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Corticotrophin-releasing factor produces a long-lasting enhancement of synaptic efficacy in the hippocampus (1998)

Wang, H. L. ; Wayner, M. J. ; Chai, C. Y. ; [et al.]

Oxford, UK : Blackwell Science Ltd

European journal of neuroscience 10 (1998), S. 0

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ISSN: 1460-9568

Source: Blackwell Publishing Journal Backfiles 1879-2005

Topics: Medicine

Notes: We have previously demonstrated that intra-hippocampal injection of corticotrophin-releasing factor improved memory retention of an inhibitory avoidance learning in rats; while the electrophysiological effects corticotrophin-releasing factor produces on hippocampal neurons are largely uncharacterized. In the present study, we found that corticotrophin-releasing factor injected into the dentate gyrus of hippocampus produced a dose-dependent and long-lasting enhancement in synaptic efficacy of these neurons, as measured by an increase in the amplitude and slope of population excitatory postsynaptic potentials, as well as the amplitude of population spike. The onset of corticotrophin-releasing factor-induced potentiation was slow. It was observed approximately 40–60 min after corticotrophin-releasing factor administration and lasted for more than 5 h. This effect of corticotrophin-releasing factor was blocked by pretreatment with the cyclase-adenosine-3,5-monophosphate (cAMP) inhibitor Rp-adenosine-3,5-cyclic monophosphothiolate triethylamine (Rp-cAMPS) and partially blocked by the N-methyl-D-aspartate receptor antagonist MK-801. Further, pretreatment with corticotrophin-releasing factor receptor antagonist dose-dependently diminished tetanization-induced long-term potentiation, and corticotrophin-releasing factor and tetanic stimuli had an additive effect on hippocampal neuron excitation. Moreover, direct injection of corticotrophin-releasing factor increased cAMP level in the dentate gyrus. These results together suggest that corticotrophin-releasing factor-induced potentiation simulates the late phase of tetanization-induced long-term potentiation and cAMP seems to be the messenger mediating this effect. Moreover, corticotrophin-releasing factor-induced potentiation and long-term potentiation may share some similar mechanisms, and corticotrophin-releasing factor is probably involved in the neural circuits underlying long-term potentiation. Thus, corticotrophin-releasing factor may play an important role in modulating synaptic plasticity in the hippocampus.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1046/j.1460-9568.1998.00352.x

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Interactive effects of nicotine and MPTP on striatal tetrahydrobiopterin in mice (1996)

Tsai, M. J. ; Wang, H. L. ; Lee, E. H. Y.

Springer

Journal of biomedical science 3 (1996), S. 47-53

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ISSN: 1423-0127

Keywords: Nicotine ; 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine ; Mecamylamine ; Biopterin ; Dopamine ; Striatum

Source: Springer Online Journal Archives 1860-2000

Topics: Biology , Medicine

Notes: Abstract 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a neurotoxin known to cause dopamine (DA) neuron degeneration, while the psychoactive compound nicotine is known to excite DA neurons. Tetrahydrobiopterin is the cofactor for tyrosine hydroxylase (TOH) in the regulation of DA biosynthesis. The present study investigated the interactions between nicotine and MPTP on striatal biopterin, DA and TOH activity in BALB/c mice. The results indicated that both acute and chronic nicotine administrations at various concentrations significantly increased biopterin and DA levels in the striatum, while MPTP markedly decreased these measures. Pretreatment with nicotine at a dose having no significant effect alone, partially protected against MPTP's toxicity on biopterin and DA. Increasing the dose of nicotine did not have a further protective action. The toxicity of MPTP on TOH was also prevented by nicotine. Further, the above effects of nicotine were probably mediated through the cholinergic nicotinic receptors since mecamylamine reversed the effects of nicotine. These results suggest that nicotine interacts with the dopaminergic system probably at the level of DA biosynthesis through activating TOH and its coenzyme tetrahydrobiopterin.