The corticopontine projection: Axotomy-induced loss of high affinity l-glutamate and d-aspartate uptake, but not of γ-aminobutyrate uptake, glutamate decarboxylase or choline acetyltransferase, in the pontine nuclei
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Axon-terminals expressing EAAT2 (GLT-1; Slc1a2) are common in the forebrain and not limited to the hippocampus
2019, Neurochemistry InternationalCitation Excerpt :Alexa fluor goat anti-mouse 488 antibodies were purchased from Molecular probes (Eugene, OR, USA). Crude tissue homogenates were prepared as described before (Thangnipon et al., 1983). Mice (8–14 weeks old) were killed by cervical dislocation.
Toward a more precise, clinically-informed pathophysiology of pathological laughing and crying
2013, Neuroscience and Biobehavioral ReviewsCitation Excerpt :Volitional glutamatergic corticopontine projections (Thangnipon et al., 1983; Dinopoulos et al., 1991) activate inhibitory interneurons (Sasaki et al., 1970; Allen et al., 1977), synapsing on basis pontis GABAergic neuronal somata (Thangnipon et al., 1983; Border and Mihailoff, 1985; Mihailoff et al., 1988; Brodal and Bjaalie, 1992), consistent with documented GABAergic regulation of the PAG (Jürgens, 1994; Lonstein and De Vries, 2000; Morgan et al., 2003; Griffiths and Lovick, 2005; Xiao et al., 2008) and hypothalamus (Ford et al., 1995). Corticopontine fiber transection dramatically increases markers of pontine cholinergic transmission (Thangnipon et al., 1983) and M1-3 muscarinic receptor activation inhibits GABA transmission within the PAG (Lau and Vaughan, 2008), disinhibiting the PAG by cholinergic inhibition of the GABAergic inhibition on PAG glutamatergic excitatory fibers (Jürgens, 1994; Lau and Vaughan, 2008). In addition to this mechanism operant in diseases such as CVA, MS, and TBI, the PAG is also inhibited by DA, NE, and 5HT (Jürgens, 1994), neurotransmitters diminished in PD and other diseases associated with IEED.
In vivo glutamate measured with magnetic resonance spectroscopy: Behavioral correlates in aging
2013, Neurobiology of AgingCitation Excerpt :Advanced age is associated with impairments in various cognitive and motor functions and structural and biochemical changes in selective brain regions (Seidler et al., 2010). A candidate substrate to contribute to decline in function with age is glutamate (Glu), a key molecule in cellular metabolism, the most abundant neurotransmitter in the mammalian nervous system, and the principal neurotransmitter of cortical efferents (Fonnum, 1984; Thangnipon et al., 1983). Alterations to the glutamatergic system have been shown to contribute to compromised cognitive performance in individuals with neuropsychiatric disorders (Krystal et al., 1999b; Newcomer et al., 1999; Parwani et al., 2005; Robbins and Murphy, 2006) and might also contribute to altered cognitive function in healthy aging.
Glutamate uptake
2001, Progress in NeurobiologyCitation Excerpt :The idea has been that glutamatergic nerve terminals have glutamate transporters (see Section 4.2) and that destruction of the axons (either by transection of the fiber tracts or ablation of the neuronal cell bodies) leads to a loss of glutamate uptake activity because the nerve terminals harboring the uptake sites degenerate. Ablation of the cerebral cortex has been shown to give reductions in glutamate uptake (as determined by autoradiography of tissue slices or in synaptosome containing tissue homogenates) in striatum, thalamus, amygdala, olfactory tubercle, pontine nuclei, spinal cord as well as some other regions (Divac et al., 1977; McGeer et al., 1977; Storm-Mathisen, 1977a; Fonnum et al., 1981; Kerkerian et al., 1983; Thangnipon et al., 1983; Walker and Fonnum, 1983a,b; Taxt and Storm-Mathisen, 1984; Potashner et al., 1988), while transection of fornix leads to reductions of glutamate uptake in corpus mammilare and lateral septum (Walaas and Fonnum, 1980). When antibodies to glutamate transporters became available, scientists were quick to repeat the lesion experiments and measure changes in glutamate transporter immunoreactivities.
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W. T. was on leave of absence from the Faculty of Science, Mahidol University, Rama VI Road, Bangkok 4, Thailand. Present address: MRC Developmental Neurobiology Unit, Institute of Neurology, 33 John's Mews, London WC1N 2NS, England.
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Institute of Physiology, University of Oslo, Oslo 1, Norway.