TFTara L. Fidler

Tara L. Fidler

*This is an algorithmically generated author record based on publicly available information.

Current Organizations / Institutes

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Previous Organizations / Institutes

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Tara L. Fidler has a total of 7 co-authors. Here are the top co-authors by number of shared publications:

  • Christopher L. Cunningham

    From the Department of Behavioral Neuroscience and Portland Alcohol Research Center, Oregon Health & Science University, Portland, Oregon

    2 shared publications
  • Lee Bakner

    2 shared publications
  • Amanda M. Struthers

    From the Department of Behavioral Neuroscience and Portland Alcohol Research Center, Oregon Health & Science University, Portland, Oregon

    1 shared publication
  • Brandon G. Oberlin

    From the Department of Behavioral Neuroscience and Portland Alcohol Research Center, Oregon Health & Science University, Portland, Oregon

    1 shared publication
  • Christopher L Cunningham

    1 shared publication
  • Christopher L. Cunningham

    Pittsburgh Hearing Research Center, Department of Otolaryngology, University of Pittsburgh

    1 shared publication

Latest Publications

  • Schedule of Passive Ethanol Exposure Affects Subsequent Intragastric Ethanol Self‐Infusion

    by Tara L. Fidler, Brandon G. Oberlin, Amanda M. Struthers, Christopher L. Cunningham

    Background: Many studies have shown that chronic ethanol exposure can enhance later self‐administration of ethanol, but only a few studies have identified critical parameters for such exposure. The present studies examined temporal and other parameters of chronic ethanol exposure on subsequent intragastric (IG) self‐infusion of ethanol.Methods: Sprague–Dawley rats implanted with IG catheters were passively infused with ethanol for 5 to 6 days and then allowed to self‐infuse ethanol or water using a procedure in which infusions were contingent upon licking fruit‐flavored solutions. Experiment 1 examined the time interval between consecutive periods of passive infusion (Massed Group: 12 hours vs. Spaced Group: 36 hours). Experiment 2 studied the interval between the final passive infusion and onset of self‐infusion (12 vs. 36 hours). Finally, Experiment 3 tested the effect of inserting self‐infusion days within the passive infusion phase.Results: Passive ethanol exposure on consecutive days induced relatively large amounts of ethanol self‐infusion (4.1 to 7.9 g/kg/d). Increasing the duration of the ethanol‐free interval between periods of passive exposure to 36 hours significantly reduced ethanol self‐infusion (2.2 g/kg/d; Exp. 1). The time delay between the last passive ethanol exposure and onset of self‐infusion had no effect on self‐infusion (Exp. 2). Moreover, inserting no‐choice self‐infusion days between the last few passive exposure days did not increase self‐infusion (Exp. 3).Conclusions: Measurement of withdrawal signs indicated that Massed passive exposure produced stronger dependence than Spaced passive exposure, suggesting that enhanced ethanol self‐infusion in Massed Groups might be explained by the opportunity for greater negative reinforcement by ethanol. Although enhanced negative reinforcement might also explain why the Massed Group showed a weaker aversion for the ethanol‐paired flavor than the Spaced Group, this observation could also be explained by the development of greater tolerance to ethanol’s aversive pharmacological effects in the Massed Group.


  • Reestablishing an Intragastric Ethanol Self‐infusion Model in Rats

    by Tara L. Fidler, Tara W. Clews, Christopher L. Cunningham

    Background: There is a scarcity of behavioral models that will reliably produce ethanol intakes in rodents at levels that induce or maintain dependence. The present experiments were designed to reestablish a model that uses passive intragastric (IG) infusion of ethanol to induce tolerance/dependence/withdrawal before allowing rats to self‐infuse ethanol intragastrically.Methods: Sprague–Dawley rats were surgically implanted with IG catheters and allowed to recover. During the passive infusion phase (3–6 days), rats in the experimental group were passively infused with 10% (v/v) ethanol (3.3–12.2 g/kg/d). Rats in the control group were not infused. During the self‐infusion phase (5–6 days), all rats had access to 2 flavored solutions. Licks on 1 solution were paired with ethanol infusions (20%, v/v) whereas licks on the other solution were unpaired. Experiments differed in the specific passive infusion parameters and in the ethanol intake limit during self‐infusion.Results: Rats in the experimental groups self‐infused more ethanol per day (means of 4–7 g/kg/d) than did rats in the control group (means of 0–2.6 g/kg/d). Across all 3 studies, individual total daily intakes exceeded 5 g/kg on 35% of the self‐infusion days in ethanol‐preexposed rats compared with 1.5 g/kg) compared with control rats (Conclusions: Relatively short periods of passive IG infusion of ethanol induced levels of ethanol self‐infusion in genetically heterogeneous rats that were comparable with drinking intakes previously reported in rats selectively bred for ethanol intake/preference. Although the induction of dependence/withdrawal may have played a role in this outcome, an alternative interpretation is that experimental rats self‐infused more ethanol because passive exposure produced tolerance to aversive pharmacological effects that would otherwise limit intake of the paired flavor because of development of conditioned taste aversion. The current findings provide a strong basis for future work designed to identify parametric determinants of this form of self‐administration, its sensitivity to genetic influences, and its neurobiological substrates.