Behavioural pharmacology of glutamate receptors in the basal ganglia

Schmidt, Werner; Kretschmer, Beate D.

doi:10.1016/s0149-7634(96)00044-9

Cited by 126 publications

(103 citation statements)

References 127 publications

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“…An attenuated locomotor response could be a result of a predominant activation of presynaptic dopamine D2 autoreceptors in the nucleus accumbens or the striatum (Hu and Wang, 1988) after a slightly enhanced dopamine release induced by the ADP analog. Another explanation could be a P2 receptor-mediated glutamate release in the same area (Krügel et al, 2001b), which is known to reduce locomotor activity (Schmidt and Kretschmer, 1997). The high potency of ADPbS to produce anxiolytic-like effects agrees with various in vitro studies that documented the high affinity of ADPbS to bind to rat brain P2Y 1 receptors (Vöhringer et al, 2000).…”

Section: Discussionmentioning

confidence: 53%

Stimulation of P2Y1 Receptors Causes Anxiolytic-like Effects in the Rat Elevated Plus-maze: Implications for the Involvement of P2Y1 Receptor-Mediated Nitric Oxide Production

Kittner

Franke

Fischer

et al. 2002

Neuropsychopharmacol

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(ADPbS), the P2X 1,3 receptor agonist a,b-methylene ATP (a,bmeATP), the unspecific P2 receptor antagonist pyridoxalphosphate-6-azopheny l-2 0 ,4 0 -disulfonic acid (PPADS), and the specific P2Y 1 receptor antagonist N 6 -methyl-2 0 -deoxyadenosine-3 0 ,5 0 -bisphosphate (MRS 2179) on the elevated plus-maze behavior of the rat were investigated. All tested compounds were given intracerebroventricularly (0.5 ml). ADPbS (50 and 500 fmol) produced an anxiolytic-like behavioral profile reflected by an increase of the open arm exploration. The anxiolytic-like effects were antagonized by pretreatment with PPADS (5 pmol) or MRS 2179 (5 pmol). Both compounds caused anxiogenic-like effects when given alone. Furthermore, the anxiolytic-like effects of ADPbS could be antagonized by pretreatment with the nitric oxide synthase (NOS) inhibitor N w -nitro-L-arginine methyl ester (L-NAME). In addition, the anxiogenic-like effects of PPADS were reversed by the pretreatment with L-arginine (500 pmol), which is the natural substrate for NOS, but not by D-arginine (500 pmol), which is not. Immunofluorescence staining revealed the presence of P2Y 1 receptors on neurons in different brain regions such as hypothalamus, amygdala, hippocampus and the periaqueductal gray. Furthermore, the colocalization of P2Y 1 receptors and neuronal NOS (nNOS) on some neurons in these regions could be demonstrated. The highest density of P2Y 1 -and nNOS-immunoreactivity was detected in the dorsomedial hypothalamic nucleus. Taken together, the present results suggest that P2Y 1 receptors are involved in the modulation of anxiety in the rat. The anxiolytic-like effects after stimulation of P2Y 1 receptors seem to be in close connection with the related nitric oxide production.

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Section: Discussionmentioning

confidence: 53%

Stimulation of P2Y1 Receptors Causes Anxiolytic-like Effects in the Rat Elevated Plus-maze: Implications for the Involvement of P2Y1 Receptor-Mediated Nitric Oxide Production

Kittner

Franke

Fischer

et al. 2002

Neuropsychopharmacol

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“…The 13 C turnover of amino acids from [1,[6][7][8][9][10][11][12][13] C 2 ]glucose was measured ex vivo using 1 H-[ 13 C]-NMR spectroscopy. The astroglial Glu pool size was estimated using a short-time infusion of [2][3][4][5][6][7][8][9][10][11][12][13] C]acetate. The ratio V cyc /V TCA for glutamatergic and GABAergic neurons was measured from the steady-state [2][3][4][5][6][7][8][9][10][11][12][13] C]acetate measurement.…”

