Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Learning deficiency and alterations in acetylcholine receptors and protein kinase C in the brain of senescence-accelerated mouse (SAM)-P10.

Mechanisms of ageing and development - 14 Apr 2000

Okuma Y, Murayama T, Tha K K, Yamada C, Hosokawa M, Ishikawa A, Watanabe R, Maekawa M, Nomura Y

Abstract excerpt

The senescence-accelerated mouse (SAM) is known to be a murine model for accelerated aging. A novel inbred SAMP10 has shown age-related brain atrophy and learning deficiency. In the present study, we investigated the changes in learning ability and in ligand binding with muscarinic acetylcholine (mACh) receptors, alpha adrenoceptors and protein kinase C in SAMP10. In Morris's water maze task, in a control strain...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Aging, Premature
Share to Behavior, Animal

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Learning Disabilities

Share to Maze Learning

Share to Mice, Mutant Strains

Share to Motor Activity

Share to Protein Kinase C

Share to Receptors, Cholinergic

Source

Identifiers

PMID: 10802123
DOI: 10.1016/s0047-6374(00)00103-2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Learning deficiency and alterations in acetylcholine receptors and protein kinase C in the brain of senescence-accelerated mouse (SAM)-P10.PMID 10802123Read ↗

Senescence-Accelerated Mouse (SAM) as an Animal Model of Senile Dementia: Pharmacological, Neurochemical and Molecular Biological ApproachSemantic proximity Read ↗

Cognitive Decline and BPSD Are Concomitant with Autophagic and Synaptic Deficits Associated with G9a Alterations in Aged SAMP8 MiceSemantic proximity Read ↗

Neuropathological studies on strains of senescence-accelerated mice (SAM) with age-related deficits in learning and memory.Semantic proximity Read ↗

Effects of aging on spatial learning and hippocampal protein kinase C in mice.Semantic proximity Read ↗

Effects of accelerated senescence on learning and memory, locomotion and anxiety-like behavior in APP/PS1 mouse model of Alzheimer's disease.Semantic proximity Read ↗

Genetic analysis of learning and memory deficits in senescence-accelerated mouse (SAM).Semantic proximity Read ↗

Pathological and non-pathological aging, SAMP8 and SAMR1. What do hippocampal neuronal populations tell us?Semantic proximity Read ↗

Hyperactivity, neuromotor defects, and impaired learning and memory in a mouse model for metachromatic leukodystrophy.Semantic proximity Read ↗

DSTYK kinase domain ablation impaired the mice capabilities of learning and memory in water maze test.Semantic proximity Read ↗

The SAMP8 mouse for investigating memory and the role of insulin in the brain.Semantic proximity Read ↗

Combination of modified SHIRPA and pharmacological approach uncovers neuronal alteration in senescence-accelerated mouse prone 6 (SAMP6) strain.Semantic proximity Read ↗

Mice lacking leukocyte common antigen-related (LAR) protein tyrosine phosphatase domains demonstrate spatial learning impairment in the two-trial water maze and hyperactivity in multiple behavioural tests.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.