Co-release of acetylcholine and gamma-aminobutyric acid by a retinal neuron.

O’Malley, Donald M.; Masland, Richard H.

doi:10.1073/pnas.86.9.3414

Cited by 133 publications

(88 citation statements)

References 34 publications

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“…GABAergic amacrine cells generally have wider dendritic fields than those of glycinergic cells and they comprise ~40% of all amacrine cells in the mouse retina (Marquardt et al, 2001;Pourcho and Goebel, 1983;Vaney, 1990). Many GABAergic amacrine cells contain other neurotransmitters such as acetylcholine and dopamine in addition to GABA (Vaney, 1990;Wassle and Boycott, 1991), as exemplified by the direction-selective starburst amacrine cells which are not only GABAergic but cholinergic as well (Brecha et al, 1988;Fried et al, 2002;Kosaka et al, 1988;O'Malley and Masland, 1989;O'Malley et al, 1992;Vaney and Young, 1988).…”

Section: Introductionmentioning

confidence: 99%

Role of theBarhl2homeobox gene in the specification of glycinergic amacrine cells

Yang

et al. 2004

Development

115

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The mammalian retina contains numerous morphological and physiological subtypes of amacrine cells necessary for integrating and modulating visual signals presented to the output neurons. Among subtypes of amacrine cells grouped by neurotransmitter phenotypes, the glycinergic andγ-aminobutyric acid (GABA)ergic amacrine cells constitute two major subpopulations. To date, the molecular mechanisms governing the specification of subtype identity of amacrine cells remain elusive. We report here that during mouse development, the Barhl2 homeobox gene displays an expression pattern in the nervous system that is distinct from that of its homologue Barhl1. In the developing retina, Barhl2expression is found in postmitotic amacrine, horizontal and ganglion cells,while Barhl1 expression is absent. Forced expression of Barhl2 in retinal progenitors promotes the differentiation of glycinergic amacrine cells, whereas a dominant-negative form of Barhl2 has the opposite effect. By contrast, they exert no effect on the formation of GABAergic neurons. Moreover, misexpressed Barhl2 inhibits the formation of bipolar and Müller glial cells, indicating that Barhl2 is able to function both as a positive and negative regulator, depending on different types of cells. Taken together, our data suggest that Barhl2 may function to specify the identity of glycinergic amacrine cells from competent progenitors during retinogenesis.

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Section: Introductionmentioning

confidence: 99%

Role of theBarhl2homeobox gene in the specification of glycinergic amacrine cells

Yang

et al. 2004

Development

115

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“…Type b cells have perikarya displaced to the ganglion cell layer, processes ramifying in stratum 4 (S4) of the IPL and ON responses to light (Famiglietti, 1983;Tauchi and Masland, 1984;Vaney, 1984;Bloomfield and Miller, 1986). In rabbits, starburst amacrine cells are known to receive synaptic inputs from cone (Brandon, 1987;Millar and Morgan, 1987;Famiglietti, 1991).Starburst amacrine cells synthesize and release both γ-aminobutyric acid (GABA) and acetylcholine (ACh) when depolarized (Masland and Livingstone, 1976;Massey and Neal, 1979;O'Malley and Masland, 1989). ACh release from the rabbit retina increases at both light onset and light offset and is maximally stimulated by large stimuli at temporal frequencies of 1-4 Hz (Massey and Neal, 1979;Massey and Redburn, 1985;O'Malley and Masland, 1993).…”

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confidence: 99%

“…Starburst amacrine cells synthesize and release both γ-aminobutyric acid (GABA) and acetylcholine (ACh) when depolarized (Masland and Livingstone, 1976;Massey and Neal, 1979;O'Malley and Masland, 1989). ACh release from the rabbit retina increases at both light onset and light offset and is maximally stimulated by large stimuli at temporal frequencies of 1-4 Hz (Massey and Neal, 1979;Massey and Redburn, 1985;O'Malley and Masland, 1993).…”

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confidence: 99%

AMPA receptors mediate acetylcholine release from starburst amacrine cells in the rabbit retina

