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Despite the well\u2010documented evidence that aging decreases bone formation, there remains little understanding whereby cellular aging alters skeletal homeostasis. We, and others, have previously demonstrated that gap junctions\u2014membrane\u2010spanning channels that allow direct cell\u2010to\u2010cell conductance of small signaling molecules\u2014are critically involved in osteoblast differentiation and skeletal homeostasis. We examined whether the capacity of rat osteoblastic cells to form gap junctions and respond to known modulators of gap junction intercellular communication (GJIC) was dependent on the age of the animal from which they were isolated. We observed no effect of age upon osteoblastic Cx43 mRNA, protein or GJIC. We also examined age\u2010related changes in PTH\u2010stimulated GJIC. PTH demonstrated age\u2010dependent effects upon GJIC: Osteoblastic cells from young rats increased GJIC in response to PTH, whereas there was no change in GJIC in response to PTH in osteoblastic cells from mature or old rats. PTH\u2010stimulated GJIC occurred independently of changes in Cx43 mRNA or protein expression. Cholera toxin significantly increased GJIC in osteoblastic cells from young rats compared to those from mature and old rats. These data demonstrate an age\u2010related impairment in the capacity of osteoblastic cells to generate functional gap junctions in response to PTH, and suggest that an age\u2010related defect in G protein\u2010coupled adenylate cyclase activity at least partially contributes to decreased PTH\u2010stimulated GJIC. \u00a9 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. 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