6 and

0.7 mg/kg, s.c.) or ethanol (0.5 g/kg, i.p.) improved WIN-induced memory impairment, suggesting a cross state-dependent memory retrieval between the drugs. Pre-test intra-CA1 microinjection of nicotine (1 and 2 mu g/mouse) before systemic administration of an ineffective SP600125 solubility dmso dose of nicotine (0.5 mg/kg, s.c.) or ethanol (0.25 g/kg) significantly reversed WIN-induced memory impairment. Pre-test intra-CA1 microinjection of mecamylamine (1 and 3 mu g/mouse) inhibited cross state-dependent memory between WIN and nicotine or ethanol. Moreover, pre-test intra-MS microinjection of nicotine (1 and 2 mu g/mouse) in combination with systemic administration of a lower dose of nicotine (0.5 mg/kg), but not ethanol (0.25 g/kg), improved memory impairment induced by pre-training administration of WIN. On the other hand, in the animals that received pre-training WIN and pretest systemic administration of nicotine (0.7 mg/kg), but not ethanol (0.5 g/kg), pre-test intra-MS microinjection of mecamylamine (1-5 mu g/mouse) inhibited

selleck products WIN-nicotine state-dependent memory retrieval. It should be noted that pre-test intra-CA1 or intra-MS microinjection of nicotine or mecamylamine by itself had no effect on memory retrieval and also could not reverse memory impairment induced by pre-training administration of WIN. It can be concluded that WIN and nicotine or WIN and ethanol can induce state-dependent memory retrieval. In addition, our results showed that a cross-state dependency between these drugs may be mediated through a cholinergic nicotinic mechanism. (C) 2013 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Reticulospinal (RS) neurons are critical for initiation of locomotor behavior, and following spinal cord injury (SCI) in the lamprey, the axons of these neurons regenerate and restore locomotor behavior within a few weeks. For lamprey RS neurons learn more in culture, experimental induction of calcium influx, either in the growth cone or cell body, is inhibitory for neurite outgrowth. Following SCI, these neurons partially downregulate calcium channel expression, which would be expected to reduce calcium influx and possibly provide supportive

conditions for axonal regeneration. In the present study, it was tested whether activation of second messenger signaling pathways stimulates neurite outgrowth of lamprey RS neurons without altering their electrical properties (e.g. spike broadening) so as to possibly increase calcium influx and compromise axonal growth. First, activation of cAMP pathways with forskolin or dbcAMP stimulated neurite outgrowth of RS neurons in culture in a PKA-dependent manner, while activation of cGMP signaling pathways with dbcGMP inhibited outgrowth. Second, neurophysiological recordings from uninjured RS neurons in isolated lamprey brain spinal cord preparations indicated that dbcAMP or dbcGMP did not significantly affect any of the measured electrical properties.