine-glutamate interactions._In: Di Chiara G, ed. Dopamine in the CNS II. Vol. 154. Berlin; Springer, 2002:117–133.
Cepeda C, Levine MS. Dopamine and N-methyl-d-aspartate receptor interactions in the neostriatum. Dev Neurosci 1998; 20:1–18.
Cepeda C, Buchwald NA, Levine MS. Neuromodulatory actions of dopamine in the neostriatum are dependent upon the excitatory amino acid receptor subtypes activated. Proc Natl Acad Sci USA 1993; 90:9576–9580.
Levine MS, Li Z, Cepeda C, Cromwell HC, Altemus KL. Neuromodulatory actions of dopamine on synaptically-evoked neostriatal responses in slices. Synapse 1996; 24:65–78.
Surmeier DJ, Bargas J, Hemmings HC Jr, Nairn AC, Greengard P. Modulation of calcium currents by a D1 dopaminergic protein kinase/phosphatase cascade in rat neostriatal neurons. Neuron 1995; 14:385–397.
Hernández-López S, Bargas J, Surmeier DJ, Reyes A, Galarraga E. D1 receptor activation enhances evoked discharge in neostriatal medium spiny neurons by modulating an L-type Ca2+ conductance. J Neurosci 1997; 17:3334–3342.
Cepeda C, Colwell CS, Itri JN, Chandler SH, Levine MS. Dopaminergic modulation of NMDA-induced whole cell currents in neostriatal neurons in slices: contribution of calcium conductances. J Neurophysiol 1998; 79:82–94.
Blank T, Nijholt I, Teichert U, et al. The phosphoprotein DARPP-32 mediates cAMP-dependent potentiation of striatal N-methyl-d-aspartate responses. Proc Natl Acad Sci U S A 1997; 94:14859–14864.
Colwell CS, Levine MS. Excitatory synaptic transmission in neostriatal neurons: regulation by cyclic AMP-dependent mechanisms. J Neurosci 1995; 15:1704–1713.
Flores-Hernández J, Cepeda C, Hernández-Echeagaray E, et al. Dopamine enhancement of NMDA currents in dissociated medium-sized striatal neurons: role of D1 receptors and DARPP-32. J Neurophysiol 2002; 88:3010–3020.
Rajadhyaksha A, Leveque J, Macias W, Barczak A, Konradi C. Molecular components of striatal plasticity: the various routes of cyclic AMP pathways. Dev Neurosci 1998; 20: 204–215.
Snyder GL, Fienberg AA, Huganir RL, Greengard P. A dopamine/D1 receptor/protein kinase A/dopamine-and cAMP-regulated phosphoprotein (Mr 32 kDa)/protein phosphatase-1 pathway regulates dephosphorylation of the NMDA receptor. J Neurosci 1998; 18: 10,297–10,303.
Dunah AW, Standaert DG. Dopamine D1 receptor-dependent trafficking of striatal NMDA glutamate receptors to the postsynaptic membrane. J Neurosci 2001; 21: 5546–5558.
Scott L, Kruse MS, Forssberg, H et al. Selective up-regulation of dopamine D1 receptors in dendritic spines by NMDA receptor activation. Proc Natl Acad Sci USA 2002; 99: 1661–1664.
Fiorentini C, Gardoni F, Spano P, Di Luca M, Missale C. Regulation of dopamine D1 receptor trafficking and desensitization by oligomerization with glutamate NMDA receptors. J Biol Chem Mar 2003; 228:20,196–20,202.
Colwell CS, Levine MS. Glutamate receptor-induced toxicity in neostriatal cells. Brain Res 1996; 724:205–212.
Cepeda C, Colwell CS, Itri JN, Gruen E, Levine MS. Dopaminergic modulation of early signs of excitotoxicity in visualized rat neostriatal neurons. Eur J Neurosci 1998; 10: 3491–3497.
Coyle JT, Schwarcz R. Lesion of striatal neurones with kainic acid provides a model for Huntington’s chorea. Nature 1976; 263:244–246.
McGeer EG, McGeer PL. Duplication of biochemical changes of Huntington’s chorea by intrastriatal injections of glutamic and kainic acids. Nature 1976; 263:517–519.
Mason ST, Fibiger HC. Kainic acid lesions of the striatum: behavioural sequalae similar to Huntington’s chorea. Brain Res 1978; 155:313–329.
Coyle JT. An animal model for Huntington’s disease. Biol Psychiatry 1979; 14:251–276.
Beal MF, Kowall NW, Ellison DW, Mazurek MF, Swartz KJ, Martin JB. Replication of the neurochemical characteristics of Huntington’s disease by quinolinic acid. Nature 1986; 321:168–171.
Doble A. The role of excitotoxicity in neurodegenerative disease: implications for therapy. Pharmacol Ther 1999; 81:163–221.
Taylor-Robinson SD, Weeks RA, Bryant DJ, et al. Proton magnetic resonance spectroscopy in Huntington’s disease: evidence in favour of the glutamate excitotoxic theory. Mov Disord 1996; 11:167–173.
Nicoli F, Vion-Dury J, Maloteaux JM, et al. CSF and serum metabolic profile of patients with Huntington’s chorea: a study by high resolution proton NMR spectroscopy and HPLC. Neurosci Lett 1993; 154:47–51.
Dure LSt, Young AB, Penney JB. Excitatory amino acid binding sites in the caudate nucleus and frontal cortex of Huntington’s disease. Ann Neurol 1991; 30:785–793.
Young AB, Greenamyre JT, Hollingsworth Z, et al. NMDA receptor losses in putamen from patients with Huntington’s disease. Science 1988; 241:981–983.
