@article{MTMT:1482495,
	title = {The Role of Extracellular Adenosine in Chemical Neurotransmission in the Hippocampus and Basal Ganglia: Pharmacological and Clinical Aspects.},
	url = {https://m2.mtmt.hu/api/publication/1482495},
	author = {Sperlágh, Beáta and Vizi, E. Szilveszter},
	doi = {10.2174/156802611795347564},
	journal-iso = {CURR TOP MED CHEM},
	journal = {CURRENT TOPICS IN MEDICINAL CHEMISTRY},
	volume = {11},
	unique-id = {1482495},
	issn = {1568-0266},
	abstract = {Now there is general agreement that the purine nucleoside adenosine is an important neuromodulator in the central nervous system, playing a crucial role in neuronal excitability and synaptic/non-synaptic transmission in the hippocampus and basal ganglia. Adenosine is derived from the breakdown of extra- or intracellular ATP and is released upon a variety of physiological and pathological stimuli from neuronal and non-neuronal sources, i.e. from glial cells and exerts effects diffusing far away from release sites. The resultant elevation of adenosine levels in the extracellular space reaches micromolar level, and leads to the activation A(1), A(2A), A(2B) and A(3) receptors, localized to pre- and postsynaptic as well as extrasynaptic sites. Activation of presynaptic A(1) receptors inhibits the release of the majority of transmitters including glutamate, acetylcholine, noradrenaline, 5-HT and dopamine, whilst the stimulation of A(2A) receptors facilitates the release of glutamate and acetylcholine and inhibits the release of GABA. These actions underlie modulation of neuronal excitability, synaptic plasticity and coordination of neural networks and provide intriguing target sites for pharmacological intervention in ischemia and Parkinson's disease. However, despite that adenosine is also released during ischemia, A(1) adenosine receptors do not participate in the modulation of excitotoxic glutamate release, which is nonsynaptic and is due to the reverse operation of transporters. Instead, extrasynaptic A(1) receptors might be responsible for the neuroprotection afforded by A(1) receptor activation.},
	year = {2011},
	eissn = {1873-4294},
	pages = {1034-1046},
	orcid-numbers = {Vizi, E. Szilveszter/0000-0002-9557-4597}
}

@article{MTMT:1228647,
	title = {Ecto-nucleoside triphosphate diphosphohydrolase 3 in the ventral and lateral hypothalamic area of female rats: morphological characterization and functional implications},
	url = {https://m2.mtmt.hu/api/publication/1228647},
	author = {Kiss, Dávid Sándor and Zsarnovszky, Attila and Horvath, Krisztina and Győrffy, Andrea and Bartha, Tibor and Novák-Hazai, Diana and Sótonyi, Péter and Somogyi, Virág and Frenyó V., László and Diano, Sabrina},
	doi = {10.1186/1477-7827-7-31},
	journal-iso = {REPROD BIOL ENDOCRIN},
	journal = {REPRODUCTIVE BIOLOGY AND ENDOCRINOLOGY},
	volume = {7},
	unique-id = {1228647},
	issn = {1477-7827},
	abstract = {Abstract 
		 
		Background: Based on its distribution in the brain, ecto-nucleoside triphosphate 
		diphosphohydrolase 3 (NTPDase3) may play a role in the hypothalamic regulation of 
		homeostatic systems, including feeding, sleep-wake behavior and reproduction. To further 
		characterize the morphological attributes of NTPDase3-immunoreactive (IR) hypothalamic 
		structures in the rat brain, here we investigated: 1.) The cellular and subcellular localization of 
		NTPDase3; 2.) The effects of 17-estradiol on the expression level of hypothalamic 
		NTPDase3; and 3.) The effects of NTPDase inhibition in hypothalamic synaptosomal 
		preparations. 
		Methods: Combined light- and electron microscopic analyses were carried out to characterize 
		the cellular and subcellular localization of NTPDase3-immunoreactivity. The effects of 
		estrogen on hypothalamic NTPDase3 expression was studied by western blot technique. 
		Finally, the effects of NTPDase inhibition on mitochondrial respiration were investigated 
		using a Clark-type oxygen electrode. 
		Results: Combined light- and electron microscopic analysis of immunostained hypothalamic 
		slices revealed that NTPDase3-IR is linked to ribosomes and mitochondria, is predominantly 
		present in excitatory axon terminals and in distinct segments of the perikaryal plasma 
		membrane. Immunohistochemical labeling of NTPDase3 and glutamic acid decarboxylase 
		(GAD) indicated that -amino-butyric-acid- (GABA) ergic hypothalamic neurons do not 
		express NTPDase3, further suggesting that in the hypothalamus, NTPDase3 is predominantly 
		present in excitatory neurons. We also investigated whether estrogen influences the expression 
		level of NTPDase3 in the ventrobasal and lateral hypothalamus. A single subcutaneous 
		injection of estrogen differentially increased NTPDase3 expression in the medial and lateral 
		parts of the hypothalamus, indicating that this enzyme likely plays region-specific roles in 
		estrogen-dependent hypothalamic regulatory mechanisms. Determination of mitochondrial 
		respiration rates with and without the inhibition of NTPDases confirmed the presence of 
		NTPDases, including NTPDase3 in neuronal mitochondria and showed that blockade of 
		mitochondrial NTPDase functions decreases state 3 mitochondrial respiration rate and total 
		mitochondrial respiratory capacity. 
		Conclusions: Altogether, these results suggest the possibility that NTPDases, among them 
		NTPDase3, may play an estrogen-dependent modulatory role in the regulation of intracellular 
		availability of ATP needed for excitatory neuronal functions including neurotransmission.},
	year = {2009},
	eissn = {1477-7827},
	orcid-numbers = {Győrffy, Andrea/0000-0001-7110-1464}
}