Molecular Tolerance of Voltage‐Gated Calcium Channels is Evident After Short Exposures to Alcohol in Vasopressin‐Releasing Nerve Terminals

Abstract

These data indicate that a brief alcohol exposure affects subsequent alcohol sensitivity of VGCCs and neuropeptide release from presynaptic terminals.

Further characterization of the effect of ethanol on voltage-gated Ca2+ channel function in developing CA3 hippocampal pyramidal neurons

“…Therefore, it is possible that voltage-gated Ca 2+ channel function is inhibited while ethanol is present and fully recovers during withdrawal. Indeed, rapid development of tolerance of L-type voltage-gated Ca 2+ channels to ethanol has been documented in neurohypophysial terminals (Pietrzykowski et al, 2013). Moreover, the pups were older at the time of slice collection in the present study (P6-8 and 13-15) vs. our previous study (P4-6), suggesting that the effect of ethanol on voltage-gated Ca 2+ channels is age-dependent.…”

P/Q-type voltage-gated calcium channels mediate the ethanol and CRF sensitivity of central amygdala GABAergic synapses

“…Previous studies have implicated voltage-gated calcium channels in several alcohol-related behaviors, including alcohol consumption and withdrawal syndrome (Newton et al, 2004; Varodayan et al, 2017b; Walter and Messing, 1999; Watson and Little, 2002). Multiple groups have also reported that alcohol both inhibits (Belia et al, 1995; Maldve et al, 2004; Mullikin-Kilpatrick and Treistman, 1993; Pietrzykowski et al, 2013; Xiao et al, 2005; Zucca and Valenzuela, 2010) and enhances (Belia et al, 1995; Pietrzykowski et al, 2013; Simasko et al, 1999) voltage-gated calcium channel activity, and alcohol’s actions on voltage-gated calcium channels regulate GABA release in several brain regions (Hirono et al, 2009; Varodayan et al, 2017b; Zucca and Valenzuela, 2010). Similarly, the CRF system can inhibit (Tao et al, 2008, 2009, 2006) or enhance (Yu and Shinnick-Gallagher, 1998) voltage-gated calcium channel activity to modulate CeA synaptic transmission (Krishnan et al, 2010; Pollandt et al, 2006).…”

Molecular Mechanisms Underlying the Development of Functional and Behavioral Tolerance to Alcohol

“…Reprinted with permission (Pietrzykowski et al, 2013). In particular, scaffolding ance in BK and voltage-gated calcium channels.…”

“…A recent study from our laboratory has examined acute tolerance to alcohol in voltage-gated calcium channels (VGCCs) recorded in rat neurohypophysial terminals (i.e., within the posterior pituitary), allowing comparison with previous results obtained in this preparation for BK channels (Pietrzykowski et al, 2004;Pietrzykowski et al, 2013). Thus it was possible to compare the temporal characteristics of molecular tolerance for two different channel proteins within the same cellular membrane (although possibly different microdomains within that membrane).…”

“…Previously published work had shown that voltage-gated calcium channels (VGCCs) in neurohypophysial terminals, which are inhibited by acute ethanol, exhibit molecular tolerance to alcohol, including desensitization to the drug and increased current density (in contrast to the decreased density seen in BK channels, which are potentiated by acute exposure), after three weeks of alcohol drinking (Knott, Dopico, Dayanithi, Lemos, & Treistman, 2002). In the latest publication on the topic, technical advances improved temporal resolution of alcohol exposure from weeks to minutes (Pietrzykowski et al, 2013). Indeed, after three weeks, terminals from drinking rats exhibit diminished alcohol inhibition of vasopressin (AVP) release (Knott et al, 2002).…”