Reilmann R, Rolf LH, Lange HW. Huntington’s disease: N-methyl-d-aspartate receptor coagonist glycine is increased in platelets. Exp Neurol 1997; 144:416–419.
Wagster MV, Hedreen JC, Peyser CE, Folstein SE, Ross CA. Selective loss of [3H]kainic acid and [3H]AMPA binding in layer VI of frontal cortex in Huntington’s disease. Exp Neurol 1994; 127:70–75.
Orlando LR, Alsdorf SA, Penney JB, Jr., Young AB. The role of group I and group II metabotropic glutamate receptors in modulation of striatal NMDA and quinolinic acid toxicity. Exp Neurol 2001; 167:196–204.
Coyle JT, Puttfarcken P. Oxidative stress, glutamate, and neurodegenerative disorders. Science 1993; 262:689–695.
Beal MF, Hyman BT, Koroshetz W. Do defects in mitochondrial energy metabolism underlie the pathology of neurodegenerative diseases? Trends Neurosci 1993; 16:125–131.
Beal MF, Brouillet E, Jenkins BG, et al. Neurochemical and histologic characterization of striatal excitotoxic lesions produced by the mitochondrial toxin 3-nitropropionic acid. J Neurosci 1993; 13:4181–4192.
Bossi SR, Simpson JR, Isacson O. Age dependence of striatal neuronal death caused by mitochondrial dysfunction. Neuroreport 1993; 4:73–76.
Novelli A, Reilly JA, Lysko PG, Henneberry RC. Glutamate becomes neurotoxic via the N-methyl-d-aspartate receptor when intracellular energy levels are reduced. Brain Res 1988; 451:205–212.
Simpson JR, Isacson O. Mitochondrial impairment reduces the threshold for in vivo NMDA-mediated neuronal death in the striatum. Exp Neurol 1993; 121:57–64.
Wüllner U, Young AB, Penny JB, Beal MF. 3-Nitropropionic acid toxicity in the striatum. J Neurochem 1994; 63:1772–1781.
Nishino H, Shimano Y, Kumazaki M, et al. Hypothalamic neurons are resistant to the intoxication with 3-nitropropionic acid that induces lesions in the striatum and hippocampus via the damage in the blood-brain barrier. Neurobiology 1995; 3:257–267.
Shimano Y, Kumazaki M, Sakurai T, et al. Chronically administered 3-nitropropionic acid produces selective lesions in the striatum and reduces muscle tonus. Obes Res 1995; 3 (Suppl 5):779S–784S.
Reynolds DS, Carter RJ, Morton AJ. Dopamine modulates the susceptibility of striatal neurons to 3-nitropropionic acid in the rat model of Huntington’s disease. J Neurosci 1998; 18:10,116–10,127.
Nishino H, Hida H, Kumazaki M, et al. The striatum is the most vulnerable region in the brain to mitochondrial energy compromise: a hypothesis to explain its specific vulnerability. J Neurotrauma 2000; 17:251–260.
Filloux F, Townsend JJ. Pre-and postsynaptic neurotoxic effects of dopamine demonstrated by intrastriatal injection. Exp Neurol 1993; 119:79–88.
Hastings TG, Lewis DA, Zigmond MJ. Role of oxidation in the neurotoxic effects of intrastriatal dopamine injections. Proc Natl Acad Sci USA 1996; 93:1956–1961.
Hattori A, Luo Y, Umegaki H, Munoz J, Roth GS. Intrastriatal injection of dopamine results in DNA damage and apoptosis in rats. Neuroreport 1998; 9:2569–2572.
McLaughlin BA, Nelson D, Erecinska M, Chesselet MF. Toxicity of dopamine to striatal neurons in vitro and potentiation of cell death by a mitochondrial inhibitor. J Neurochem 1998; 70:2406–2415.
Stokes AH, Hastings TG, Vrana KE. Cytotoxic and genotoxic potential of dopamine. J Neurosci Res 1999; 55:659–665.
Jakel RJ, Maragos WF. Neuronal cell death in Huntington’s disease: a potential role for dopamine. Trends Neurosci 2000; 23:239–245.
Olney JW, Zorumski CF, Stewart GR, Price MT, Wang GJ, Labruyere J. Excitotoxicity of l-dopa and 6-OH-dopa: implications for Parkinson’s and Huntington’s diseases. Exp Neurol 1990; 108:269–272.
Globus MY, Ginsberg MD, Dietrich WD, Busto R, Scheinberg P. Substantia nigra lesion protects against ischemic damage in the striatum. Neurosci Lett 1987; 80:251–256.
Chapman AG, Durmuller N, Lees GJ, Meldrum BS. Excitotoxicity of NMDA and kainic acid is modulated by nigrostriatal dopaminergic fibres. Neurosci Lett 1989; 107: 256–260.
Eradiri OL, Starr MS. Striatal dopamine depletion and behavioural sensitization induced by methamphetamine and 3-nitropropionic acid. Eur J Pharmacol 1999; 386:217–226.
Ferger B, Eberhardt O, Teismann P, de Groote C, Schulz JB. Malonate-induced generation of reactive oxygen species in rat striatum depends on dopamine release but not on NMDA receptor activation. J Neurochem 1999; 73:1329–1332.
Bowyer JF, Clausing P, Schmued L, et al. Parenterally administered 3-nitropropionic acid and amphetamine can combine to produce damage to terminals and cell bodies in the striatum. Brain Res 1996; 712:221–229.
Garside S, Furtado JC, Mazurek MF. Dopamine-glutamate interactions in the striatum: behaviourally relevant modification of excitotoxicity by dopamine receptor-mediated mechanisms. Neuroscience 1996; 75:1065–1074.
