Meg Kirkpatrick - Academia.edu (original) (raw)

Papers by Meg Kirkpatrick

Journal of undergraduate neuroscience education : JUNE : a publication of FUN, Faculty for Undergraduate Neuroscience, 2009

This article describes a two-part laboratory module taught at Wheaton College and provides resour... more This article describes a two-part laboratory module taught at Wheaton College and provides resources to allow instructors to recreate this module at their own institutions. This module introduces students to basic surgical techniques and allows for in-depth discussion of 1) effects of hormones on behavior, 2) ethics of animal use in research, 3) psychopharmacology, 4) experimental design and 5) empirical data collection. This exercise provides students with the opportunity to replicate a classic behavioral neuroendocrinology study while developing critical thinking, experimental design and empirical data collection skills.

NeuroToxicology, 2015

Methylmercury (MeHg) is a widely distributed environmental neurotoxin with established effects on... more Methylmercury (MeHg) is a widely distributed environmental neurotoxin with established effects on locomotor behaviors and cognition in both human populations and animal models. Despite well-described neurobehavioral effects, the mechanisms of MeHg toxicity are not completely understood. Previous research supports a role for oxidative stress in the toxic effects of MeHg. However, comparing findings across studies has been challenging due to differences in species, methodologies (in vivo or in vitro studies), dosing regimens (acute vs. long-term) and developmental life stage. The current studies assess the behavioral effects of MeHg in adult mice in conjunction with biochemical and cellular indicators of oxidative stress using a consistent dosing regimen. In Experiment 1, adult male C57/BL6 mice were orally administered 5mg/kg/day MeHg or the vehicle for 28 days. Impact of MeHg exposure was assessed on inverted screen and Rotor-Rod behaviors as well as on biomarkers of oxidative stress (thioredoxin reductase (TrxR), glutathione reductase (GR) and glutathione peroxidase (GPx)) in brain and liver. In Experiment 2, brain tissue was immunohistochemically labeled for 8-hydroxy-2&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-deoxyguanosine (8-OHdG), a biomarker of DNA oxidation and an indicator of oxidative stress, following the same dosing regimen. 8-OHdG immunoreactivity was measured in the motor cortex, the magnocellular red nucleus (RMC) and the accessory oculomotor nucleus (MA3). Significant impairments were observed in MeHg-treated animals on locomotor behaviors. TrxR and GPx was significantly inhibited in brain and liver, whereas GR activity decreased in liver and increased in brain tissue of MeHg-treated animals. Significant MeHg-induced alterations in DNA oxidation were observed in the motor cortex, the RMC and the MA3.

Hormones and behavior, 2003

Physiology & Behavior, 2011

Sexual receptivity induced in ovariectomized rats by the long-term administration of estradiol be... more Sexual receptivity induced in ovariectomized rats by the long-term administration of estradiol benzoate (EB) can be inhibited by concurrent administration of androgens. Experiment 1 examined the role of time course and dose of androgens in the inhibition of estrogen-induced sexual receptivity. Ovariectomized rats were treated with EB (2.0 µg per rat per day) for 6 days and tested for sexual receptivity (Test Day I). EB treatment continued for 15 days concomitant with daily administration of one of three doses of dihydrotestosterone propionate (DHTP; 7.5, 0.75, 0.075 mg/kg) or 3α-androstanediol (3α-Adiol; 3.75, 1.0, 0.375 mg/kg). Four tests for sexual receptivity were conducted on days 3, 6, 14, and 15 of the androgen/vehicle treatment period (Test Days II -V). On Day 15 (Test Day V), the rats received progesterone (1.0 mg per rat) 4 h before testing. Using the same experimental design, Experiment 2 examined the effect of increasing the dose of estrogen on the androgenic inhibition of sexual receptivity. Ovariectomized rats were treated with one of two doses of EB (2.0 or 10.0 µg per rat per day) concomitant with daily administration of DHTP (7.5 mg/kg) or 3α-Adiol (3.75 mg/kg). In Experiment 1, the highest doses of both DHTP and 3α-Adiol significantly inhibited estrogen-induced sexual receptivity. Data from Experiment 2 indicate that the inhibitory effects of DHTP but not 3α-Adiol can be moderated by an increased dose of EB.

