Cerebral cortex, acetylcholine release

Celesia, G. G. Jasper, H. H. (1966). Acetylcholine released from cerebral cortex in relation to state of activation. Neurology 16, 1053-64. 

Mitchell, J. F. (1963). The spontaneous and evoked release of acetylcholine from the cerebral cortex. J. Physiol. Lond. 163, 98-116. 

Several indirect neurochemical effects of methyixanthines contribute to their effects. Micromolar concentrations of caffeine enhance release of acetylcholine (Pedata et al. 1984). However, this effect is biphasic, augmenting release at 50 pM, but decreasing it at 0.5 pM. This effect is also modulatory, affecting stimulated, but not basal, release. Caffeine enhances acetylcholine release in the hippocampus, which is due to adenosine Al receptor subtypes (Carter et al. 1995). Conversely, chronic caffeine reduces the excitatory effect of acetylcholine in the cerebral cortex (Lin and Phillis... 

Opioids dose-dependently reduce the release of acetylcholine in several brain areas, including the hippocampus, striatum, and cerebral cortex... 

Lapchak PA, Araujo DM, Collier B. (1989). Regulation of endogenous acetylcholine release from mammalian brain slices by opiate receptors hippocampus, striatum, and cerebral cortex of guinea-pig and rat. Neuroscience. 31(2) 313-25. 

The available data are consistent with the present thesis that cholinergic inputs to cerebral cortex mediate intradendritic events fundamental to conscious activity as a primary role, and that cholinergic modulation of electrophysiological activity may be secondary, even epiphenomenal. Transduction pathways exist whereby muscarinic receptors (and possibly nicotinic receptors acting presynaptically to inhibit acetylcholine release) may lead to actions on the cytoskeleton directly relevant to consciousness. The thesis presented here describes these pathways and also suggests a possible explanation for the diversity of neuromodulators and metabotropic receptors. Accordingly, qualitative aspects of our consciousness would be finely tuned by a number of neurochemicals, prominent among which is acetylcholine. 

Maura G, Andrioli SC, Cavazzani P S-hydroxytryptaminej receptor sites on cholinergic axon terminals of human cerebral cortex mediate inhibition of acetylcholine release. J Neurochem 58 2334-2337, 1992 Mavissakalian M, Turner SM, Michelson L, et al Tricyclic antidepressants in obsessive-compulsive disorder antiobsessional or antidepressant agents 11. Am J Psychiatry 142 572-576, 1985... 

Fig. 1. Occurrence of H3 receptors inhibiting release of acetylcholine, of amino acid and monoamine neurotransmitters in the mammalian CNS in vitro. The schematic drawing represents a midsagittal section of the human brain three areas with a more lateral position are shown by broken line (substantia nigra and part of the hippocampus and of the striatum). For each of the six regions of the CNS (subregions given in brackets), in which H3 heteroreceptors have been identified, the neurotransmitter(s) and the species are indicated. The superscripts refer to the numbers of the papers as listed under References. Own unpublished data suggest that an H3 receptor-mediated inhibition of noradrenaline release also occurs in the human cerebral cortex and hippocampus and in the guinea-pig cerebral cortex. Note that a presynaptic location has not been verified for each of the H3 heteroreceptors or has been even excluded (for details, see Table 1). Abbreviations ACh, acetylcholine DA, dopamine GABA, y-aminobutyric acid Glu, glutamate 5-HT, 5-hydroxytryptamine, serotonin NA, noradrenaline...

High densities of H3 receptors were found in ACh-rich areas such as the cerebral cortex [40]. Furthermore, two different laboratories reported that H3 receptors are involved in the inhibitory effects of histamine on potassium-evoked release of [3H]-acetylcholine (ACh) [53, 54]. However, H3 receptor activation failed to inhibit [3H]-ACh release from rat cortical synaptosomes [54]. Since, as noted above, prudence must always be exerted in in-vivo extrapolation of in-vitro observations, we investigated the effect of histamine on the release of ACh from the cortex of freely moving rats and characterized the underlying mechanisms [55-58]. 

Cox SL, Schelb V, Trendelenburg AU et al (2000) Enhancement of noradrenaline release by angiotensin II and bradykinin in mouse atria evidence for cross talk between Gq/11 protein- and Gi/o protein-coupled receptors. Br J Pharmacol 129 1095-1102 Cunha RA, Milusheva E, Vizi ES et al (1994a) Excitatory and inhibitory effects of Ai and A2a adenosine receptor activation on the electrically evoked [3H] acetylcholine release from different areas of the rat hippocampus. J Neurochem 63 207-14 Cunha RA, Ribeiro JA, Sebastiao AM (1994b) Purinergic modulation of the evoked release of [3 H] acetylcholine from the hippocampus and cerebral cortex of the rat role of the ectonucleotidases. Eur J Neurosci 6 33 42... 

Maura G, et al. 5-Hydroxytryptamine3 receptors sited on cholineigic axon terminals of human cerebral cortex mediate inhibition of acetylcholine release. J Neurochem... 

Shikimi et al. (113) observed that Ca + was necessary in the incubation medium before high concentrations of morphine (10 3 m) could inhibit K+-stimulated acetylcholine release from cerebral cortical slices. Also morphine inhibition of acetylcholine release from the cerebral cortex in vivo is antagonized by both subcutaneous (114,115) and intraventricular injection of Ca + (116) as well as in the guinea pig ileum (36). 

Several pharmacologically active substances are present in superfusates of the cerebral cortex, including acetylcholine, 5-hydroxytryptamine, substance P and the prostaglandins. Members of this latter family of hydroxy-unsaturated fatty acids are released from a great variety of tissues on nerve and hormone stimulation (Ramwell and Shaw 1970), and have been shown to possess a wide range of biological activity (Horton, 1969). 

Galea, E. and Estrada, C., Periendothelial acetylcholine synthesis and release in bovine cerebral cortex capillaries, J. Cereb. Blood Flow Metah, 11(5), 868, 1991. 

Effect of morphine, nalorphine, naloxone, pentazocine, cyclazocine, and oxotremorine on the synthesis and release of acetylcholine by mouse cerebral cortex slices in vitro Howes, John F. Harris, Louis Selig Dewey, William L. 

The apparently wide distribution of cholinergic neurones presumably accounts for the ease with which it is possible to demonstrate drug-induced changes in the acetylcholine content of brain and in the rate of its release from the irrigated cerebral cortex. 

Cimsolo, S., Baldi. G., Gioigi, S., and Nannini, L, (1996). The cerebral cortex and parafascicular thalamic nucleus fticili-tate in vivo acetylcholine release in the rat striatum through distinct glutamate receptor subtypes. Eur. J. Neurosci. 8, 2702-2710. 

Macintosh F. C and Obonn P E (1953) Release of acetylcholine from intact cerebral cortex. Proc. XIX Int Cong Physiol, pp. 580-581. 

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