Whittemore ER, Ilyin VI, Woodward RM. subtype-selectivity and mechanisms of inhibition. J Pharmacol Exp Ther 1997; 282:326–338.
Garrett MC, Soares-da-Silva P. Increased cerebrospinal fluid dopamine and 3,4-dihydroxyphenylacetic acid levels in Huntington’s disease: evidence for an overactive dopaminergic brain transmission. J Neurochem 1992; 58:101–106.
Berman SB, Zigmond MJ, Hastings TG. Modification of dopamine transporter function: effect of reactive oxygen species and dopamine. J Neurochem 1996; 67:593–600.
Maragos WF, Jakel RJ, Pang Z, Geddes JW. 6-Hydroxydopamine injections into the nigrostriatal pathway attenuate striatal malonate and 3-nitropropionic acid lesions. Exp Neurol 1998; 154:637–644.
Bernheimer H, Birkmayer W, Hornykiewicz O, Jellinger K, Seitelberger F. Brain dopamine and the syndromes of Parkinson and Huntington. Clinical, morphological and neurochemical correlations. J Neurol Sci 1973; 20:415–455.
Backman L, Farde L. Dopamine and cognitive functioning: brain imaging findings in Huntington’s disease and normal aging. Scand J Psychol 2001; 42:287–296.
Sedvall G, Karlsson P, Lundin A, et al. Dopamine D1 receptor number—a sensitive PET marker for early brain degeneration in Huntington’s disease. Eur Arch Psychiatry Clin Neurosci 1994; 243:249–255.
Antonini A, Leenders KL, Spiegel R, et al. Striatal glucose metabolism and dopamine D2 receptor binding in asymptomatic gene carriers and patients with Huntington’s disease. Brain 1996; 119:2085–2095.
Augood SJ, Faull RL, Emson PC. Dopamine D1 and D2 receptor gene expression in the striatum in Huntington’s disease. Ann Neurol 1997; 42:215–221.
Weeks RA, Piccini P, Harding AE, Brooks DJ. Striatal D1 and D2 dopamine receptor loss in asymptomatic mutation carriers of Huntington’s disease. Ann Neurol 1996; 40:49–54.
Ginovart N, Lundin A, Farde L, et al. PET study of the pre-and post-synaptic dopaminergic markers for the neurodegenerative process in Huntington’s disease. Brain 1997; 120:503–514.
Cross A, Rossor M. Dopamine D-1 and D-2 receptors in Huntington’s disease. Eur J Pharmacol 1983; 88:223–229.
Richfield EK, O’Brien CF, Eskin T, Shoulson I. Heterogeneous dopamine receptor changes in early and late Huntington’s disease. Neurosci Lett 1991; 132:121–126.
Leenders KL, Frackowiak RS, Quinn N, Marsden CD. Brain energy metabolism and dopaminergic function in Huntington’s disease measured in vivo using positron emission tomography. Mov Disord 1986; 1:69–77.
Turjanski N, Weeks R, Dolan R, Harding AE, Brooks DJ. Striatal D1 and D2 receptor binding in patients with Huntington’s disease and other choreas. A PET study. Brain 1995; 118:689–696.
Sanchez-Pernaute R, Kunig G, del Barrio Alba A, de Yebenes JG, Vontobel P, Leenders KL. Bradykinesia in early Huntington’s disease. Neurology 2000; 54:119–125.
Bibb JA, Yan Z, Svenningsson P, et al. Severe deficiencies in dopamine signaling in presymptomatic Huntington’s disease mice. Proc Natl Acad Sci USA 2000; 97: 6809–6814.
Hickey MA, Reynolds GP, Morton AJ. The role of dopamine in motor symptoms in the R6/2 transgenic mouse model of Huntington’s disease. J Neurochem 2002; 81:46–59.
Hantraye P, Loc HC, Maziere B, et al. 6-[18F]fluoro-l-dopa uptake and [76Br]bromolisuride binding in the excitotoxically lesioned caudate-putamen of nonhuman primates studied using positron emission tomography. Exp Neurol 1992; 115:218–227.
Cha JH, Kosinski CM, Kerner JA, et al. Altered brain neurotransmitter receptors in transgenic mice expressing a portion of an abnormal human Huntington disease gene. Proc Natl Acad Sci USA 1998; 95:6480–6485.
Ariano MA, Aronin N, Difiglia M, et al. Striatal neurochemical changes in transgenic models of Huntington’s disease. J Neurosci Res 2002; 68:716–729.
Petersén A, Larsen KE, Behr GG, et al. Expanded CAG repeats in exon 1 of the Huntington’s disease gene stimulate dopamine-mediated striatal neuron autophagy and degeneration. Hum Mol Genet 2001; 10:1243–1254.
Spektor BS, Miller DW, Hollingsworth ZR, et al. Differential D1 and D2 receptor-mediated effects on immediate early gene induction in a transgenic mouse model of Huntington’s disease. Brain Res Mol Brain Res 2002; 102:118–128.
Menalled LB, Chesselet MF. Mouse models of Huntington’s disease. Trends Pharmacol Sci 2002; 23:32–39.
Rubinsztein DC. Lessons from animal models of Huntington’s disease. Trends Genet 2002; 18:202–209.
Mangiarini L, Sathasivam K, Seller M, et al. Exon 1 of the HD gene with an expanded CAG repeat is sufficient to cause a progressive neurological phenotype in transgenic mice. Cell 1996; 87:493–506.
Hodgson JG, Agopyan N, Gutekunst CA, et al. AYAC mouse model for Huntington’s disease with full-length mutant huntingtin, cytoplasmic toxicity, and selective striatal neurodegeneration. Neuron 1999; 23:181–192.
