Characterization of activity-dependent changes in flavoprotein fluorescence in cerebellar slices from juvenile rats. (1st January 2015)

• Record Type: Journal Article
• Authors: Jotty, Karick; Shuttleworth, C. William; Valenzuela, C. Fernando
• Is Part Of: Neuroscience letters. Volume 584(2015)
• Page Start: 17
• Page End: 22
• Publication Date: 2015-01-01
• Subjects: Cerebellum -- Purkinje neurons -- Mitochondria -- Flavoproteins -- Intrinsic imaging -- Ethanol; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2014.09.052
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: We characterized flavoprotein autofluorescence responses in rat cerebellar slices. Molecular layer stimulation initially increased fluorescence, which then decreased. Responses were abolished by Na + channel or AMPA receptor antagonists. Neither a GABAA receptor antagonist nor ethanol affected the responses. This technique could be used to study cerebellar effects of pharmacological agents. Abstract: Flavoprotein autofluorescence signals attributed to neuronal metabolism have been used to assess synaptic function. Here, we characterized flavoprotein autofluorescence responses in the molecular layer of rat cerebellar slices. High frequency stimulation elicited a transient fluorescence increase (peak phase) that was followed by a longer-lasting fluorescence decrease (valley phase). The peak phase was restricted to the molecular layer, whereas the valley phase extended into the Purkinje cell layer and a portion of the granule cell layer. Responses were abolished by either the Na + channel antagonist, tetrodotoxin, or a combination of the AMPA receptor antagonists, NBQX and GIKI-53655, and were also reduced by a flavoprotein inhibitor (diphenyleneiodonium). These findings are consistent with responses being mediated by an increase in mitochondrial activity triggered by increased energy demands evoked by AMPA receptor-mediated synaptic transmission. The GABAA receptor antagonist picrotoxin did not significantly influence evoked responses. Likewise, exogenous application of ethanol, at concentrations known to increase GABAA receptor-mediated synaptic transmission at Purkinje cells, did not modify peak responses. These observations indicate that flavoprotein autofluorescence imaging could be useful to assess the coupling between glutamatergic synaptic transmission and neuronal metabolism in cerebellar slices.