| dc.contributor.author | Bennett, Hilary Jane. | en_US |
| dc.date.accessioned | 2014-10-21T12:35:39Z | |
| dc.date.available | 2000 | |
| dc.date.issued | 2000 | en_US |
| dc.identifier.other | AAINQ60664 | en_US |
| dc.identifier.uri | http://hdl.handle.net/10222/55729 | |
| dc.description | Adenosine is an inhibitory neuromodulator in the central nervous system. For extracellular adenosine to play a physiological role in the brain, it must be present at effective concentrations. The purpose of these studies was to identify the neurotransmitters that evoke an increase in extracellular adenosine in the cerebral cortex and to identify the receptor subtypes that mediate these effects using in vivo microdialysis. | en_US |
| dc.description | Activation of ionotropic receptors by glutamate has been shown to increase adenosine in cortical slice. However, the possible effects of metabotropic glutamate receptor activation on the concentration of extracellular adenosine has not been examined. We tested whether activation of metabotropic and ionotropic glutamate receptors increases the extracellular concentration of adenosine in vivo. The group I/II metabotropic glutamate receptor agonist trans-(+/-)-1-amino(1S,3R)-cyclopenyanedicarboxylic acid increased extracellular adenosine as did the specific group I agonist (S)-3,5-dihydroxyphenylglycine. Activation of the group II or III metabotropic receptors did not affect extracellular adenosine levels. NMDA, AMPA and kainic acid also significantly increased the concentration of extracellular adenosine. | en_US |
| dc.description | Previous experiments using cortical slice and in vivo preparations have shown that activation of muscarinic receptors alone has no effect on basal adenosine release but enhanced the evoked release of adenosine. Given the role of nicotinic receptors in the modulation of neurotransmitter release, we tested whether activation of nicotinic receptors increases extracellular adenosine levels in vivo. Acetylcholine and the acetylcholinesterase inhibitor neostigmine increased extracellular adenosine levels, and the effects of neostigmine were blocked by the nicotinic receptor antagonist mecamylamine. Activation of muscarinic receptors using the nonselective agonist oxotremorine and a selective M1 receptor agonist also increased extracellular adenosine levels. Both nicotine and the nicotinic receptor agonist epibatidine increased the concentration of extracellular adenosine. | en_US |
| dc.description | Given the role of noradrenaline in modulating the activity of cortical neurons, it is important to determine whether noradrenaline evokes the release of adenosine in the cerebral cortex in vivo. Noradrenaline and the noradrenergic reuptake inhibitor desipramine increased extracellular adenosine levels. The alpha1-adrenergic receptor agonist phenylephrine and the beta-adrenergic agonist isoproterenol increased extracellular adenosine levels, whereas the alpha2-adrenergic receptor agonist clonidine did not have an effect. | en_US |
| dc.description | Taken together, these studies suggest that glutamatergic, cholinergic and noradrenergic transmission may contribute to the regulation of extracellular adenosine levels in vivo and may represent a mechanism for controlling neuronal excitability in the cerebral cortex. | en_US |
| dc.description | Thesis (Ph.D.)--Dalhousie University (Canada), 2000. | en_US |
| dc.language | eng | en_US |
| dc.publisher | Dalhousie University | en_US |
| dc.publisher | | en_US |
| dc.subject | Biology, Anatomy. | en_US |
| dc.subject | Biology, Neuroscience. | en_US |
| dc.title | An in vivo microdialysis study of neurotransmitter evoked adenosine release in the rat cerebral cortex. | en_US |
| dc.type | text | en_US |
| dc.contributor.degree | Ph.D. | en_US |
