Nicotine prevents disruption of the late phase LTP‐related molecular cascade in adult‐onset hypothyroidism

Abstract

We have shown previously that chronic nicotine treatment reverses adult-onset hypothyroidism-induced impairment of late-phase long-term potentiation (L-LTP) in area CA1 of the hippocampus. In the present study, basal and stimulated levels of signaling molecules essential for the expression of L-LTP were determined in area CA1. Immunoblots analysis showed that chronic nicotine treatment of hypothyroid rats prevented the reduction in the basal protein levels of adenylyl cyclase I (ACI), mitogen-activated protein kinases [MAPKp44/42 (ERK1/2)], calcium-calmodulin-dependent protein kinase IV (CaMKIV), and cyclic-AMP response element binding protein [CREB; phosphorylated (P-) and total]. A significant increase in the levels of P-CREB, P-MAPKp44, P-MAPKp42 and brain derived neurotrophic factor (BDNF) was seen 4 h after multiple train high frequency stimulation (MHFS) in nicotine-treated hypothyroid and control animals, but not in hypothyroid animals. The levels of total CREB, total MAPKp44, total MAPKp42, and CaMKIV were elevated in all groups 4 h after MHFS. These findings suggest that prevention of the reduced basal level of CaMKIV, MAPKp44/42, and CREB by nicotine along with the regained ability of MHFS to induce MAPKp44/42 and CREB phosphorylation in nicotine treated hypothyroid animals may be responsible for the reversal of L-LTP impairment by chronic nicotine treatment in this disease model.

Chronic psychosocial stress accelerates impairment of long‐term memory and late‐phase long‐term potentiation in an at‐risk model of Alzheimer's disease

“…Several lines of evidence have suggested that BDNF is involved in the L-LTP and long-term memory (Barco et al, 2005;Alzoubi et al, 2007b). L-LTP is impaired in knockout mice and mice with mutations in the BDNF receptor (Minichiello et al, 2002;Pang and Lu, 2004).…”

“…Standard procedures for in vivo recording from the Cornu Ammonis field 1 (CA1) brain region of anesthetized rats were performed as described (Alzoubi et al, 2007b). Rats were anesthetized with urethane (1.2 g/kg i.p.…”

Treadmill Exercise Prevents Learning and Memory Impairment in Alzheimer’s Disease-Like Pathology

“…Seventeen days after implantation surgery, in vivo electrophysiological recordings from area Cornu Ammonis 1 (CA1) of the hippocampus was accomplished as described [24, 25]. Briefly, rats were urethane-anesthetized (1.2 g/kg, i.p., Sigma Aldrich, USA) and two holes were stereotaxically drilled for placing the stimulating and recording electrodes.…”

“…The magnitude of E-LTP, evoked by one train of HFS (8 pulses of 400 Hz every 10 seconds, repeated 8 times), is quantified by changes in the field excitatory post-synaptic potential (fEPSP) slope and pspike amplitude recorded for 1 hour following HFS. The fEPSP slope and pspike amplitude represent synaptic strength and the number of neurons reaching firing threshold respectively [24, 25]. …”

Chronic Psychosocial Stress Exacerbates Impairment of Synaptic Plasticity in β-Amyloid Rat Model of Alzheimers Disease: Prevention by Nicotine

“…L-LTP was induced in the CA1 region of the hippocampus, and five hours after MHFS, the rats were sacrificed and the septal and temporal parts of the right hippocampus were dissected out. As stated in the Method section, to minimize individual variation, the temporal side was used as an internal control [52,53,63,64].…”