Physiology & Behavior, 1998

effects on the rat estrous cycle. PHYSIOL BEHAV 63(2) [287][288][289][290][291][292][293][294][29... more effects on the rat estrous cycle. PHYSIOL BEHAV 63(2) [287][288][289][290][291][292][293][294][295] 1998.-Anabolic-androgenic steroid (AAS) effects on the estrous cycle of adult Long-Evans rats were examined in four different experiments. Sexual receptivity, vaginal cytology, and body weight were monitored throughout two-week baseline, AAS treatment, and recovery periods. In Experiments 1-3, rats were administered stanozolol, oxymetholone, or testosterone cypionate within dose ranges selected to mimic the human abuse levels of each compound. In these studies, the highest doses of stanozolol (5 mg/kg), oxymetholone (12 mg/kg), or testosterone cypionate (7.5 mg/kg) disrupted the cyclical display of sexual receptivity and vaginal estrus. To compare effects on estrous cyclicity across AAS compounds, rats in Experiment 4 received a single dose (7.5 mg/kg) of each compound for 2 weeks. At the 7.5 mg/kg dose, all AAS compounds interfered with the cyclical display of vaginal estrus, although effects on sexual receptivity were not uniform. No striking AAS effects on body weight were seen in any experiment. The short-term administration of AAS compounds at high doses disrupts female neuroendocrine function in rats.

Journal of Neuroendocrinology, 2002

Sensory cues from male rats, such as odours and vaginal-cervical stimulation (VCS), play a modula... more Sensory cues from male rats, such as odours and vaginal-cervical stimulation (VCS), play a modulatory role in female rat sexual behaviour. For example, exposure to male odours and VCS appears to be at least partially responsible for increases in sexual behaviour following repeated mating of oestradiol-primed female rats. Although there is evidence that VCS influences sexual behaviour via a ligand-independent progestin receptor (PR)-dependent mechanism, the mechanism by which odours influence sexual behaviour is not known. We tested the hypothesis that, similar to VCS, the effects of male odours on sexual behaviour are mediated by progestin receptors. Female rats were injected with the progestin antagonist, RU486, or oil vehicle and were then exposed to male-soiled bedding or clean bedding. Although exposure to male-soiled bedding resulted in higher levels of Fos immunoreactivity in brain areas associated with female sexual behaviour, the progestin antagonist did not reduce this effect. Furthermore, there was minimal coexpression of odour-induced Fos and progestin receptors in brain areas associated with female sexual behaviour. Together, these results suggest that the effects of male odours are not mediated by a PR-dependent mechanism. Therefore, we tested the hypothesis that oestrogen receptor (ER)-containing cells are involved in the effects of olfactory cues. Although there was virtually no coexpression of ERb and odour-induced Fos in brain areas associated with female sexual behaviour, exposure to male odours slightly increased the number of cells coexpressing ERa and odour-induced Fos in the posterodorsal medial amygdala. Although, these results do not support the hypothesis that the effects of odours are mediated by a PR-dependent mechanism, they suggest that integration of male odours and hormonal cues may occur in ERa-containing cells in the posterodorsal medial amygdala.

Hormones and Behavior, 2001

Repeated mating of estradiol-primed female rats increases sexual receptivity. Two studies were co... more Repeated mating of estradiol-primed female rats increases sexual receptivity. Two studies were conducted to determine the contribution of vaginal-cervical stimulation (VCS) to this increase. In the first study, female rats were repeatedly mated for 165 min. The vaginas of half of the females were covered with tape (masked) to prevent intromissions by the males. The remaining females were unmasked. Only females receiving intromissions (unmasked) showed a significant increase in sexual receptivity during repeated mating, suggesting that VCS from intromissions is necessary for repeated mating to increase sexual receptivity. In the second experiment, female rats received either experimentally administered VCS or control scapular stimulation administered with a plastic probe 1 h prior to testing for sexual receptivity. VCS applied in this manner significantly increased sexual receptivity. Together, these findings suggest that VCS from intromissions is one of the primary factors responsible for increases in sexual receptivity following repeated mating.

