Problems with timing and time perception have been suggested as key characteristics of autism spectrum condition (ASC). Studies and personal accounts from clinicians, parents, caregivers, and self‐reports from autistic people themselves often refer to problems with time. Although a number of empirical studies have examined aspects relating to time in autistic individuals, there remains no clear consensus on whether or how timing mechanisms may be affected in autism. A key reason for this lack of clarity is the wide range of timing processes that exist and subsequently the wide range of methodologies, research paradigms, and samples that time‐based studies have used with autism populations. In order to summarize and organize the available literature on this issue, a systematic review was conducted. Five electronic databases were consulted. From an initial 597 records (after duplicates were removed), 45 papers were selected and reviewed. The studies are reviewed within different sections based on the different types of timing ability that have been explored in the neurotypical (NT) population: time sensitivity, interval timing, and higher‐order time perception. Within each section cognitive models, methodologies, possible clinical implications, and research results are discussed. The results show different consistency across studies between the three types of timing ability. The highest consistency of results showing atypical time perception abilities is found in high‐level time perception studies. It remains unclear if autism is characterized by a fundamental time perception impairment. Suggestions for future research are discussed. Autism Res 2019, 12: 1440–1462. © 2019 International Society for Autism Research, Wiley Periodicals, Inc.Lay SummaryThis systematic review examines the different types of timing and time perception behavior that have been investigated in autism. Overall, there are a number of studies that show differences between autistic and non‐autistic individuals, but some studies do not find such differences. Group differences are more consistent across studies using complex tasks rather than simpler more fundamental timing tasks. We suggest that experiments across a range of timing tasks would be fruitful to address gaps in our knowledge.

A growing body of literature provides evidence of a prominent role for bone morphogenetic proteins (BMPs) in regulating various stages of ovarian follicle development. Several actions for BMP6 have been previously reported in the hen ovary, yet only within postselection (preovulatory) follicles. The initial hypothesis tested herein is that BMP6 increases FSH receptor (FSHR) mRNA expression within the granulosa layer of prehierarchal (6-8 mm) follicles (6-8 GC). BMP6 mRNA is expressed at higher levels within undifferentiated (1-8 mm) follicles compared with selected (R9 mm) follicles. Recombinant human (rh) BMP6 initiates SMAD1, 5, 8 signaling in cultured 6-8 GC and promotes FSHR mRNA expression in a dose-related fashion. In addition, a 21 h preculture with rhBMP6 followed by a 3 h challenge with FSH increases cAMP accumulation, STAR (StAR) expression, and progesterone production. Interestingly, rhBMP6 also increases expression of anti-Mü llerian hormone (AMH) mRNA in cultured 6-8 GC. This related BMP family member has previously been implicated in negatively regulating FSH responsiveness during follicle development. Considering these data, we propose that among the paracrine and/or autocrine actions of BMP6 within prehierarchal follicles is the maintenance of both FSHR and AMH mRNA expression. We predict that before follicle selection, one action of AMH within granulosa cells from 6 to 8 mm follicles is to help suppress FSHR signaling and prevent premature granulosa cell differentiation. At the time of selection, we speculate that the yet undefined signal directly responsible for selection initiates FSH responsiveness. As a result, FSH signaling suppresses AMH expression and initiates the differentiation of granulosa within the selected follicle.

The corpus luteum (CL) produces oxytocin (OXT), which has been proposed to regulate the pulsatile release of prostaglandin F2alpha during luteolysis in ruminants. This action of OXT is mediated via oxytocin receptors (OXTRs) present on uterine epithelial cells. It is hypothesized that luteal OXT acts as a paracrine regulator of resident immune cells. In the present study, OXTR mRNA expression in bovine lymphocytes was analyzed, as well as its regulation during the estrous cycle. OXTR transcripts were observed in freshly purified bovine peripheral blood mononuclear cells and T lymphocytes. OXTR mRNA in bovine lymphocytes on Day 3 was numerically greater than but not significantly different from that of Day 19 of the estrous cycle (P=0.091). In cultured T cells, estradiol (E2) treatment significantly increased the steady-state concentrations of OXTR mRNA, but the stimulatory effect of E2 was inhibited by the addition of progesterone (P4). Each of the major T cell subsets (CD4+, CD8+, and gamma delta+) expressed OXTR mRNA, with no significant difference in expression among them. Western blot analyses demonstrated the presence of the bovine OXTR protein at about 45 kDa in lymphocytes, as well as expression of the 14-kDa precursor of OXT. When lymphocytes were treated with OXT, intracellular concentrations of calcium ([Ca2+]i) were rapidly and dramatically increased. This study demonstrated that bovine lymphocytes express OXTRs and that this expression can be regulated in a steroid-dependent manner. Furthermore, OXT elicited a functional [Ca2+]i response in T lymphocytes, supporting the possibility that OXT within the CL could act as a paracrine or autocrine regulator of resident T lymphocytes.

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