[Abstract Title]. - Society for Neuroscience

1 Dept. of Neurol., Nagoya City Univ. Med. Sch., Nagoya, Japan; 2 Inst. for Med. Sci. of Aging,
Nagakute, Japan
Abstract: The cholinergic neuronal system of septo-hippocampus is known to play a important
role in memory. The reduction of acethylcholine, due to the inactivation of
cholineacethyltransferase (ChAT), was ascertained in this cholinergic system in animal models
of dementia and in patients with Alzheimer‟s disease.
Hippocampal cholinergic neurostimulating peptide (HCNP), originally purified from young rat
hippocampus, stimulates the synthesis of acetylcholine in the septal nucleus, inducing the
activity of ChAT in vitro, and can be released from the neurons of hippocampus by the
stimulation of N-methyl-D-asparate (NMDA)-type receptor in vitro.
To examine directly the involvement of HCNP and HCNP-precursor protein(HCNP-pp) in
memory formation, we generated the conditional transgenic mouse of HCNP-pp, driven by
αCaMKII promoter. In transgenic mouse, we confirmed the amelioration of learning ability, and
the increase of ChAT positive neurons in medial septal nucleus in vivo. These results suggest
that HCNP and HCNP-pp can be one of key molecules to play a crucial role in memory in vivo.
Disclosures: N. Uematsu, None; N. Matsukawa, None; T. Toyoda, None; T. Sagisaka,
None; T. Kanamori, None; K. Ojika , None; Y. Hashizume, None.
Poster
292. Acetylcholine, Neurotrophins, and Cognition
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 292.3/SS16
Topic: F.02.d. Cognitive learning and memory systems
Support: NINDS Grant RO1NS054272
Title: The effects of tacrine on spontaneous alternation performance and hippocampal
acetylcholine release in an animal model of diencephalic amnesia
Authors: *J. J. ROLAND, M. LEVINSON, J. PATEL, L. M. SAVAGE;
Psychology, Univ. Binghamton, Binghamton, NY
Abstract: Tacrine, an acetylcholinesterase inhibitor (AChE-I), has been used to treat the
memory deficits associated with amnesia and dementia. However, AChE-Is have had mixed
efficacy in human patients as well as in a variety of animal models of cognitive dysfunction. In
the present study, pyrithiamine-induced thiamine deficiency (PTD) was used to create a rodent
model of diencephalic amnesia. PTD treatment results in diencephalic lesions, septohippocampal