The effect of insulin receptor deletion in neuropeptide Y neurons on hippocampal dependent cognitive function in aging mice.

Goodman, EK; Mitchell, CS; Teo, JD; Gladding, JM; Abbott, KN; Rafiei, N; Zhang, L; Herzog, H; Begg, DP

The effect of insulin receptor deletion in neuropeptide Y neurons on hippocampal dependent cognitive function in aging mice.

Goodman, EK Mitchell, CS Teo, JD Gladding, JM Abbott, KN Rafiei, N Zhang, L Herzog, H Begg, DP

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Publisher:: IMR Press
Publication Type:: Journal Article
Citation:: J Integr Neurosci, 2022, 21, (1), pp. 6
Issue Date:: 2022-01-28

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Field	Value	Language
dc.contributor.author	Goodman, EK
dc.contributor.author	Mitchell, CS
dc.contributor.author	Teo, JD
dc.contributor.author	Gladding, JM
dc.contributor.author	Abbott, KN
dc.contributor.author	Rafiei, N
dc.contributor.author	Zhang, L
dc.contributor.author	Herzog, H
dc.contributor.author	Begg, DP
dc.date.accessioned	2023-07-17T01:59:36Z
dc.date.available	2021-08-27
dc.date.available	2023-07-17T01:59:36Z
dc.date.issued	2022-01-28
dc.identifier.citation	J Integr Neurosci, 2022, 21, (1), pp. 6
dc.identifier.issn	0219-6352
dc.identifier.uri	http://hdl.handle.net/10453/171535
dc.description.abstract	Insulin is known to act in the central nervous system to regulate several physiological and behavioural outcomes, including energy balance, glucose homeostasis and cognitive functioning. However, the neuronal populations through which insulin enhances cognitive performance remain unidentified. Insulin receptors are found in neuropeptide-Y (NPY) expressing neurons, which are abundant in the hypothalamus and hippocampus; regions involved in feeding behaviour and spatial memory, respectively. Here we show that mice with a tissue specific knockout of insulin receptors in NPY expressing neurons (IRl⁢o⁢x/l⁢o⁢x; NPYC⁢r⁢e⁣/+) display an impaired performance in the probe trial of the Morris Water Maze compared with control mice at both the 6 and the 12, but not at the 24 months time point, consistent with a crucial role of insulin and NPY in cognitive functioning. By 24 months of age all groups demonstrated similar reductions in spatial memory performance. Together, these data suggest that the mechanisms through which insulin influences cognitive functioning are, at least in part, via insulin receptor signaling in NPY expressing neurons. These results also highlight that cognitive impairments observed in aging may be due to impaired insulin signaling.
dc.format	Print
dc.language	eng
dc.publisher	IMR Press
dc.relation.ispartof	J Integr Neurosci
dc.relation.isbasedon	10.31083/j.jin2101006
dc.rights	info:eu-repo/semantics/openAccess
dc.subject	09 Engineering, 11 Medical and Health Sciences, 17 Psychology and Cognitive Sciences
dc.subject.classification	Neurology & Neurosurgery
dc.subject.classification	3209 Neurosciences
dc.subject.classification	5202 Biological psychology
dc.subject.mesh	Aging
dc.subject.mesh	Animals
dc.subject.mesh	Behavior, Animal
dc.subject.mesh	Cognitive Dysfunction
dc.subject.mesh	Disease Models, Animal
dc.subject.mesh	Hippocampus
dc.subject.mesh	Maze Learning
dc.subject.mesh	Mice
dc.subject.mesh	Mice, Inbred C57BL
dc.subject.mesh	Mice, Knockout
dc.subject.mesh	Neurons
dc.subject.mesh	Neuropeptide Y
dc.subject.mesh	Receptor, Insulin
dc.subject.mesh	Spatial Memory
dc.subject.mesh	Hippocampus
dc.subject.mesh	Neurons
dc.subject.mesh	Animals
dc.subject.mesh	Mice, Inbred C57BL
dc.subject.mesh	Mice, Knockout
dc.subject.mesh	Mice
dc.subject.mesh	Disease Models, Animal
dc.subject.mesh	Receptor, Insulin
dc.subject.mesh	Neuropeptide Y
dc.subject.mesh	Behavior, Animal
dc.subject.mesh	Maze Learning
dc.subject.mesh	Aging
dc.subject.mesh	Spatial Memory
dc.subject.mesh	Cognitive Dysfunction
dc.subject.mesh	Aging
dc.subject.mesh	Animals
dc.subject.mesh	Behavior, Animal
dc.subject.mesh	Cognitive Dysfunction
dc.subject.mesh	Disease Models, Animal
dc.subject.mesh	Hippocampus
dc.subject.mesh	Maze Learning
dc.subject.mesh	Mice
dc.subject.mesh	Mice, Inbred C57BL
dc.subject.mesh	Mice, Knockout
dc.subject.mesh	Neurons
dc.subject.mesh	Neuropeptide Y
dc.subject.mesh	Receptor, Insulin
dc.subject.mesh	Spatial Memory
dc.title	The effect of insulin receptor deletion in neuropeptide Y neurons on hippocampal dependent cognitive function in aging mice.
dc.type	Journal Article
utslib.citation.volume	21
utslib.location.activity	Singapore
utslib.for	09 Engineering
utslib.for	11 Medical and Health Sciences
utslib.for	17 Psychology and Cognitive Sciences
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
utslib.copyright.status	open_access	*
dc.date.updated	2023-07-17T01:59:34Z
pubs.issue	1
pubs.publication-status	Published
pubs.volume	21
utslib.citation.issue	1

Abstract:

Insulin is known to act in the central nervous system to regulate several physiological and behavioural outcomes, including energy balance, glucose homeostasis and cognitive functioning. However, the neuronal populations through which insulin enhances cognitive performance remain unidentified. Insulin receptors are found in neuropeptide-Y (NPY) expressing neurons, which are abundant in the hypothalamus and hippocampus; regions involved in feeding behaviour and spatial memory, respectively. Here we show that mice with a tissue specific knockout of insulin receptors in NPY expressing neurons (IRl⁢o⁢x/l⁢o⁢x; NPYC⁢r⁢e⁣/+) display an impaired performance in the probe trial of the Morris Water Maze compared with control mice at both the 6 and the 12, but not at the 24 months time point, consistent with a crucial role of insulin and NPY in cognitive functioning. By 24 months of age all groups demonstrated similar reductions in spatial memory performance. Together, these data suggest that the mechanisms through which insulin influences cognitive functioning are, at least in part, via insulin receptor signaling in NPY expressing neurons. These results also highlight that cognitive impairments observed in aging may be due to impaired insulin signaling.

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http://hdl.handle.net/10453/171535