Laforet GA, Sapp E, Chase K, et al. Changes in cortical and striatal neurons predict behavioral and electrophysiological abnormalities in a transgenic murine model of Huntington’s disease. J Neurosci 2001; 21:9112–9123.
Levine MS, Klapstein GJ, Koppel A, et al. Enhanced sensitivity to N-methyl-d-aspartate receptor activation in transgenic and knockin mouse models of Huntington’s disease. J Neurosci Res 1999; 58:515–532.
Davies SW, Turmaine M, Cozens BA, et al. Formation of neuronal intranuclear inclusions underlies the neurological dysfunction in mice transgenic for the HD mutation. Cell 1997; 90:537–548.
Luthi-Carter R, Strand A, Peters NL, et al. Decreased expression of striatal signaling genes in a mouse model of Huntington’s disease. Hum Mol Genet 2000; 9:1259–1271.
Menalled L, Zanjani H, MacKenzie L, et al. Decrease in striatal enkephalin mRNA in mouse models of Huntington’s disease. Exp Neurol 2000; 162:328–342.
Tabrizi SJ, Workman J, Hart PE, et al. Mitochondrial dysfunction and free radical damage in the Huntington R6/2 transgenic mouse. Ann Neurol 2000; 47:80–86.
Higgins DS, Hoyt KR, Baic C, Vensel J, Sulka M. Metabolic and glutamatergic disturbances in the Huntington’s disease transgenic mouse. Ann NY Acad Sci 1999; 893:298–300.
Carter RJ, Lione LA, Humby T, et al. Characterization of progressive motor deficits in mice transgenic for the human Huntington’s disease mutation. J Neurosci 1999; 19:3248–3257.
Lione LA, Carter RJ, Hunt MJ, Bates GP, Morton AJ, Dunnett SB. Selective discrimination learning impairments in mice expressing the human Huntington’s disease mutation. J Neurosci 1999; 19:10,428–10,437.
Murphy KP, Carter RJ, Lione LA, et al. Abnormal synaptic plasticity and impaired spatial cognition in mice transgenic for exon 1 of the human Huntington’s disease mutation. J Neurosci 2000; 20:5115–5123.
Horikawa K, Armstrong WE. Aversatile means of intracellular labeling: injection of biocytin and its detection with avidin conjugates. J Neurosci Methods 1988; 25:1–11.
Turmaine M, Raza A, Mahal A, Mangiarini L, Bates GP, Davies SW. Nonapoptotic neurodegeneration in a transgenic mouse model of Huntington’s disease. Proc Natl Acad Sci USA 2000; 97:8093–8097.
Klapstein GJ, Fisher RS, Zanjani H, et al. Electrophysiological and morphological changes in striatal spiny neurons in R6/2 Huntington’s disease transgenic mice. J Neurophysiol 2001; 86:2667–2677.
Cepeda C, Ariano MA, Calvert CR, et al. NMDA receptor function in mouse models of Huntington disease. J Neurosci Res 2001; 66:525–539.
Zeron MM, Hansson O, Chen N, et al. Increased sensitivity to N-methyl-d-aspartate receptormediated excitotoxicity in a mouse model of Huntington’s disease. Neuron 2002; 33: 849–860.
Centonze D, Gubellini P, Picconi B, et al. An abnormal striatal synaptic plasticity may account for the selective neuronal vulnerability in Huntington’s disease. Neurol Sci 2001; 22:61–62.
Cudkowicz M, Kowall NW. Degeneration of pyramidal projection neurons in Huntington’s disease cortex. Ann Neurol 1990; 27:200–204.
de la Monte SM, Vonsattel JP, Richardson EP Jr. Morphometric demonstration of atrophic changes in the cerebral cortex, white matter, and neostriatum in Huntington’s disease. J Neuropathol Exp Neurol 1988; 47:516–525.
Halliday GM, McRitchie DA, Macdonald V, Double KL, Trent RJ, McCusker E. Regional specificity of brain atrophy in Huntington’s disease. Exp Neurol 1998; 154:663–672.
Hedreen JC, Peyser CE, Folstein SE, Ross CA. Neuronal loss in layers V and VI of cerebral cortex in Huntington’s disease. Neurosci Lett 1991; 133:257–261.
Sotrel A, Paskevich PA, Kiely DK, Bird ED, Williams RS, Myers RH. Morphometric analysis of the prefrontal cortex in Huntington’s disease. Neurology 1991; 41:1117–1123.
Morton AJ, Edwardson JM. Progressive depletion of complexin II in a transgenic mouse model of Huntington’s disease._J Neurochem 2001; 76:166–172.
Morton AJ, Faull RL, Edwardson JM. Abnormalities in the synaptic vesicle fusion machinery in Huntington’s disease. Brain Res Bull 2001; 56:111–117.
Liévens JC, Woodman B, Mahal A, Bates GP. Abnormal phosphorylation of synapsin I predicts a neuronal transmission impairment in the R6/2 Huntington’s disease transgenic mice. Mol Cell Neurosci 2002; 20:638–648.
Cepeda C, Hurst RS, Calvert CR, et al. Transient and progressive electrophysiological alterations in the corticostriatal pathway in a mouse model of Huntington’s disease. J Neurosci 2003; 23:961–969.
Berretta S, Parthasarathy HB, Graybiel AM. Local release of GABAergic inhibition in the motor cortex induces immediate-early gene expression in indirect pathway neurons of the striatum. J Neurosci 1997; 17:4752–4763.
Mitchell IJ, Cooper AJ, Griffiths MR. The selective vulnerability of striatopallidal neurons. Prog Neurobiol 1999; 59:691–719.
