Mechanisms of adenosine 5?-triphosphate-induced dopamine release in the rat nucleus accumbens in vivo

Involvement of P2X7 receptors in the regulation of neurotransmitter release in the rat hippocampus

“…7b), and BzATP was more potent than ATP, consistent with P2X 7 R activation. This finding is in agreement with recent findings of Krugel et al . (2001) who found that ATP stimulates glutamate and subsequent GABA release from the rat nucleus accumbens in vivo .…”

“…7b), and BzATP was more potent than ATP, consistent with P2X 7 R activation. This finding is in agreement with recent findings of Krugel et al (2001) who found that ATP stimulates glutamate and subsequent GABA release from the rat nucleus accumbens in vivo. It should be noted, however, that apart from [ 3 H]GABA efflux, which represents predominantly neuronal GABA release, [ 14 C]glutamate efflux could be equally derived from neuronal and non-neuronal cells, e.g.…”

Involvement of P2X7 receptors in the regulation of neurotransmitter release in the rat hippocampus

“…7b), and BzATP was more potent than ATP, consistent with P2X 7 R activation. This finding is in agreement with recent findings of Krugel et al . (2001) who found that ATP stimulates glutamate and subsequent GABA release from the rat nucleus accumbens in vivo .…”

“…7b), and BzATP was more potent than ATP, consistent with P2X 7 R activation. This finding is in agreement with recent findings of Krugel et al (2001) who found that ATP stimulates glutamate and subsequent GABA release from the rat nucleus accumbens in vivo. It should be noted, however, that apart from [ 3 H]GABA efflux, which represents predominantly neuronal GABA release, [ 14 C]glutamate efflux could be equally derived from neuronal and non-neuronal cells, e.g.…”

Purinergic modulation of extracellular glutamate levels in the nucleus accumbens in vivo

“…The presented data corroborate the previous suggestion, based on the measurement of dopamine release in the NAc and the use of various antagonists of ionotropic and metabotropic glutamate receptors, that ATP may enhance the glutamate outflow in the NAc in vivo (Krugel et al, 2001a). Electrophysiological investigations also proved a P2 receptor‐mediated release of excitatory amino acids from cultured Schwann cells (Jeftinija and Jeftinija, 1998) and trigeminal mesencephalic nerve terminals in the brain stem (Khakh and Henderson, 1998) as well as spinal cord slice preparations (Nakatsuka and Gu, 2001).…”

Modulation of feeding behaviour by blocking purinergic receptors in the rat nucleus accumbens: a combined microdialysis, electroencephalographic and behavioural study

“…Effects mediated by adenosine in the NAc probably also involve an A 2A receptor‐induced glutamate release and the subsequent activation of GABAergic projection neurons which may also generate the inhibitory input to the VTA. Glutamate and NMDA applied to the NAc at lower concentrations, similar to those occurring under physiological conditions, were shown to decrease the DA release dependent on GABA A receptor stimulation in the VTA (Krügel et al. , 2001b).…”

“…Ã P < 0.05 in comparison with the baseline activity. NAc at lower concentrations, similar to those occurring under physiological conditions, were shown to decrease the DA release dependent on GABA A receptor stimulation in the VTA (Kru Ègel et al, 2001b). Furthermore, it has been demonstrated that activation of the GABA receptors in the VTA diminished the DA release in the NAc (Westerink et al, 1996).…”

Involvement of P2X7 receptors in the regulation of neurotransmitter release in the rat hippocampus

“…7b), and BzATP was more potent than ATP, consistent with P2X 7 R activation. This finding is in agreement with recent findings of Krugel et al . (2001) who found that ATP stimulates glutamate and subsequent GABA release from the rat nucleus accumbens in vivo .…”

“…7b), and BzATP was more potent than ATP, consistent with P2X 7 R activation. This finding is in agreement with recent findings of Krugel et al (2001) who found that ATP stimulates glutamate and subsequent GABA release from the rat nucleus accumbens in vivo. It should be noted, however, that apart from [ 3 H]GABA efflux, which represents predominantly neuronal GABA release, [ 14 C]glutamate efflux could be equally derived from neuronal and non-neuronal cells, e.g.…”

