4.8 Article

Social amnesia in mice lacking the oxytocin gene

Journal

NATURE GENETICS
Volume 25, Issue 3, Pages 284-288

Publisher

NATURE AMERICA INC
DOI: 10.1038/77040

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Funding

  1. NCRR NIH HHS [RR0016] Funding Source: Medline
  2. NICHD NIH HHS [HD33438] Funding Source: Medline
  3. PHS HHS [R01M56538-01] Funding Source: Medline

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The development of social familiarity in rodents depends predominantly on olfactory cues and can critically influence reproductive success(1,2). Researchers have operationally defined this memory by a reliable decrease in olfactory investigation in repeated or prolonged encounters with a conspecific(3-6). Brain oxytocin (OT) and vasopressin (AVP) seem to modulate a range of social behaviour from parental care to mate guarding(7). Pharmacological studies indicate that AVP administration may enhance social memory(8-10), whereas OT administration may either inhibit or facilitate social memory depending on dose, route or paradigm(1,11-13). We found that male mice mutant for the oxytocin gene (Oxt(-/-)) failed to develop social memory, whereas wild-type (Oxt(+/+)) mice showed intact social memory. Measurement of both olfactory foraging and olfactory habituation tasks indicated that olfactory detection of non-social stimuli is intact in Oxt(-/-) mice. Spatial memory and behavioural inhibition measured in a Morris water-maze, Y-maze. or habituation of an acoustic startle also seemed intact. Treatment with OT but not AVP rescued social memory in Oxt(-/-) mice, and treatment with an OT antagonist produced a social amnesia-like effect in Oxt(+/+) mice. Our data indicate that OT is necessary for the normal development of social memory in mice and support the hypothesis that social memory has a neural basis distinct from other forms of memory.

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