Uhl GR, Navia B, Douglas J. Differential expression of preproenkephalin and preprodynorphin mRNAs in striatal neurons: high levels of preproenkephalin expression depend on cerebral cortical afferents._J Neurosci 1988; 8:4755–4764.
Lovinger DM, Tyler E, Fidler S, Merritt A. Properties of a presynaptic metabotropic glutamate receptor in rat neostriatal slices. J Neurophysiol 1993; 69:1236–1244.
Lovinger DM, Choi S. Activation of adenosine A1 receptors initiates short-term synaptic depression in rat striatum. Neurosci Lett 1995; 199:9–12.
Liévens JC, Woodman B, Mahal A, et al. Impaired glutamate uptake in the R6 Huntington’s disease transgenic mice. Neurobiol Dis 2001; 8:807–821.
NicNiocaill B, Haraldsson B, Hansson O, O’Connor WT, Brundin P. Altered striatal amino acid neurotransmitter release monitored using microdialysis in R6/1 Huntington transgenic mice. Eur J Neurosci 2001; 13:206–210.
Behrens PF, Franz P, Woodman B, Lindenberg KS, Landwehrmeyer GB. Impaired glutamate transport and glutamate-glutamine cycling: downstream effects of the Huntington mutation. Brain 2002; 125:1908–1922.
Zuccato C, Ciammola A, Rigamonti D, et al. Loss of huntingtin-mediated BDNF gene transcription in Huntington’s disease. Science 2001; 293:493–498.
Hansson O, Petersén A, Leist M, Nicotera P, Castilho RF, Brundin P. Transgenic mice expressing a Huntington’s disease mutation are resistant to quinolinic acid-induced striatal excitotoxicity. Proc Natl Acad Sci USA 1999; 96:8727–8732.
Morton AJ, Leavens W. Mice transgenic for the human Huntington’s disease mutation have reduced sensitivity to kainic acid toxicity. Brain Res Bull 2000; 52:51–59.
MacGibbon GA, Hamilton LC, Crocker SF, et al. Immediate-early gene response to methamphetamine, haloperidol, and quinolinic acid is not impaired in Huntington’s disease transgenic mice. J Neurosci Res 2002; 67:372–378.
Bizière K, Coyle JT. Effects of cortical ablation on the neurotoxicity and receptor binding of kainic acid in striatum. J Neurosci Res 1979; 4:383–398.
McGeer EG, McGeer PL, Singh K. Kainate-induced degeneration of neostriatal neurons: dependency upon corticostriatal tract. Brain Res 1978; 139:381–383.
Petersén A, Chase K, Puschban Z, et al. Maintenance of susceptibility to neurodegeneration following intrastriatal injections of quinolinic acid in a new transgenic mouse model of Huntington’s disease. Exp Neurol 2002; 175:297–300.
Schiefer J, Alberty A, Dose T, Oliva S, Noth J, Kosinski CM. Huntington’s disease transgenic mice are resistant to global cerebral ischemia. Neurosci Lett 2002; 334:99–102.
Hickey MA, Morton AJ. Mice transgenic for the Huntington’s disease mutation are resistant to chronic 3-nitropropionic acid-induced striatal toxicity. J Neurochem 2000; 75:2163–2171.
Petersén A, Hansson O, Puschban Z, et al. Mice transgenic for exon 1 of the Huntington’s disease gene display reduced striatal sensitivity to neurotoxicity induced by dopamine and 6-hydroxydopamine. Eur J Neurosci 2001; 14:1425–1435.
Petersén A, Puschban Z, Lotharius J, et al. Evidence for dysfunction of the nigrostriatal pathway in the R6/1 line of transgenic Huntington’s disease mice. Neurobiol Dis 2002; 11:134–146.
Ariano MA, Cepeda, C, Calvert CR, et al. Alterations in K+ channels in Huntington’s disease transgenic mice. Soc Neurosci Abst 2000; 26:1030.
Eubanks JH, Altherr M, Wagner-McPherson C, McPherson JD, Wasmuth JJ, Evans GA. Localization of the D5 dopamine receptor gene to human chromosome 4p15.1–p15.3, centromeric to the Huntington’s disease locus. Genomics 1992; 12:510–516.
Levine MS, Altemus KL, Cepeda C, et al. Modulatory actions of dopamine on NMDA receptor-mediated responses are reduced in D1A-deficient mutant mice. J Neurosci 1996; 16:5870–5882.
Ingham CA, Hood SH, Arbuthnott GW. Spine density on neostriatal neurones changes with 6-hydroxydopamine lesions and with age. Brain Res 1989; 503:334–338.
Arbuthnott GW, Ingham CA, Wickens JR. Dopamine and synaptic plasticity in the neostriatum. J Anat 2000; 196:587–596.
van Dellen A, Welch J, Dixon RM, et al. N-Acetylaspartate and DARPP-32 levels decrease in the corpus striatum of Huntington’s disease mice. Neuroreport 2000; 11:3751–3757.
Sieradzan KA, Mann DM. The selective vulnerability of nerve cells in Huntington’s disease. Neuropathol Appl Neurobiol 2001; 27:1–21.
Ferrante RJ, Gutekunst CA, Persichetti F, et al. Heterogeneous topographic and cellular distribution of huntingtin expression in the normal human neostriatum. J Neurosci 1997; 17:3052–3063.
Fusco FR, Chen Q, Lamoreaux WJ, et al. Cellular localization of huntingtin in striatal and cortical neurons in rats: lack of correlation with neuronal vulnerability in Huntington’s disease. J Neurosci 1999; 19:1189–1202.
Landwehrmeyer GB, Standaert DG, Testa CM, Penny JB Jr, Young AB. NMDA receptor subunit mRNA expression by projection neurons and interneurons in rat striatum. J Neurosci 1995; 15:5297–5307.