Purinergic modulation of extracellular glutamate levels in the nucleus accumbens in vivo

“…The presented data corroborate the previous suggestion, based on the measurement of dopamine release in the NAc and the use of various antagonists of ionotropic and metabotropic glutamate receptors, that ATP may enhance the glutamate outflow in the NAc in vivo (Krugel et al, 2001a). Electrophysiological investigations also proved a P2 receptor‐mediated release of excitatory amino acids from cultured Schwann cells (Jeftinija and Jeftinija, 1998) and trigeminal mesencephalic nerve terminals in the brain stem (Khakh and Henderson, 1998) as well as spinal cord slice preparations (Nakatsuka and Gu, 2001).…”

Modulation of feeding behaviour by blocking purinergic receptors in the rat nucleus accumbens: a combined microdialysis, electroencephalographic and behavioural study

“…Effects mediated by adenosine in the NAc probably also involve an A 2A receptor‐induced glutamate release and the subsequent activation of GABAergic projection neurons which may also generate the inhibitory input to the VTA. Glutamate and NMDA applied to the NAc at lower concentrations, similar to those occurring under physiological conditions, were shown to decrease the DA release dependent on GABA A receptor stimulation in the VTA (Krügel et al. , 2001b).…”

“…Ã P < 0.05 in comparison with the baseline activity. NAc at lower concentrations, similar to those occurring under physiological conditions, were shown to decrease the DA release dependent on GABA A receptor stimulation in the VTA (Kru Ègel et al, 2001b). Furthermore, it has been demonstrated that activation of the GABA receptors in the VTA diminished the DA release in the NAc (Westerink et al, 1996).…”

Involvement of P2X7 receptors in the regulation of neurotransmitter release in the rat hippocampus

“…7b), and BzATP was more potent than ATP, consistent with P2X 7 R activation. This finding is in agreement with recent findings of Krugel et al . (2001) who found that ATP stimulates glutamate and subsequent GABA release from the rat nucleus accumbens in vivo .…”

“…7b), and BzATP was more potent than ATP, consistent with P2X 7 R activation. This finding is in agreement with recent findings of Krugel et al (2001) who found that ATP stimulates glutamate and subsequent GABA release from the rat nucleus accumbens in vivo. It should be noted, however, that apart from [ 3 H]GABA efflux, which represents predominantly neuronal GABA release, [ 14 C]glutamate efflux could be equally derived from neuronal and non-neuronal cells, e.g.…”

Purinergic modulation of extracellular glutamate levels in the nucleus accumbens in vivo

“…The presented data corroborate the previous suggestion, based on the measurement of dopamine release in the NAc and the use of various antagonists of ionotropic and metabotropic glutamate receptors, that ATP may enhance the glutamate outflow in the NAc in vivo (Krugel et al, 2001a). Electrophysiological investigations also proved a P2 receptor‐mediated release of excitatory amino acids from cultured Schwann cells (Jeftinija and Jeftinija, 1998) and trigeminal mesencephalic nerve terminals in the brain stem (Khakh and Henderson, 1998) as well as spinal cord slice preparations (Nakatsuka and Gu, 2001).…”

Modulation of feeding behaviour by blocking purinergic receptors in the rat nucleus accumbens: a combined microdialysis, electroencephalographic and behavioural study

“…Effects mediated by adenosine in the NAc probably also involve an A 2A receptor‐induced glutamate release and the subsequent activation of GABAergic projection neurons which may also generate the inhibitory input to the VTA. Glutamate and NMDA applied to the NAc at lower concentrations, similar to those occurring under physiological conditions, were shown to decrease the DA release dependent on GABA A receptor stimulation in the VTA (Krügel et al. , 2001b).…”

“…Ã P < 0.05 in comparison with the baseline activity. NAc at lower concentrations, similar to those occurring under physiological conditions, were shown to decrease the DA release dependent on GABA A receptor stimulation in the VTA (Kru Ègel et al, 2001b). Furthermore, it has been demonstrated that activation of the GABA receptors in the VTA diminished the DA release in the NAc (Westerink et al, 1996).…”