Hormones and Behavior, 2003

Sexual behavior in female rats depends on the action of estradiol on estrogen receptors (ERs) fou... more Sexual behavior in female rats depends on the action of estradiol on estrogen receptors (ERs) found in particular brain regions. While hormonal regulation of female sexual behavior requires ER␣, the possible functions of ER␤ remain to be clarified. Mating stimulation has several behavioral and physiological consequences and induces Fos expression in many brain areas involved in the regulation of reproductive behavior and physiology. In addition, some cells in which mating induces Fos expression coexpress ER␣. To determine whether cells in which Fos is induced by a particular mating stimulus coexpress ER␣, ER␤, or both, we used a triple-label immunofluorescent technique to visualize ER␣-, ER␤-, and mating-induced Fos-immunoreactivity (Fos-ir) in neurons in which mating stimulation reliably increases Fos expression. Ovariectomized, hormone-primed rats were either unmated, received 15 mounts, or received 15 intromissions. In the rostral medial preoptic area, Fos-ir was induced by mounts alone primarily in cells coexpressing ER␣-ir, while Fos-ir was induced by intromissions mainly in cells coexpressing both ER␣-ir and ER␤-ir (ER␣/ER␤-ir). In the dorsal part of the posterodorsal medial amygdala, Fos-ir was induced by intromissions in cells coexpressing ER␣-ir and ER␣/ER␤-ir. However, in the ventral part of the posterodorsal medial amygdala, Fos-ir was induced by intromissions primarily in cells coexpressing only ER␤-ir. These data suggest that qualitatively different sexual stimuli may be integrated through distinct ER-containing circuits in the rostral medial preoptic area and posterodorsal medial amygdala. The diversity in coexpression of type of ER in cells in different brain areas after various mating stimuli suggests a role for both ER␣ and ER␤ in the integration of hormonal information and information related to mating stimuli.

Hormones and Behavior, 1998

Both naturally occurring and synthetic androgens have been shown to inhibit estrogen-induced sexu... more Both naturally occurring and synthetic androgens have been shown to inhibit estrogen-induced sexual receptivity when administered to ovariectomized (OVX) rats. The mechanisms by which androgens exert these effects, however, remain unclear. Experiments were conducted to determine the role of the androgen receptor in the inhibition of estrogen-induced sexual receptivity in OVX rats by using flutamide, an androgen receptor antagonist. In each experiment, OVX Long-Evans rats received 6 consecutive days of estradiol benzoate (EB; 2.0 g/ day) followed by 15 days of EB concurrent with flutamide (10.0 mg/kg; twice daily) or the vehicle and one of the following androgens or the vehicle: dihydrotestosterone propionate (7.5 mg/kg), 3␣-androstanediol (3.75 mg/kg), 17␣-methyltestosterone (7.5 mg/kg), stanozolol (7.5 mg/ kg), or nandrolone decanoate (7.5 mg/kg). On Day 15, all female rats received progesterone (P; 1.0 mg/rat) 4 h before testing. Tests for sexual receptivity were conducted on Days 3, 6, 14, and 15 of androgen/flutamide treatment. Each androgen inhibited sexual receptivity as expected, and concurrent treatment with flutamide reversed the inhibitory effects of all androgens on sexual receptivity on all test days. High levels of sexual receptivity were displayed in response to P on Day 15, regardless of experimental treatment. These results suggest that naturally occurring and synthetic androgens act at the androgen receptor to inhibit estrogen-induced sexual receptivity in OVX rats.

Neurobiology of Learning and Memory, 1997

In the adult rat, hippocampal dendritic synaptic connec-