http://www.cnr.it/ontology/cnr/individuo/prodotto/ID37758
Cannabinoids modulate neuronal firing in the rat basolateral amygdala: evidence for CB1- and non-CB1-mediated actions. (Articolo in rivista)
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- Cannabinoids modulate neuronal firing in the rat basolateral amygdala: evidence for CB1- and non-CB1-mediated actions. (Articolo in rivista) (literal)
- Anno
- 2004-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1016/j.neuropharm.2003.08.003 (literal)
- Alternative label
Marco Pistis (1,3); Simona Perra (1,3); Giuliano Pillolla (1,3); Miriam Melis (1,3);
Gian Luigi Gessa (1,3); Anna Lisa Muntoni (2,3) (2004)
Cannabinoids modulate neuronal firing in the rat basolateral amygdala: evidence for CB1- and non-CB1-mediated actions.
in Neuropharmacology
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- Marco Pistis (1,3); Simona Perra (1,3); Giuliano Pillolla (1,3); Miriam Melis (1,3);
Gian Luigi Gessa (1,3); Anna Lisa Muntoni (2,3) (literal)
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- (1) B.B. Brodie Department of Neuroscience, University of Cagliari, Monserrato, Italy;
(2) CNR Institute of Neuroscience-Section of Cagliari, University of Cagliari, Monserrato, Italy;
(3) Center of Excellence \"Neurobiology of Addiction\", University of Cagliari, Italy (literal)
- Titolo
- Cannabinoids modulate neuronal firing in the rat basolateral amygdala: evidence for CB1- and non-CB1-mediated actions. (literal)
- Abstract
- Recent evidence indicates that the basolateral amygdala (BLA) may be involved in behavioural effects induced by cannabinoids.
High levels of CB1 cannabinoid receptors have been shown in this region, where they modulate excitatory and inhibitory synaptic
transmission. However, the neurophysiological effects of these opposing synaptic actions have not been investigated in vivo. To
this purpose, single-unit extracellular recordings were performed in urethane anaesthetized rats in order to determine whether exogenously
applied cannabinoids influenced the spontaneous or evoked electrical activity of neurons in the BLA. The effects of cannabinoids
were found to be dependent on the characteristics of the neurons examined and on the properties of the agents used. We
tested and compared two structurally different synthetic cannabinoid receptor agonists, the highly potent HU-210 (0.125-1.0 mg/kg,
i.v.) and WIN55212-2 (WIN, 0.125-1.0 mg/kg, i.v.). With a CB1 cannabinoid receptor-dependent mechanism, HU-210 potently
inhibited the firing rate of BLA interneurons whereas WIN modulated the discharge rate in a biphasic manner. By contrast, BLA
projection neurons, antidromically identified from the shell of the nucleus accumbens, were significantly inhibited by WIN at all
doses tested, while HU-210 administration led to less consistent effects, since only 1.0 mg/kg inhibited firing rate in the majority
of recorded neurons. Additionally, WIN, but not HU-210, significantly attenuated short-latency spiking activity in BLA projection
neurons evoked by electrical stimulation of the medial prefrontal cortex. In these neurons, WIN-induced effects were antagonised
by the non-selective cannabinoid receptor antagonist SR141716A and by the vanilloid receptor antagonist capsazepine, but not by
the selective CB1 antagonist AM-251. Taken together, our findings indicate that the overall excitability of efferent neurons in the
BLA is strongly reduced by WIN in a non-CB1-dependent manner. In this effect, the contribution of a novel cannabinoid-vanilloid-sensitive
putative non-CB1 receptors, the existence of which was postulated in recent reports, might play a role. (literal)
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