Section: Introductionmentioning

confidence: 99%

“…The astroglial Glu pool size was estimated using a short-time infusion of [2][3][4][5][6][7][8][9][10][11][12][13] C]acetate. The ratio V cyc /V TCA for glutamatergic and GABAergic neurons was measured from the steady-state [2][3][4][5][6][7][8][9][10][11][12][13] C]acetate measurement. The 13 C turnover of cerebral amino acids from [1,[6][7][8][9][10][11][12][13] C 2 ]glucose was analyzed using a three-compartment metabolic model to determine metabolic rates associated with the glutamatergic and GABAergic pathway in different regions of the mouse brain.…”

Section: Introductionmentioning

confidence: 99%

Glutamatergic and GABAergic TCA Cycle and Neurotransmitter Cycling Fluxes in Different Regions of Mouse Brain

Tiwari

Ambadipudi

Patel

2013

J Cereb Blood Flow Metab

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The 13 C nuclear magnetic resonance (NMR) studies together with the infusion of 13 C-labeled substrates in rats and humans have provided important insight into brain energy metabolism. In the present study, we have extended a three-compartment metabolic model in mouse to investigate glutamatergic and GABAergic tricarboxylic acid (TCA) cycle and neurotransmitter cycle fluxes across different regions of the brain. ]glucose were analyzed using a threecompartment metabolic model to estimate the rates of the TCA cycle and neurotransmitter cycle associated with glutamatergic and GABAergic neurons. The glutamatergic TCA cycle rate was found to be highest in the cerebral cortex (0.91 ± 0.05 mmol/g per minute) and least in the hippocampal region (0.64±0.07 mmol/g per minute) of the mouse brain. In contrast, the GABAergic TCA cycle flux was found to be highest in the thalamus-hypothalamus (0.28±0.01 mmol/g per minute) and least in the cerebral cortex (0.24 ± 0.02 mmol/g per minute). These findings indicate that the energetics of excitatory and inhibitory function is distinct across the mouse brain.

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“…Glutamate (Glu) is the major excitatory neurotransmitter in the brain involved in functions such as motor behavior, cognition and emotion, which are affected in the course of the normal aging process [9,20,34]. Several lines of evidence also implicate glutamate toxicity as a contributing factor in the pathogenesis of age-related neurological conditions, including Parkinson's disease, Alzheimer's dementia, and Amyotrophic lateral sclerosis (for reviews see Refs.…”

Section: Introductionmentioning

confidence: 99%

Age-related glutamate and glutamine concentration changes in normal human brain: 1H MR spectroscopy study at 4 T

Kaiser

Schuff

Cashdollar

et al. 2005

Neurobiology of Aging

217

150

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Proton magnetic resonance spectroscopy was performed at 4 T to determine effects of age, region and gender on glutamate and glutamine in the normal human brain. Furthermore, glutamate and glutamine alterations with age were tested for correlations with other cerebral metabolites. Two 8 cm 3 volumes were selected in corona radiata and mesial motor cortex in normal subjects (N = 24) between 24 and 68 years old. Older subjects had lower glutamate concentration in the motor cortex compared to younger subjects (p < 0.001). In corona radiata, older subjects demonstrated a trend in higher glutamine compared to younger subjects (p = 0.05). Glutamate in the motor cortex was positively correlated with glutamine, N-acetyl aspartate and creatine. Reduced glutamate and Nacetyl aspartate in the motor cortex is consistent with neuronal loss/shrinkage with age. In conclusion, different patterns in association with normal aging in these brain regions were detected in this study.

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Behavioural pharmacology of glutamate receptors in the basal ganglia

Cited by 126 publications

References 127 publications

Stimulation of P2Y1 Receptors Causes Anxiolytic-like Effects in the Rat Elevated Plus-maze: Implications for the Involvement of P2Y1 Receptor-Mediated Nitric Oxide Production

Stimulation of P2Y1 Receptors Causes Anxiolytic-like Effects in the Rat Elevated Plus-maze: Implications for the Involvement of P2Y1 Receptor-Mediated Nitric Oxide Production

Glutamatergic and GABAergic TCA Cycle and Neurotransmitter Cycling Fluxes in Different Regions of Mouse Brain

Age-related glutamate and glutamine concentration changes in normal human brain: 1H MR spectroscopy study at 4 T

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