Amino Acids Released from the Cerebral Cortex in Relation to Its State of Activation

Jasper, Herbert H.; Khan, Rifat; Elliott, K. A. C.

doi:10.1126/science.147.3664.1448

Cited by 154 publications

(15 citation statements)

References 13 publications

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“…For example. Mitchell and co-workers (Mitchell & Srinivasan, 1969;Iversen, Mitchell & Srinivasan, 1971), in an elegant series of experiments, demonstrated a Ca2+-dependent release of endogenous GABA following electrical stimulation of the cortical surface and of the lateral geniculate nucleus and an increase in GABA release following brain stem transaction has also been described (Jasper, Khan & Elliott, 1965;Jasper & Koyama, 1969). Apart from work in this laboratory (Clark & Collins, 1975;Collins 1975) there have been no reports of stimulation achieving a significant R. M. CLARK AND G. G. S COLLINS release of endogenous taurine although Jasper & Koyama (1969) reported an increase in release accompanying electrical stimulation of the mid brain reticular formation.…”

Section: Discussionmentioning

confidence: 99%

The release of endogenous amino acids from the rat visual cortex.

Clark¹,

Collins²

1976

The Journal of Physiology

109

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SUMMARY1. The release of endogenous taurine, GABA, glycine, aspartate, glutamate, glutamine and alanine from the rat visual cortex was measured using a cortical cup technique. The electrocorticogram (ECoG) was monitored throughout most experiments.2. Spreading depression, evoked by the dropwise placement of 10 % KCl solution on to the brain outside the cup was associated with a significant increase in the release of GABA and glutamine but a marked fall in that of glutamate. The evoked release of GABA and glutamate but not of glutamine was Ca2+-dependent.3. A solution containing 50 mM-K+ placed within the cup elicited a significant increase in the release of taurine and GABA, whereas 100 mM-K+ additionally released aspartate and glutamate. The K+-evoked release of these amino acids with the exceptions of taurine and glutamine was Ca2+-dependent.4. Three series of experiments were carried out in which the preparations were stimulated electrically. Bipolar stimulation (100 Hz, 1 msec pulse width, 2-5 mA for 5 min) with the electrode within the cup was followed by significant increases in taurine, GABA and glutamate release; using a 5 mA current, there was an additional release of aspartate and alanine. Only the evoked release of GABA and glutamate was Ca2+-dependent.5. In the second and third series of experiments, the electrode was sited adjacent to the cup or on the contralateral cortex respectively. Following stimulation (100 Hz, 1 msec pulse width, 2-5 mA for 5 min) there was a significant increase in taurine and GABA release and a significant fall in the release of aspartate and glutamate. With the exception of taurine, these changes in release were Ca2+-dependent. Reducing the stimulus current to 1P5 mA or the period of stimulation to 2-5 min initiated similar but statistically insignificant changes in release. A range (10-100 Hz) of stimulation frequencies was examined: the evoked release of GABA was R. M. CLARK AND G. G. S. COLLINS linearly related to frequency whereas that of taurine was frequencyindependent. The fall in aspartate and glutamate release was maximal at a frequency of about 50 Hz.6. The results are discussed in relation to (a) the possible sites of release of the amino acids and (b) the proposed neurotransmitter roles of the physiologically active amino acids.

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Section: Discussionmentioning

confidence: 99%

The release of endogenous amino acids from the rat visual cortex.

Clark¹,

Collins²

1976

The Journal of Physiology

109

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“…Of the studies that have examined effects of sleep on glutamate, most concentrate on the effects of sleep and sleep loss in the cortex. These studies have observed that glutamate in the cortex levels fluctuate progressively through sleep/wake states (Jasper et al 1965;Lopez-Rodriguez et al 2007). Few have examined the effects of sleep deprivation on cortical glutamate levels.…”

Section: Glutamatementioning

confidence: 99%

The impact of sleep loss on hippocampal function

2013

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Hippocampal cellular and molecular processes critical for memory consolidation are affected by the amount and quality of sleep attained. Questions remain with regard to how sleep enhances memory, what parameters of sleep after learning are optimal for memory consolidation, and what underlying hippocampal molecular players are targeted by sleep deprivation to impair memory consolidation and plasticity. In this review, we address these topics with a focus on the detrimental effects of post-learning sleep deprivation on memory consolidation. Obtaining adequate sleep is challenging in a society that values "work around the clock." Therefore, the development of interventions to combat the negative cognitive effects of sleep deprivation is key. However, there are a limited number of therapeutics that are able to enhance cognition in the face of insufficient sleep. The identification of molecular pathways implicated in the deleterious effects of sleep deprivation on memory could potentially yield new targets for the development of more effective drugs.

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“…In 1965, it was first reported [33] that glutamate is released from the cortex of cats with the surface superfusion approach. It is also found that the release of glutamate was accompanied by the release of aspartate, glycine, and taurine after electrical stimulation.…”

Section: Glutamate In the Central Nervous Systemmentioning

confidence: 99%

Selective detection of neurotransmitters by fluorescence and chemiluminescence imaging

Wang

Yeung

2001

Pure and Applied Chemistry

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In recent years, luminescence imaging has been widely employed in neurochemical analysis. It has a number of advantages for the study of neuronal and other biological cells: (1) a particular molecular species or cellular constituent can be selectively visualized in the presence of a large excess of other species in a heterogeneous environment; (2) low concentration detection limits can be achieved because of the inherent sensitivity associated with fluorescence and chemiluminescence; (3) low excitation intensities can be used so that long-term observation can be realized while the viability of the specimen is preserved; and (4) excellent spatial resolution can be obtained with the light microscope so subcellular compartments can be identified. With good sensitivity, temporal and spatial resolution, the flux of ions and molecules and the distribution and dynamics of intracellular species can be measured in real time with specific luminescence probes, substrates, or with native fluorescence. A noninvasive detection scheme based on glutamate dehydrogenase (GDH) enzymatic assay combined with microscopy was developed to measure the glutamate release in cultured cells from the central nervous system (CNS). The enzyme reaction is very specific and sensitive. The detection limit with CCD imaging is down to µM levels of glutamate with reasonable response time. We also found that chemiluminescence associated with the ATP-dependent reaction between luciferase and luciferin can be used to image ATP at levels down to 10 nM in the millisecond time scale. Similar imaging experiments should be feasible in a broad spectrum of biological systems.

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Amino Acids Released from the Cerebral Cortex in Relation to Its State of Activation

Cited by 154 publications

References 13 publications

The release of endogenous amino acids from the rat visual cortex.

The release of endogenous amino acids from the rat visual cortex.

The impact of sleep loss on hippocampal function

Selective detection of neurotransmitters by fluorescence and chemiluminescence imaging

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