Standaert DG, Friberg IK, Landwehrmeyer GB, Young AB, Penney JB Jr. Expression of NMDA glutamate receptor subunit mRNAs in neurochemically identified projection and interneurons in the striatum of the rat. Brain Res Mol Brain Res 1999; 64:11–23.
Cepeda C, Itri JN, Flores-Hernández J, Hurst RS, Calvert CR, and Levine MS. Differential sensitivity of medium-and large-sized striatal neurons to NMDA but not kainate receptor activation in the rat. Eur J Neurosci 2001; 14:1577–1589.
Calabresi P, Centonze D, Pisani A, et al. Striatal spiny neurons and cholinergic interneurons express differential ionotropic glutamatergic responses and vulnerability: implications for ischemia and Huntington’s disease. Ann Neurol 1998; 43:586–597.
Bennett BD, Wilson CJ. Spontaneous activity of neostriatal cholinergic interneurons in vitro. J Neurosci 1999; 19:5586–5596.
Lapper SR, Bolam JP. Input from the frontal cortex and the parafascicular nucleus to cholinergic interneurons in the dorsal striatum of the rat. Neuroscience 1992; 51:533–545.
Wüllner U, Standaert DG, Testa CM, et al. Glutamate receptor expression in rat striatum: effect of deafferentation. Brain Res 1994; 647:209–219.
Gottmann K, Mehrle A, Gisselmann G, Hatt H. Presynaptic control of subunit composition of NMDA receptors mediating synaptic plasticity. J Neurosci 1997; 17:2766–2774.
Kullmann DM, Asztely F. Extrasynaptic glutamate spillover in the hippocampus: evidence and implications. Trends Neurosci 1998; 21:8–14.
Lozovaya NA, Kopanitsa MV, Boychuk YA, Krishtal OA. Enhancement of glutamate release uncovers spillover-mediated transmission by N-methyl-D-aspartate receptors in the rat hippocampus. Neuroscience 1999; 91:1321–1330.
Tovar KR, Westbrook GL. The incorporation of NMDA receptors with a distinct subunit composition at nascent hippocampal synapses in vitro. J Neurosci 1999; 19:4180–4188.
Sattler R, Xiong Z, Lu WY, MacDonald JF, Tymianski M. Distinct roles of synaptic and extrasynaptic NMDA receptors in excitotoxicity. J Neurosci 2000; 20:22–33.
Hardingham GE, Fukunaga Y, Bading H. Extrasynaptic NMDARs oppose synaptic NMDARs by triggering CREB shut-off and cell death pathways. Nat Neurosci 2002; 5:405–414.
Gardoni F, Bellone C, Viviani B, et al. Lack of PSD-95 drives hippocampal neuronal cell death through activation of an alpha CaMKII transduction pathway. Eur J Neurosci 2002; 16:777–786.
Halpain S, Hipolito A, Saffer L. Regulation of F-actin stability in dendritic spines by glutamate receptors and calcineurin. J Neurosci 1998; 18:9835–9844.
Segal M. Dendritic spines for neuroprotection: a hypothesis. Trends Neurosci 1995; 18:468–471.
Carter RJ, Hunt MJ, Morton AJ. Environmental stimulation increases survival in mice transgenic for exon 1 of the Huntington’s disease gene. Mov Disord 2000; 15:925–937.
Hockly E, Cordery PM, Woodman B, et al. Environmental enrichment slows disease progression in R6/2 Huntington’s disease mice. Ann Neurol 2002; 51:235–242.
van Dellen A, Blakemore C, Deacon R, York D, Hannan AJ. Delaying the onset of Huntington’s in mice. Nature 2000; 404:721–722.
Schrott LM. Effect of training and environment on brain morphology and behavior. Acta Paediatr Suppl 1997; 422:45–47.
Caplen NJ, Taylor JP, Statham VS, Tanaka F, Fire A, Morgan RA. Rescue of polyglutaminemediated cytotoxicity by double-stranded RNA-mediated RNA interference. Hum Mol Genet 2002; 11:175–184.
Feigin A, Zgaljardic D. Recent advances in Huntington’s disease: implications for experimental therapeutics. Curr Opin Neurol 2002; 15:483–489.
McMurray CT. Huntington’s disease: new hope for therapeutics. Trends Neurosci 2001; 24:S32–S38.
Jankowsky JL, Savonenko A, Schilling G, Wang J, Xu G, Borchelt DR. Transgenic mouse models of neurodegenerative disease: opportunities for therapeutic development. Curr Neurol Neurosci Rep 2002; 2:457–464.
Smith DL, Portier R, Woodman B, et al. Inhibition of polyglutamine aggregation in R6/2 HD brain slices-complex dose-response profiles. Neurobiol Dis 2001; 8:1017–1026.
Sanchez I, Mahlke C, Yuan J. Pivotal role of oligomerization in expanded polyglutamine neurodegenerative disorders. Nature 2003; 42:373–379.
Chen M, Ona VO, Li M, et al. Minocycline inhibits caspase-1 and caspase-3 expression and delays mortality in a transgenic mouse model of Huntington disease. Nat Med 2000; 6:797–801.
Ona VO, Li M, Vonsattel JP, et al. Inhibition of caspase-1 slows disease progression in a mouse model of Huntington’s disease. Nature 1999; 399:263–267.
Thomas M, Le WD, Jankovic J. Minocycline and other tetracycline derivatives: a neuroprotective strategy in Parkinson’s disease and Huntington’s disease. Clin Neuropharmacol. 2003; 26:18–23.
