Environmental and intraperitoneal ethanol influences morphine antinociceptive effect in mice

Peris, Laura Climent; Peiró, Ana M.; Zapater, Pedro; Parte, José Francisco Horga de la

doi:10.1016/j.lfs.2004.10.077

Cited by 3 publications

(1 citation statement)

References 27 publications

(34 reference statements)

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“…Animal studies have shown that acute alcohol exposure can induce locomotor stimulation (Humeniuk, White, & Ong, 1993; Koob, 1992; Kornetsky, Bain, Unterwald, & Lewis, 1988) and is also anxiolytic (Morales-Mulia et al, 2012; Sharko, Kaigler, Fadel, & Wilson, 2013). Alcohol exposure also modifies pain perception and the anti-nociceptive effects of opiates (Peris, Peiro, Hernandez, & de la Parte, 2005). Chronic alcohol exposure produces very different behavioral effects during withdrawal.…”

Section: Introductionmentioning

confidence: 99%

Alcohol effects on synaptic transmission in periaqueductal gray dopamine neurons

McCall

López

et al. 2013

Alcohol

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The role of dopamine (DA) signaling in regulating the rewarding properties of drugs, including alcohol, has been widely studied. The majority of these studies, however, have focused on the DA neurons located in the ventral tegmental area (VTA), and their projections to the nucleus accumbens. DA neurons within the ventral periaqueductal gray (vPAG) have been shown to regulate reward but little is known about the functional properties of these neurons, or how they are modified by drugs of abuse. This lack of knowledge is likely due to the highly heterogeneous cell composition of the vPAG, with both γ-amino-butyric acid (GABA) and glutamate neurons present in addition to DA neurons. In this study, we performed whole-cell recordings in a TH–eGFP transgenic mouse line to evaluate the properties of vPAG-DA neurons. Following this initial characterization, we examined how both acute and chronic alcohol exposure modify synaptic transmission onto vPAG-DA neurons. We found minimal effects of acute alcohol exposure on GABA transmission, but a robust enhancement of glutamatergic synaptic transmission in vPAG-DA. Consistent with this effect on excitatory transmission, we also found that alcohol caused an increase in firing rate. These data were in contrast to the effects of chronic intermittent alcohol exposure, which had no significant impact on either inhibitory or excitatory synaptic transmission on the vPAG-DA neurons. These data add to a growing body of literature that points to alcohol having both region-dependent and cell-type dependent effects on function.

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