Chronic haloperidol, but not clozapine, produces altered oral movements and increased extracellular glutamate in rats
References (51)
- et al.
Subcortical excitatory amino acid levels after acute and subchronic administration of typical and atypical neuroleptics
Eur. J. Pharmacol.
(1993) - et al.
High sensitivity HPLC assay for GABA in brain dialysis studies
J. Neurosci. Meth.
(1991) - et al.
Free radicals and tardive dyskinesia
Trends Neurosci.
(1986) - et al.
Actions of clozapine and haloperidol on the extracellular levels of excitatory amino acids in the prefrontal cortex and striatum of conscious rats
Neurosci. Lett.
(1993) - et al.
Spontaneous chewing movements in rats during acute and chronic antipsychotic drug administration
Pharmacol. Biochem. Behav.
(1986) - et al.
Presynaptic dopaminergic modulation of cortical input to the striatum
Life Sci.
(1986) - et al.
Subchronic haloperidol and sulpiride treatment induces region-specific changes in tissue levels of putative amino acid transmitters in rat brain
Neurosci. Lett.
(1987) - et al.
Increased indices of free radical activity in the cerebrospinal fluid of patients with tardive dyskinesia
Biol. Psychiatry
(1990) - et al.
Normalization of extracellular dopamine in striatum following recovery from a partial unilateral 6-OHDA lesion of the substantia nigra: a microdialysis study in freely moving rats
Brain Res.
(1988) Striatal dopamine metabolism increases during long-term haloperidol administration in rats but shows tolerance to acute challenge with raclopride
Neurosci. Lett.
(1991)
Comparison of chronic administration of haloperidol and the atypical neuroleptics, clozapine and raclopride, in an animal model of tardive dyskinesia
Eur. J. Pharmacol.
Chronic neuroleptic treatment in rats produces persisting changes in GABAA and dopamine D-2, but not dopamine D-1 receptors
Life Sci.
Chronic neuroleptic administration decreases extracellular GABA in the nucleus accumbens but not in the caudate-putamen of rats
Brain Res.
Regional differences in chronic neuroleptic effects on extracellular dopamine activity
Brain Res. Bull.
Blood to brain distribution of neuroleptics
Psychiat. Res.
Schizophrenia, affective psychoses, and other disorders treated with neuroleptic drugs: the enigma of tardive dyskinesia, its neurobiological determinants, and the conflict of paradigms
Int. Rev. Neurobiol.
Instrumental assessment of lingual motor instability in tardive dyskinesia
Neuropsychopharmacology
Tardive dyskinesia
Clozapine: neuroleptic-induced EPS and tardive dyskinesia
Psychopharmacology
The risks and benefits of clozapine versus chlorpromazine
J. Clin. Psychopharmacol.
Oxidative stress, glutamate, and neurodegenerative disorders
Science
Excitotoxic mechanisms may be involved in the pathophysiology of tardive dyskinesia
Clin. Neuropharmacol.
Opposite effects of short and long-term haloperidol treatment on levels of mRNA encoding glutamic acid decarboxylase (GAD 67) in rat globus pallidus
The Physiologist
Extracellular glutamate levels increase with age in the lateral striatum: potential involvement of presynaptic D-2 receptors
Synapse
Rats administered chronic neuroleptics develop oral movements which are similar in form to those in humans with tardive dyskinesia
Psychopharmacology
Cited by (83)
Antipsychotic treatment leading to dopamine supersensitivity persistently alters nucleus accumbens function
2015, NeuropharmacologyCitation Excerpt :Finally, glutamate modulates dopamine function, and chronic exposure to typical versus atypical antipsychotics can evoke different neuroadaptations within the glutamate system. Chronic exposure to HAL but not to the atypical antipsychotic clozapine enhances basal extracellular glutamate levels in the striatum (See and Chapman, 1994; Yamamoto and Cooperman, 1994). In addition, chronic exposure to HAL versus to OLZ or clozapine has differential effects on the density of the NR1 subunit of the NMDA receptor in the striatum (Fitzgerald et al., 1995), and on the density of type II metabotropic glutamate receptors in the frontal cortex (Tascedda et al., 2001).
Antipsychotic medications, glutamate, and cell death: A hidden, but common medication side effect?
2013, Medical HypothesesCitation Excerpt :In summary, elevated extracellular glutamate levels have been consistently observed in caudate, frontal cortex, and nucleus accumbens in rats treated chronically with the typical antipsychotic medication haloperidol, but not with the atypical antipsychotic medication clozapine. In contrast to effects of typical antipsychotic medications on extracellular glutamate, multiple studies have demonstrated that the atypical antipsychotic medication clozapine does not affect extracellular glutamate in stratum or frontal cortex [15–17,20]. However, widespread clinical use of clozapine is limited because of metabolic side effects and risk of agranulocytosis.
Co-administration of nitric oxide (NO) donors prevents haloperidol-induced orofacial dyskinesia, oxidative damage and change in striatal dopamine levels
2009, Pharmacology Biochemistry and BehaviorLess Is More: Antipsychotic Drug Effects Are Greater with Transient Rather Than Continuous Delivery
2008, Biological PsychiatryCitation Excerpt :However, chronic haloperidol treatment (either via minipump, the drinking water, or daily SC injection) decreases striatal dopamine levels (15,37–41), suggesting that nondopaminergic mechanisms might be involved. One candidate is glutamate, which remains elevated in the striatum during chronic haloperidol treatment (42–44) and is involved in antipsychotic-induced striatal c-fos expression (45–47). Whatever the underlying mechanisms, the positive correlation between c-fos mRNA expression and antipsychotic efficacy suggests that gene regulation might be a step in a chain of intracellular events that contribute to and/or maintain antipsychotic efficacy over time.
Novel oral drug administration in an animal model of neuroleptic therapy
2005, Journal of Neuroscience MethodsAntipsychotic drugs elevate mRNA levels of presynaptic proteins in the frontal cortex of the rat
2005, Biological Psychiatry