Electrophysiology of dopamine in normal and denervated striatal neurons

Parkinson's disease (PD) symptoms originate from the loss of the dopaminergic control of neuronal activity in the striatum. Permanent loss of dopaminergic terminals in the striatum results in an abnormal activity of striatal neurons. The therapeutic treatment with exogenous dopamine, therefore, temporarily restores a balanced synaptic excitation of striatal neurons, counteracting pre- and postsynaptically the excessive glutamate release caused by the degeneration of nigrostriatal dopaminergic fibers. However, chronic treatment is associated with adverse effects that might reflect nonphysiological dopamine replacement. Basic studies on experimental animal models of PD are of crucial importance for the development of therapeutic agents able to provide relief to individuals with PD, without the adverse effects associated with currently available drugs.

[1]  C. Cepeda,et al.  Neuromodulatory actions of dopamine in the neostriatum are dependent upon the excitatory amino acid receptor subtypes activated. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[2]  G. Bernardi,et al.  The action of dopamine on rat caudate neurones intracellularly recorded , 1978, Neuroscience Letters.

[3]  Thomas H. McNeill,et al.  Atrophy of medium spiny I striatal dendrites in advanced Parkinson's disease , 1988, Brain Research.

[4]  R. Roth,et al.  Effect ofl-glutamate on the release of striatal dopamine: in vivo dialysis and electrochemical studies , 1990, Brain Research.

[5]  P. Calabresi,et al.  Unilateral dopamine denervation blocks corticostriatal LTP. , 1999, Journal of neurophysiology.

[6]  U. Ungerstedt,et al.  Bilateral regulation of glutamate tissue and extracellular levels in caudate-putamen by midbrain dopamine neurons , 1990, Neuroscience Letters.

[7]  A M Graybiel,et al.  The basal ganglia and adaptive motor control. , 1994, Science.

[8]  P. Calabresi,et al.  Long-term synaptic depression in the striatum: physiological and pharmacological characterization , 1992, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[9]  T. F. Freund,et al.  Tyrosine hydroxylase-immunoreactive boutons in synaptic contact with identified striatonigral neurons, with particular reference to dendritic spines , 1984, Neuroscience.

[10]  P. Calabresi,et al.  The corticostriatal projection: from synaptic plasticity to dysfunctions of the basal ganglia , 1996, Trends in Neurosciences.

[11]  P. Calabresi,et al.  Intracellular studies on the dopamine-induced firing inhibition of neostriatal neurons in vitro: Evidence for D1 receptor involvement , 1987, Neuroscience.

[12]  A. Lang,et al.  New developments in understanding the etiology of Parkinson's disease and in its treatment , 1998, Current Opinion in Neurobiology.

[13]  A. Grace,et al.  Alterations in electrophysiological activity and dye coupling of striatal spiny and aspiny neurons in dopamine‐denervated rat striatum recorded in vivo , 1999, Synapse.

[14]  M. Starr.  Glutamate/dopamine D1/D2 balance in the basal ganglia and its relevance to Parkinson' disease , 1995, Synapse.

[15]  E. Vaadia,et al.  Physiological aspects of information processing in the basal ganglia of normal and parkinsonian primates , 1998, Trends in Neurosciences.

[16]  R. Romo,et al.  In vivo presynaptic control of dopamine release in the cat caudate nucleus—II. Facilitatory or inhibitory influence ofl-glutamate , 1986, Neuroscience.

[17]  Y. J. Lin,et al.  Permeation and block of dopamine-modulated potassium channels on rat striatal neurons by cesium and barium ions. , 1996, Journal of neurophysiology.

[18]  P. Groves.  A theory of the functional organization of the neostriatum and the neostriatal control of voluntary movement , 1983, Brain Research Reviews.

[19]  F. Tarazi,et al.  Localization of dopamine receptor subtypes in corpus striatum and nucleus accumbens septi of rat brain: comparison of D1-, D2- and D4-like receptors , 1998, Neuroscience.

[20]  J. Bouyer,et al.  Chemical and structural analysis of the relation between cortical inputs and tyrosine hydroxylase-containing terminals in rat neostriatum , 1984, Brain Research.

[21]  B. Yamamoto,et al.  Dopaminergic Modulation of Glutamate Release in Striatum as Measured by Microdialysis , 1992, Journal of neurochemistry.

[22]  J. P. Huston,et al.  The unilateral 6-hydroxydopamine lesion model in behavioral brain research. Analysis of functional deficits, recovery and treatments , 1996, Progress in Neurobiology.

[23]  P. Blanchet,et al.  Neostriatal mechanisms in Parkinson's disease , 1998, Neurology.

[24]  S. Sesack,et al.  Ultrastructural localization of D2 receptor-like immunoreactivity in midbrain dopamine neurons and their striatal targets , 1994, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[25]  J. Hagan,et al.  Parkinson's disease: prospects for improved drug therapy. , 1997, Trends in pharmacological sciences.

[26]  Paolo Calabresi,et al.  Neurophysiology of Parkinson's disease: from basic research to clinical correlates , 1999, Clinical Neurophysiology.

