Activation of nicotinic acetylcholine receptors induces long‐term potentiation in vivo in the intact mouse dentate gyrus

Abstract

The present study was conducted to clarify the role of nicotinic ACh receptors (nAChRs) on long-term potentiation (LTP) in vivo in the intact mouse dentate gyrus using extracellular recording techniques. Intraperitoneal application of nicotine at a dose of 3.0 mg/kg but not 0.03 or 0.3 mg/kg produced a gradually developing, long-lasting increase for 120 min similar to tetanic LTP. Nicotine at a dose of 9. 0 mg/kg caused a temporary increase followed by depression. The long-lasting potentiation induced by nicotine at 3.0 mg/kg, which was named nicotinic long-term potentiation (LTPn), and tetanic LTP were significantly suppressed by pretreatment with mecamylamine (0.5 mg/kg i.p.), a nonselective nicotinic antagonist, but not affected by postapplication of mecamylamine. Interestingly, choline, a selective alpha7 nAChR agonist, at 3.0-90 mg/kg, induced the long-lasting potentiation similar to LTPn in a dose-dependent manner in vivo in the intact mouse dentate gyrus. The long-lasting potentiation induced by choline (30 mg/kg i.p.) was additionally increased by postapplication of nicotine (3.0 mg/kg i.p.) or tetanic stimulation. The present study revealed that systemic application of nicotine or choline induced the long-lasting potentiation in vivo in the intact mouse dentate gyrus, suggesting that alpha7 nAChRs may contribute to the induction of LTP by nicotine, and supporting in vivo animal studies that nicotine improves learning and memory performance.

Epibatidine Induces Long-Term Potentiation (LTP) via Activation of α4β2 Nicotinic Acetylcholine Receptors (nAChRs) In Vivo in the Intact Mouse Dentate Gyrus: Both α7 and α4β2 nAChRs Essential to Nicotinic LTP

“…Indeed, activation of a 7 nAChRs facilitates LTP induction in the rat hippocampus (21) and produces LTP induction in the rat midbrain (22). We also showed that intraperitoneal application of choline, a selective a7 nAChR agonist, induced smaller LTPn in the mouse dentate gyrus (7). However, there is no evidence about the involvement of a 4b2 nAChRs, which are the most abundant subtype of nAChRs in the brain, in LTP.…”

“…We used mecamylamine at a dose of 0.5 mg / kg as a non-selective nAChRs antagonist as shown in our previous report (7). Mecamylamine and epibatidine were applied to examine how the a 4b2 nAChRs are involved in LTPn in vivo in the intact mouse dentate gyrus.…”

“…Indeed, nicotine facilitates LTP induction in hippocampal slice preparations (6). Moreover, we showed that intraperitoneal application of nicotine caused a long-lasting potentiation, which was named nicotinic LTP (LTPn), in vivo in the intact mouse dentate gyrus (7), suggesting that the intact preparation is especially relevant because all of the normal neural connections of the hippocampal formation are preserved.…”

The effects of rapid eye movement sleep deprivation and recovery on spatial reference memory of young rats

“…(Monmaur, Collet, Puma, Frankel-Kohn, & Sharif, 1997;Yoder & Pang, 2005). Previous studies have shown that acetylcholine during REM sleep following a learning task plays an important role in memory consolidation (Matsuyama, Matsumoto, Enomoto, & Nishizaki, 2000;Smith, Tenn, & Annett, 1991). In addition, a more recent study by Davis et al (2006) indicated that RSD severely hampers cytoskeletal reorganization in the hippocampus, a process that is essential for synaptic plasticity and memory consolidation.…”

D1/D5 receptors and histone deacetylation mediate the Gateway Effect of LTP in hippocampal dentate gyrus

“…Either application of nicotine in brain slices or subcutaneous injection of nicotine, in vivo, enhances LTP in dentate gyrus (Sawada et al 1994;Curran and Connor 2003;Welsby et al 2006Welsby et al , 2009. Acute nicotine treatment prevents sleep deprivation-induced impairment of LTP in the DG (Aleisa et al 2011) and administration of a highdose of nicotine causes synaptic potentiation in the DG, without pairing of tetanic stimulation (Matsuyama et al 2000;Tang and Dani 2009). These studies in the DG have, however, focused on the effects of nicotine alone.…”