Firth

Massey

et al. 2003

J of Comparative Neurology

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The light response of starburst amacrine cells is initiated by glutamate released from bipolar cells. To identify the receptors that mediate this response, we used a combination of anatomical and physiological techniques. An in vivo, rabbit eyecup was preloaded with [ 3 H]-choline, and the [ 3 H]-acetylcholine (ACh) released into the superfusate was monitored. A photopic, 3 Hz flashing light increased ACh release, and the selective AMPA receptor antagonist, GYKI 53655, blocked this light-evoked response. Nonselective AMPA/kainate agonists increased the release of ACh, but the specific kainate receptor agonist, SYM 2081, did not increase ACh release. Selective AMPA receptor antagonists, GYKI 53655 or GYKI 52466, also blocked the responses to agonists. We conclude that the predominant excitatory input to starburst amacrine cells is mediated by AMPA receptors. We also labeled lightly fixed rabbit retinas with antisera to choline acetyltransferase (ChAT), AMPA receptor subunits GluR1, GluR2/3, or GluR4, and kainate receptor subunits GluR6/7 and KA2. Labeled puncta were observed in the inner plexiform layer with each of these antisera to glutamate receptors, but only GluR2/3-IR puncta and GluR4-IR puncta were found on the ChAT-IR processes. The same was true of starburst cells injected intracellularly with Neurobiotin, and these AMPA receptor subunits were localized to two populations of puncta. The AMPA receptors are expected to desensitize rapidly, enhancing the sensitivity of starburst amacrine cells to moving or other rapidly changing stimuli. Indexing termsglutamate; ionotropic receptors; localization; cholinergic; interneuron; confocal microscopy Starburst amacrine cells are one of the most common types of amacrine cells in rabbit retina (MacNeil et al., 1999), and there are two subtypes. Type a cells have perikarya in the inner nuclear layer, processes ramifying in the outer half of the inner plexiform layer (IPL) in stratum 2 (S2) and OFF responses to light. Type b cells have perikarya displaced to the ganglion cell layer, processes ramifying in stratum 4 (S4) of the IPL and ON responses to light (Famiglietti, 1983;Tauchi and Masland, 1984;Vaney, 1984;Bloomfield and Miller, 1986). In rabbits, starburst amacrine cells are known to receive synaptic inputs from cone (Brandon, 1987;Millar and Morgan, 1987;Famiglietti, 1991).Starburst amacrine cells synthesize and release both γ-aminobutyric acid (GABA) and acetylcholine (ACh) when depolarized (Masland and Livingstone, 1976;Massey and Neal, 1979;O'Malley and Masland, 1989). ACh release from the rabbit retina increases at both light onset and light offset and is maximally stimulated by large stimuli at temporal frequencies of 1-4 Hz (Massey and Neal, 1979;Massey and Redburn, 1985;O'Malley and Masland, 1993). The majority of the synaptic output from the starburst cells is onto ganglion cell dendrites (Brandon, 1987;Millar and Morgan, 1987;Famiglietti, 1991 . The agonist α-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) is more potent than kainate or...

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“…Neurons signal using more than one chemical transmission mechanism, including co-transmission of different classes of neurotransmitter from distinct vesicles or co-release from the same vesicle [178][179][180][181][182][183]. This has long been recognized [181,184], but modern techniques provide excellent tools to detect co-transmission/release while mapping it onto defined neurons.…”

Section: Questions Limitations and Future Directionsmentioning

confidence: 99%

“…This has long been recognized [181,184], but modern techniques provide excellent tools to detect co-transmission/release while mapping it onto defined neurons. As described above, we now know that some dopamine neurons also transmit glutamate [105,185], as well as GABA [108], even through non-canonical mechanisms [106,186], including co-release [106].…”

Section: Questions Limitations and Future Directionsmentioning

confidence: 99%

Contemporary approaches to neural circuit manipulation and mapping: focus on reward and addiction

Saunders

Janak

2015

Phil. Trans. R. Soc. B

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One contribution of 15 to a theme issue 'Controlling brain activity to alter perception, behaviour and society'. Tying complex psychological processes to precisely defined neural circuits is a major goal of systems and behavioural neuroscience. This is critical for understanding adaptive behaviour, and also how neural systems are altered in states of psychopathology, such as addiction. Efforts to relate psychological processes relevant to addiction to activity within defined neural circuits have been complicated by neural heterogeneity. Recent advances in technology allow for manipulation and mapping of genetically and anatomically defined neurons, which when used in concert with sophisticated behavioural models, have the potential to provide great insight into neural circuit bases of behaviour. Here we discuss contemporary approaches for understanding reward and addiction, with a focus on midbrain dopamine and cortico-striato-pallidal circuits.

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Co-release of acetylcholine and gamma-aminobutyric acid by a retinal neuron.

Cited by 133 publications

References 34 publications

Role of theBarhl2homeobox gene in the specification of glycinergic amacrine cells

Role of theBarhl2homeobox gene in the specification of glycinergic amacrine cells

AMPA receptors mediate acetylcholine release from starburst amacrine cells in the rabbit retina

Contemporary approaches to neural circuit manipulation and mapping: focus on reward and addiction

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