Dedeoglu A, Kubilus JK, Jeitner TM, et al. Therapeutic effects of cystamine in a murine model of Huntington’s disease. J Neurosci 2002; 22:8942–8950.
Lesort M, Lee M, Tucholski J, Johnson GV. Cystamine inhibits caspase activity. Implications for the treatment of polyglutamine disorders. J Biol Chem 2003; 278:3825–3830.
Heiser V, Engemann S, Brocker W, et al. Identification of benzothiazoles as potential polyglutamine aggregation inhibitors of Huntington’s disease by using an automated filter retardation assay. Proc Natl Acad Sci USA 2002; 99:16,400–16,406.
Kornhuber J, Weller M, Shoppmeyer K, Riederer P. Amantadine and memantine are NMDA receptor antagonists with neuroprotective properties. J Neural Transm 1994; 43:91–104.
Lucetti C, Gambaccini G, Bernardini S, et al. Amantadine in Huntington’s disease: openlabel video-blinded study. Neurol Sci 2002; 23:S83–S84.
Verhagen Metman L, Morris MJ, Farmer C, et al. Huntington’s disease: a randomized, controlled trial using the NMDA-antagonist amantadine. Neurology 2002; 59:694–699.
Schilling G, Coonfield ML, Ross CA, Borchelt DR. Coenzyme Q10 and remacemide hydrochloride ameliorate motor deficits in a Huntington’s disease transgenic mouse model. Neurosci Lett 2001; 315:149–153.
Ferrante RJ, Andreassen OA, Dedeoglu A, et al. Therapeutic effects of coenzyme Q10 and remacemide in transgenic mouse models of Huntington’s disease. J Neurosci 2002; 22:1592–1599.
Colwell CS, Altemus KL, Cepeda C, Levine MS. Regulation of N-methyl-d-aspartate-induced toxicity in the neostriatum: a role for metabotropic glutamate receptors? Proc Natl Acad Sci USA 1996; 93:1200–1204.
Orlando LR, Standaert DG, Penney JB, Jr., Young AB. Metabotropic receptors in excitotoxicity: (S)-4-carboxy-3-hydroxyphenylglycine ((S)-4C3HPG) protects against rat striatal quinolinic acid lesions. Neurosci Lett 1995; 202:109–112.
Blum D, Gall D, Galas MC, d’Alcantara P, Bantubungi K, Schiffmann SN. The adenosine A1 receptor agonist adenosine amine congener exerts a neuroprotective effect against the development of striatal lesions and motor impairments in the 3-nitropropionic acid model of neurotoxicity. J Neurosci 2002; 22:9122–9133.
Popoli P, Pintor A, Domenici MR, et al. Blockade of striatal adenosine A2A receptor reduces, through a presynaptic mechanism, quinolinic acid-induced excitotoxicity: possible relevance to neuroprotective interventions in neurodegenerative diseases of the striatum. J Neurosci 2002; 22:1967–1975.
Schiefer J, Landwehrmeyer GB, Luesse HG, et al. Riluzole prolongs survival time and alters nuclear inclusion formation in a transgenic mouse model of Huntington’s disease. Mov Disord 2002; 17:748–757.
Wei H, Qin ZH, Senatorov VV, et al. Lithium suppresses excitotoxicity-induced striatal lesions in a rat model of Huntington’s disease. Neuroscience 2001; 106:603–612.
Hockly E, Richon VM, Woodman B, et al. Suberoylanilide hydroxamic acid, a histone deacetylase inhibitor, ameliorates motor deficits in a mouse model of Huntington’s disease. Proc Natl Acad Sci USA 2003; 100:2041–2046.
Steffan JS, Bodai L, Pallos J, et al. Histone deacetylase inhibitors arrest polyglutaminedependent neurodegeneration in Drosophila. Nature 2001; 413:739–743.
Corsini GU, Onali P, Masala C, Cianchetti C, Mangoni A, Gessa G. Apomorphine hydrochloride-induced improvement in Huntington’s chorea: stimulation of dopamine receptor. Arch Neurol 1978; 35:27–30.
Albanese A, Cassetta E, Carretta D, Bentivoglio AR, Tonali P. Acute challenge with apomorphine in Huntington’s disease: a double-blind study. Clin Neuropharmacol 1995; 18:427–434.
Tyler A, Scourfield J, Morris MR. Management and therapy of Huntington’s disease. In: Harper PS, ed. Huntington’s Disease. London: Saunders, 1996:161–201.
Kartzinel R, Hunt RD, Calne DB. Bromocriptine in Huntington chorea. Arch Neurol 1976; 33:517–518.
Loeb C, Roccatagliata G, Albano C, Besio G. Bromocriptine and dopaminergic function in Huntington disease. Neurology 1979; 29:730–734.
Quinn N, Marsden CD. A double blind trial of sulpiride in Huntington’s disease and tardive dyskinesia. J Neurol Neurosurg Psychiatry 1984; 47:844–847.
Melamed E, Hefti F, Bird ED. Huntington chorea is not associated with hyperactivity of nigrostriatal dopaminergic neurons: studies in postmortem tissues and in rats with kainic acid lesions. Neurology 1982; 32:640–644.
Clifford JJ, Drago J, Natoli AL, et al. Essential fatty acids given from conception prevent topographies of motor deficit in a transgenic model of Huntington’s disease. Neuroscience 2002; 109:81–88.
Duan W, Guo Z, Jiang H, Ware M, Li XJ, Mattson MP. Dietary restriction normalizes glucose metabolism and BDNF levels, slows disease progression, and increases survival in huntingtin mutant mice. Proc Natl Acad Sci U S A 2003; 100:2911–2916.