[27]  R. Riesenberg,et al.  Synaptic reorganisation in the rat striatum after dopaminergic deafferentation: An ultrastructural study using glutamate decarboxylase immunocytochemistry , 1995, Synapse.

[28]  Charles J. Wilson,et al.  Membrane potential synchrony of simultaneously recorded striatal spiny neurons in vivo , 1998, Nature.

[29]  P. Calabresi,et al.  Vulnerability of Medium Spiny Striatal Neurons to Glutamate: Role of Na+/K+ ATPase , 1995, The European journal of neuroscience.

[30]  C. Cepeda,et al.  Dopaminergic modulation of NMDA-induced whole cell currents in neostriatal neurons in slices: contribution of calcium conductances. , 1998, Journal of neurophysiology.

[31]  G Bernardi,et al.  Electrophysiology of dopamine-denervated striatal neurons. Implications for Parkinson's disease. , 1993, Brain : a journal of neurology.

[32]  P. Calabresi,et al.  Depletion of catecholamines reveals inhibitory effects of bromocryptine and lysuride on neostriatal neurones recorded intracellularly in vitro , 1988, Neuropharmacology.

[33]  J. Hell,et al.  Biochemical properties and subcellular distribution of an N-type calcium hannel α1 subunit , 1992, Neuron.

[34]  F. J. White,et al.  Review: D1 dopamine receptor—the search for a function: A critical evaluation of the D1/D2 dopamine receptor classification and its functional implications , 1987 .

[35]  P. Calabresi,et al.  Glutamate-Triggered Events Inducing Corticostriatal Long-Term Depression , 1999, The Journal of Neuroscience.

[36]  P. Calabresi,et al.  Abnormal Synaptic Plasticity in the Striatum of Mice Lacking Dopamine D2 Receptors , 1997, The Journal of Neuroscience.

[37]  J. Vincent,et al.  Dopamine D1 receptor modulates the voltage‐gated sodium current in rat striatal neurones through a protein kinase A. , 1995, The Journal of physiology.

[38]  P. Calabresi,et al.  Chronic neuroleptic treatment: D2 dopamine receptor supersensitivity and striatal glutamatergic transmission , 1992, Annals of neurology.

[39]  P. Greengard,et al.  Modulation of calcium currents by a D1 dopaminergic protein kinase/phosphatase cascade in rat neostriatal neurons , 1995, Neuron.

[40]  Y. Agid,et al.  Synaptic plasticity in the caudate nucleus of patients with Parkinson's disease. , 1996, Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration.

[41]  A. D. Smith,et al.  The neural network of the basal ganglia as revealed by the study of synaptic connections of identified neurones , 1990, Trends in Neurosciences.

[42]  R. Malenka,et al.  Modulation of synaptic transmission by dopamine and norepinephrine in ventral but not dorsal striatum. , 1998, Journal of neurophysiology.

[43]  R. Kötter.  Postsynaptic integration of glutamatergic and dopaminergic signals in the striatum , 1994, Progress in Neurobiology.

[44]  P. Calabresi,et al.  Role of Ca2+ in striatal LTD and LTP , 1996 .

[45]  J. Bolam,et al.  Input from the frontal cortex and the parafascicular nucleus to cholinergic interneurons in the dorsal striatum of the rat , 1992, Neuroscience.

[46]  P. Calabresi,et al.  Long‐term Potentiation in the Striatum is Unmasked by Removing the Voltage‐dependent Magnesium Block of NMDA Receptor Channels , 1992, The European journal of neuroscience.

[47]  Rodolfo Llinás,et al.  P-type calcium channels in the somata and dendrites of adult cerebellar purkinje cells , 1992, Neuron.

[48]  A. Graybiel.  Neurotransmitters and neuromodulators in the basal ganglia , 1990, Trends in Neurosciences.

[49]  U. Ungerstedt,et al.  N‐methyl‐d‐Aspartic Acid Differentially Regulates Extracellular Dopamine, GABA, and Glutamate Levels in the Dorsolateral Neostriatum of the Halothane‐Anesthetized Rat: An In Vivo Microdialysis Study , 1993, Journal of neurochemistry.

[50]  Greg A. Gerhardt,et al.  Multiple single-unit recordings in the striatum of freely moving animals: effects of apomorphine and d-amphetamine in normal and unilateral 6-hydroxydopamine-lesioned rats , 1999, Brain Research.

[51]  G. Rebec,et al.  Striatal Neuronal Activity and Responsiveness to Dopamine and Glutamate after Selective Blockade of D1 and D2 Dopamine Receptors in Freely Moving Rats , 1999, The Journal of Neuroscience.

[52]  A. Grace,et al.  Dye coupling between rat striatal neurons recorded in vivo: compartmental organization and modulation by dopamine. , 1994, Journal of neurophysiology.

[53]  G. Arbuthnott,et al.  Spine density on neostriatal neurones changes with 6-hydroxydopamine lesions and with age , 1989, Brain Research.