Alterations in plasma and brain amino acids after administration of the glycine/NMDA receptor partial agonist, d-cycloserine, to mice and rats

Baran, Halina; Gramer, Martina; Löscher, Wolfgang

doi:10.1016/0014-2999(94)00745-s

Cited by 20 publications

(13 citation statements)

References 17 publications

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“…The enhancement by DCS persisted transiently into extinction. Because the half-life of DCS is approximately 2 hours in rats (Baran et al, 1995), it is unlikely that the transient enhancement was due to any residual drug effect.…”

Section: Discussionmentioning

confidence: 99%

NMDA receptor in conditioned flavor-taste preference learning: Blockade by MK-801 and enhancement by D-cycloserine

Golden

Houpt

2007

Pharmacology Biochemistry and Behavior

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Conditioned flavor-taste preference (CFTP) is a robust form of learning in which animals acquire a preference for a flavor (e.g. Kool-Aid) previously mixed with a highly preferred tastant (e.g. fructose) over a flavor previously mixed with a less preferred tastant (e.g. saccharin). Here, the role of the Nmethyl-D-aspartate (NMDA) glutamate-glycine receptor (NR) was probed using systemic MK-801, a non-competitive antagonist, and D-cycloserine (DCS), a glycine agonist. Rats were injected with MK-801 (100 μg/kg) or vehicle 30 min prior to a daily 2-h conditioning session with 1-bottle access to a Kool-Aid flavor (grape or cherry) mixed with either 8% fructose (CS+/F) or 0.2% saccharin (CS −/S). CFTP expression was measured in 2-bottle preference tests between the Kool-Aid flavors mixed with 0.2% saccharin (CS+/S vs. CS−/S). While vehicle-treated rats acquired a preference for CS+/ S over CS−/S, MK-801 prior to conditioning completely blocked CFTP learning. The effect of MK-801 was specific to CFTP acquisition, because follow-up experiments demonstrated that MK-801 did not induce a conditioned taste aversion, cause state-dependent learning, or affect CFTP expression. In a second approach, rats were injected with DCS (15 mg/kg) 60 min prior to daily conditioning. In contrast to MK-801, adminstration of DCS prior to conditioning enhanced CFTP learning (but not reversal conditioning). These results demonstrate that NR neurotransmission is critical for CFTP learning. Furthermore, enhancement of CFTP learning by DCS suggests that endogenous levels of glycine or D-serine may be a limiting factor in CFTP learning.

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Section: Discussionmentioning

confidence: 99%

NMDA receptor in conditioned flavor-taste preference learning: Blockade by MK-801 and enhancement by D-cycloserine

Golden

Houpt

2007

Pharmacology Biochemistry and Behavior

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“…This dosage has been shown to facilitate performance on learning tasks in rodents, a property attributed to NMDA receptor potentiation (Andersen et al 2002;Baran et al 1995;Depoortere et al 1999;Monahan et al 1989). Antagonistic effects of D-cycloserine such as its anticonvulsive properties are associated to much higher doses (160-320 mg/kg) in rodents (Baran et al 1995;Loscher et al 1994;Wlaz et al 1994). It is conceivable that the D-cycloserine dose of 20 mg/kg in rats exerts an agonistic effect similarly to the dosage proven to be effective in adjunction to haloperidol in humans.…”

Section: Discussionmentioning

confidence: 99%

Homer 1a Gene Expression Modulation by Antipsychotic Drugs Involvement of the Glutamate Metabotropic System and Effects of D-Cycloserine

Polese¹,

Serpis²,

Ambesi-Impiombato³

et al. 2002

Neuropsychopharmacology

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“…The authors have demonstrated that intraventricular infusion of a nerve growth factor-specific antibody, which blocks nerve growth factor biological activity in vitro, attenuated the cholinergic axonal sprouting of basal forebrain cholinergic neurons following seizureinduced injury in vivo. In the future, experiments with GABA-mimetic drugs or drugs characterised by N-methyl-D-aspartate receptor-mediated release of GABA [45] or even reagents that influence the sprouting of cholinergic and GABAergic neurons will be of particular significance in order to prove their anti-epileptic properties and capability to modulate the progression of neural degeneration in the chronic KA model for epilepsy and may give new insight into the treatment of chronic epilepsy.…”

Section: Discussionmentioning

confidence: 99%

Choline Acetyltransferase, Glutamic Acid Decarboxylase and Somatostatin in the Kainic Acid Model for Chronic Temporal Lobe Epilepsy

et al. 2004

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The aim of the study was to investigate neurochemical changes in a kainic acid (KA; 10 mg/kg, s.c.)-induced spontaneous recurrent seizure model of epilepsy, 6 months after the initial KA-induced seizures. The neuronal markers of cholinergic and γ-aminobutyric acid (GABA)ergic systems, i.e. choline acetyltransferase (ChAT) and glutamic acid decarboxylase (GAD) activities, and a marker for neuropeptide, i.e. level of somatostatin, have been investigated. The brain regions investigated were the hippocampus, amygdala/piriform cortex, caudate nucleus, substantia nigra and the frontal, parietal, temporal and occipital cortices. Six months after KA injection, reduced ChAT activity was observed in the amygdala/piriform cortex (47% of control; p < 0.001), increased ChAT activity in the hippocampus (119% of control; p < 0.01) and normal ChAT activity in the other brain regions. The activity of GAD was significantly increased in all analysed cortical regions (between 146 and 171% of control), in the caudate nucleus (144% of control; p < 0.01) and in the substantia nigra (126% of control; p < 0.01), whereas in the amygdala/piriform cortex, the GAD activity was moderately lowered. The somatostatin level was significantly increased in all cortical regions (between 162 and 221% of control) as well as in the hippocampus (119% of control), but reduced in the amygdala/piriform cortex (45% of control; p < 0.01). Six months after KA injection, the somatostatin:GAD ratio was lowered in the amygdala/piriform cortex (49% of control) and in the caudate nucleus (41% of control), whereas it was normal in the hippocampus and moderately increased in the cortical brain regions. A positive correlation was found between seizure severity and the reduction of both ChAT activities and somatostatin levels in the amygdala/piriform cortex. The results show a specific pattern of changes for cholinergic, GABAergic and somatostatinergic activities in the chronic KA model for epilepsy. The revealed data suggest a functional role for them in the new network that follows spontaneous repetitive seizures.

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Alterations in plasma and brain amino acids after administration of the glycine/NMDA receptor partial agonist, d-cycloserine, to mice and rats

Cited by 20 publications

References 17 publications

NMDA receptor in conditioned flavor-taste preference learning: Blockade by MK-801 and enhancement by D-cycloserine

NMDA receptor in conditioned flavor-taste preference learning: Blockade by MK-801 and enhancement by D-cycloserine

Homer 1a Gene Expression Modulation by Antipsychotic Drugs Involvement of the Glutamate Metabotropic System and Effects of D-Cycloserine

Choline Acetyltransferase, Glutamic Acid Decarboxylase and Somatostatin in the Kainic Acid Model for Chronic Temporal Lobe Epilepsy

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