Brain slices release

Chey, W. M., 1978, The application of HPLC in brain slice release studies, M.S. Thesis, University of Kansas. 

Because of their strategic localization, astrocytes play a crucial role in maintaining the extracellular ionic homeostasis, provide energetic metabolites to neurons and remove excess of neurotransmitter in schedule with synaptic activity. In addition, the strategic location of astrocytes allows them to carefully monitor and control the level of synaptic activity. Indeed, number of papers during the last 15 years have shown that cultured astrocytes can respond to a variety of neurotransmitters with a variety of different patterns of intracellular calcium increases (Verkhratsky et al. 1998). Later on, studies performed in intact tissue preparations (acute brain slices) further established that the plasma membrane receptors can sense external inputs (such as the spillover of neurotransmitters during intense synaptic activity) and transduce them as intracellular calcium elevations, mostly via release of calcium from internal stores (Dani et al. 1992 Murphy et al. 1993 Porter and McCarthy... 

There is also the interesting possibility that presynaptie inhibition of this form, with or without potential changes, need not be restricted to the effect of the NT on the terminal from which it is released. Numerous studies in which brain slices have been loaded with a labelled NT and its release evoked by high K+ or direct stimulation show... 

Figure 1.9 Comparison of the effects of an endogenously released and exogenously applied neurotransmitter on neuronal activity (identity of action). Recordings are made either of neuronal firing (extracellularly, A) or of membrane potential (intracellularly, B). The proposed transmitter is applied by iontophoresis, although in a brain slice preparation it can be added to the bathing medium. In this instance the applied neurotransmitter produces an inhibition, like that of nerve stimulation, as monitored by both recordings and both are affected similarly by the antagonist. The applied neurotransmitter thus behaves like and is probably identical to that released from the nerve...

Pali), P and Stamford, JA (1993) Real-time monitoring of endogenous noradrenaline release in rat brain slices using fast cyclic voltammetry. 2. Operational characteristics of the alpha2 autoreceptors in the bed nucleus of the stria terminalis, pars ventralis. Brain Res. 608 134-140. 

Murugaiah, KD and O Donnell, JM (1995) Facilitation of noradrenaline release from rat brain slices by beta-adrenoceptors. Naunyn-Schmiedebergs Arch. Pharmacol. 351 483--490. 

ATP certainly fulfils the criteria for a NT. It is mostly synthesised by mitochondrial oxidative phosphorylation using glucose taken up by the nerve terminal. Much of that ATP is, of course, required to help maintain Na+/K+ ATPase activity and the resting membrane potential as well as a Ca +ATPase, protein kinases and the vesicular binding and release of various NTs. But that leaves some for release as a NT. This has been shown in many peripheral tissues and organs with sympathetic and parasympathetic innervation as well as in brain slices, synaptosomes and from in vivo studies with microdialysis and the cortical cup. There is also evidence that in sympathetically innervated tissue some extracellular ATP originates from the activated postsynaptic cell. While most of the released ATP comes from vesicles containing other NTs, some... 

Inhibition of glutamate release was thought to be the mode of action of lamotrigine. It reduces MBS and kindling and also glutamate (and to a lesser extent GABA) release induced in brain slices by veratridine, which opens sodium channels. But it now seems likely that the actual block of sodium channels is its primary action (see later). 

Johnson, M.P. Hoffman, A.J. and Nichols, D.E. Effects of the enantiomers of MDA, MDMA and related analogs on [ H] serotonin and [ Hjdopamine release from superfused rat brain slices. Eur J Pharmacol 132 269-276, 1986. 

Gifford AN, Tang Y, Gatley SJ, Volkow ND, Lan R, Makriyannis A. Effect of the cannabinoid receptor SPECT agent, AM 281, on hippocampal acetylcholine release from rat brain slices. Neurosci Lett 1997 238 84-86. 

Nicotine increased DA levels both in vivo11,193 and in vitro. 94 196 Nicotine197 and its metabolites198 were found to both release and inhibit the reuptake of DA in rat brain slices, with uptake inhibition occurring at a lower concentration than that required for DA release. In addition, the (-) isomer was more potent than the (+) isomer.197 However, the effects of nicotine upon DA release and uptake were only apparent when brain slices were utilized because nicotine was unable to affect DA when a synaptosomal preparation was utilized.197 These results indicate that nicotine exerts its effects upon the DAT indirectly, most likely via nicotine acetylcholine receptors. This finding was supported by the results of Yamashita et al.199 in which the effect of nicotine on DA uptake was examined in PC 12 and COS cells transfected with rat DAT cDNA. Nicotine inhibited DA uptake in PC 12 cells that possess a nicotine acetylcholine receptor. This effect was blocked by the nicotinic antagonists hexamethonium and mecamylamine. Additionally, nicotine did not influence DA uptake in COS cells, which lack nicotinic acetylcholine receptors. 

Westfall, T.C., Effect of nicotine and other drugs on the release of 3H-norepinephrine and 3H-dopamine from rat brain slices, Neuropharmacology, 13, 693, 1974. 

Fitzgerald, J.L. and Reid, J.J., Interactions of methylenedioxymethamphetamine with monoamine transmitter release mechanisms in rat brain slices, Naunyn Schmiedeberg s Arch. Pharmacol. 347(3), 313-323, 1993. 

Sprouse, J.S., Bradberry, C.W., Roth, R.H., and Aghajanian, G.K., MDMA (3,4-methylene-dioxymethamphetamine) inhibits the firing of dorsal raphe neurons in brain slices via release of serotonin, Eur. J. Pharmacol. 167(3), 375-383, 1989. 

Experiments investigating the interactions between brain histamine and other transmitters are summarized. Unless otherwise specified, release experiments were performed in vitro with brain slices or synaptosomes. See [71,89,90] for references. 

Katz, R. 1., and Kopin, 1. J. (1969) Effect of D-LSD and related compounds on release of norepinephrine-3H and serotonin-3H evoked from brain slices by electrical stimulation. Pharmacol. Res. Commun., 1 54-62. 

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