Andreassen OA, Ferrante RJ, Huang HM, et al. Dichloroacetate exerts therapeutic effects in transgenic mouse models of Huntington’s disease. Ann Neurol 2001; 50:112–117.
Ferrante RJ, Andreassen OA, Jenkins BG, et al. Neuroprotective effects of creatine in a transgenic mouse model of Huntington’s disease. J Neurosci 2000; 20:4389–4397.
Keene CD, Rodrigues CM, Eich T, Chhabra MS, Steer CJ, Low WC. Tauroursodeoxycholic acid, a bile acid, is neuroprotective in a transgenic animal model of Huntington’s disease. Proc Natl Acad Sci USA 2002; 99:10671–10676.
Seppi K, Mueller J, Bodner T, et al. Riluzole in Huntington’s disease (HD): an open label study with one year follow up. J Neurol 2001; 248:866–869.
Isacson O, Riche D, Hantraye P, Sofroniew MV, Maziere M. A primate model of Huntington’s disease: cross-species implantation of striatal precursor cells to the excitotoxically lesioned baboon caudate-putamen. Exp Brain Res 1989; 75:213–220.
Chen GJ, Jeng CH, Lin SZ, Tsai SH, Wang Y, Chiang YH. Fetal striatal transplants restore electrophysiological sensitivity to dopamine in the lesioned striatum of rats with experimental Huntington’s disease. J Biomed Sci 2002; 9:303–310.
Hauser RA, Furtado S, Cimino CR, et al. Bilateral human fetal striatal transplantation in Huntington’s disease. Neurology 2002; 58:687–695.
Rosser AE, Barker RA, Harrower T, et al. Unilateral transplantation of human primary fetal tissue in four patients with Huntington’s disease: NEST-UK safety report ISRCTN no 36485475. J Neurol Neurosurg Psychiatry 2002; 73:678–685.
Albin RL. Fetal striatal transplantation in Huntington’s disease: time for a pause. J Neurol Neurosurg Psychiatry 2002; 73:612.
Greenamyre JT, Shoulson I. We need something better, and we need it now: fetal striatal transplantation in Huntington’s disease? Neurology 2002; 58:675–676.
Bachoud-Levi AC, Hantraye P, Peschanski M. Fetal neural grafts for Huntington’s disease: a prospective view. Mov Disord 2002; 17:439–444.
van Dellen A, Deacon R, York D, Blakemore C, Hannan AJ. Anterior cingulate cortical transplantation in transgenic Huntington’s disease mice. Brain Res Bull 2001; 56:313–318.
Gouhier C, Chalon S, Venier-Julienne MC, et al. Neuroprotection of nerve growth factorloaded microspheres on the D2 dopaminergic receptor positive-striatal neurones in quinolinic acid-lesioned rats: a quantitative autoradiographic assessment with iodobenzamide. Neurosci Lett 2000; 288:71–75.
Mittoux V, Ouary S, Monville C, et al. Corticostriatopallidal neuroprotection by adenovirusmediated ciliary neurotrophic factor gene transfer in a rat model of progressive striatal degeneration. J Neurosci 2002; 22:4478–4486.
Regulier E, Pereira de Almeida L, Sommer B, Aebischer P, Deglon N. Dose-dependent neuroprotective effect of ciliary neurotrophic factor delivered via tetracycline-regulated lentiviral vectors in the quinolinic acid rat model of Huntington’s disease. Hum Gene Ther 2002; 13:1981–1990.
Nakao N, Brundin P, Funa K, Lindvall O, Odin P. Trophic and protective actions of brainderived neurotrophic factor on striatal DARPP-32-containing neurons in vitro. Brain Res Dev Brain Res 1995; 90:92–101.
Frim DM, Simpson J, Uhler TA, et al. Striatal degeneration induced by mitochondrial blockade is prevented by biologically delivered NGF. J Neurosci Res 1993; 35:452–458.
Petersén AA, Larsen KE, Behr GG, et al. Brain-derived neurotrophic factor inhibits apoptosis and dopamine-induced free radical production in striatal neurons but does not prevent cell death. Brain Res Bull 2001; 56:331–335.
Funa K, Yamada N, Brodin G, Pietz K, Ahgren A, Wictoria K, et al. Enhanced synthesis of platelet-derived growth factor following injury induced by 6-hydroxydopamine in rat brain. Neuroscience 1996; 74:825–833.
Zhou J, Pliego-Rivero B, Bradford HF, Stern GM. The BDNF content of postnatal and adult rat brain: the effects of 6-hydroxydopamine lesions in adult brain. Brain Res Dev Brain Res 1996; 97:297–303.
Numan S, Seroogy KB. Increased expression of trkB mRNA in rat caudate-putamen following 6-OHDA lesions of the nigrostriatal pathway. Eur J Neurosci 1997; 9:489–495.
Mizuta I, Ohta M, Ohta K, Nishimura M, Mizuta E, Kuno S. Riluzole stimulates nerve growth factor, brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor synthesis in cultured mouse astrocytes. Neurosci Lett 2001; 310:117–120.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2005 Humana Press Inc., Totowa, NJ
About this chapter
Cite this chapter
Cepeda, C., Ariano, M.A., Levine, M.S. (2005). Dopamine and Glutamate in Huntington’s Disease. In: Schmidt, W.J., Reith, M.E.A. (eds) Dopamine and Glutamate in Psychiatric Disorders. Humana Press. https://doi.org/10.1007/978-1-59259-852-6_23
Download citation
DOI: https://doi.org/10.1007/978-1-59259-852-6_23
Publisher Name: Humana Press
Print ISBN: 978-1-58829-325-1
Online ISBN: 978-1-59259-852-6
eBook Packages: MedicineMedicine (R0)