dc.contributor.author |
Cucchiaroni, ML |
en |
dc.contributor.author |
Freestone, PS |
en |
dc.contributor.author |
Berretta, N |
en |
dc.contributor.author |
Viscomi, MT |
en |
dc.contributor.author |
Bisicchia, E |
en |
dc.contributor.author |
Okano, H |
en |
dc.contributor.author |
Molinari, M |
en |
dc.contributor.author |
Bernardi, G |
en |
dc.contributor.author |
Lipski, J |
en |
dc.contributor.author |
Mercuri, NB |
en |
dc.contributor.author |
Guatteo, E |
en |
dc.date.accessioned |
2012-03-01T19:31:40Z |
en |
dc.date.available |
2012-03-01T19:31:40Z |
en |
dc.date.issued |
2011 |
en |
dc.identifier.citation |
European Journal of Neuroscience 33(9):1622-1636 2011 |
en |
dc.identifier.issn |
0953-816X |
en |
dc.identifier.other |
1460-9568 |
en |
dc.identifier.uri |
http://hdl.handle.net/2292/12443 |
en |
dc.description.abstract |
Organotypic cultures (OCs) have been widely used to investigate the midbrain dopaminergic system, but only a few studies focused on the functional properties of dopaminergic neurons and their synaptic inputs from dopaminergic and non-dopaminergic neurons also contained in such cultures. In addition, it is not clear whether the culturing process affects the intrinsic neuronal properties and the expression of specific receptors and transporters. We performed patch-clamp recordings from dopaminergic neurons in mesencephalic–striatal co-cultures obtained from transgenic mice expressing green fluorescent protein (GFP) under the tyrosine hydroxylase promoter. Some (10 ⁄ 44) GFP+ neurons displayed a bursting activity that renders the firing of these cells similar to that of the dopaminergic neurons in vivo. The culturing process reduced the hyperpolarization-activated current (Ih) and the expression of D2 receptors. Downregulation of D2 receptor mRNA and protein was confirmed with reverse transcriptase polymerase chain reaction and Western blotting. Immunocytochemistry revealed that many synaptic terminals, most likely originating from dopaminergic neurons, co-expressed the dopamine (DA) transporter and the vesicular glutamate transporter-2, suggesting a co-release of DA and glutamate. Interestingly, exogenous DA decreased glutamate release in young cultures [days in vitro (DIV) < 20] by acting on pre-synaptic D2 receptors, while in older cultures (DIV > 26) DA increased glutamate release by acting on a-1 adrenoreceptors. The facilitatory effect of DA on glutamatergic transmission to midbrain dopaminergic neurons may be important in conditions when the expression of D2 receptors is compromised, such as long-term treatment with antipsychotic drugs. Our data show that midbrain OCs at DIV > 26 may provide a suitable model of such conditions. |
en |
dc.publisher |
Federation of European Neuroscience Societies and Blackwell Publishing Ltd |
en |
dc.relation.ispartofseries |
European Journal of Neuroscience |
en |
dc.rights |
Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. Previously published items are made available in accordance with the copyright policy of the publisher. Details have been obtained from http://www.sherpa.ac.uk/romeo/issn/0953-816X/ |
en |
dc.rights.uri |
https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm |
en |
dc.source.uri |
http://dx.doi.org/10.1111/j.1460-9568.2011.07659.x |
en |
dc.title |
Properties of dopaminergic neurons in organotypic mesencephalic-striatal co-cultures - evidence for a facilitatory effect of dopamine on the glutamatergic input mediated by α-1 adrenergic receptors |
en |
dc.type |
Journal Article |
en |
dc.identifier.doi |
10.1111/j.1460-9568.2011.07659.x |
en |
pubs.issue |
9 |
en |
pubs.begin-page |
1622 |
en |
pubs.volume |
33 |
en |
dc.rights.holder |
Copyright: Federation of European Neuroscience Societies and Blackwell Publishing Ltd |
en |
pubs.end-page |
1636 |
en |
dc.rights.accessrights |
http://purl.org/eprint/accessRights/RestrictedAccess |
en |
pubs.elements-id |
210567 |
en |
pubs.org-id |
Faculty of Medical & Hlth Sci |
en |
pubs.org-id |
Medical Sciences |
en |
pubs.org-id |
Physiology Division |
en |