Samantha Penman

Samantha Penman

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

Current Organizations / Institutes

The organizations/institutes from the scholar's latest article


Samantha Penman has a total of 26 co-authors. Here are the top co-authors by number of shared publications:

  • Panayotis K. Thanos

    Behavioral Neuropharmacology and Neuroimaging Laboratory on Addictions (BNNLA), Clinical Research Institute on Addictions, Department of Pharmacology and Toxicology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY 14203, USA

    5 shared publications
  • Aidan Powell

    Behavioral Neuropharmacology and Neuroimaging Laboratory on Addictions (BNNLA), Clinical Research Institute on Addictions, Department of Pharmacology and Toxicology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY 14203, USA

    3 shared publications
  • Ayanna Varma

    Behavioral Neuropharmacology and Neuroimaging Laboratory on Addictions (BNNLA), Clinical Research Institute on Addictions, Department of Pharmacology and Toxicology, Jacobs, School of Medicine and Biomedical Sciences, University at Buffalo, 1021 Main Street, Buffalo, NY 14203, USA

    2 shared publications
  • David E. Komatsu

    Department of Orthopaedics, Stony Brook University, Stony Brook, NY, USA

    2 shared publications
  • Faisal Sadar

    Department of Orthopaedics and Rehabilitation, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY 11794, USA

    2 shared publications
  • Grace Clouse

    Behavioral Neuropharmacology and Neuroimaging Laboratory on Addictions (BNNLA), Clinical Research Institute on Addictions, Department of Pharmacology and Toxicology, Jacobs, School of Medicine and Biomedical Sciences, University at Buffalo, 1021 Main Street, Buffalo, NY 14203, USA

    2 shared publications

Latest Publications

  • Open Access

    Chronic THC Inhalation During Early Adulthood Exacerbates Ovariectomy-Induced Bone Loss in a Rat Model of Osteoporosis

    by Grace Clouse, Samantha Penman, Aidan Powell, Faisal Sadar, Nihamul Ehan, Isaiah T. Taylor, Ayanna Varma, Michael Hadjiargyrou, David E. Komatsu, Panayotis K. Thanos

    Introduction: Osteoporosis is a debilitating bone disease that affects a large segment of the population. Currently, pharmacological treatment options for osteoporosis, including antiresorptive drugs and those that prevent bone loss, are limited. Multiple studies have shown that the endocannabinoid system and cannabis may play a significant role in bone remodeling. As both the use of cannabis and high-quality research on its effects continue to grow, novel medicinal uses of selected components, such as tetrahydrocannabinol (THC), are being investigated. The present study examined the potential effect of chronic THC inhalation during early adulthood on an ovariectomized rodent model of post-menopausal osteoporosis. Materials and Methods: Young (26-week-old) adult female rats received daily either THC or air inhalation for 8 weeks. The rats then underwent an ovariectomy (OVX) or sham surgery (Sx) when they were 34 weeks old. They were then euthanized 4 weeks post-OVX, and skeletal tissues were collected for analysis. Results: MicroCT analysis of femora showed that THC + OVX rats showed a significant decrease (45%) in trabecular bone volume compared to Air + Sham Sx rats. As expected, the Air + OVX rats also showed a 17% reduction in trabecular bone volume. Discussion: Overall, early adulthood THC exposure increased susceptibility to osteoporosis following ovariectomy-induced menopause. This suggests that THC exerts long-lasting effects on bone health, which may exacerbate post-menopausal bone loss.

  • Open Access

    Chronic Δ9-Tetrahydrocannabinol Inhalation Following Osteoporosis Results in Bone Deficits

    by Aidan Powell, Grace Clouse, Samantha L. Penman, Isaiah T. Taylor, Faisal Sadar, Nihamul Ehan, Ayanna Varma, Michael Hadjiargyrou, David E. Komatsu, Panayotis K. Thanos

    Background: Osteoporosis, a debilitating bone disease characterized by low bone mineral density, poses a large burden on the population. Current pharmacological treatment options are limited, with antiresorptive drugs being the current first-line option. Recent research has shown that the endocannabinoid system, modulated by endocannabinoids and phytocannabinoids, may influence bone remodeling. As the prevalence of cannabis use and research into its medicinal potential continues to increase, its therapeutic potential has emerged. Objective: To investigate the role of Δ9-tetrahydrocannabinol (THC) inhalation in treating osteoporosis in a rodent model. Methods: Adult female Sprague–Dawley rats underwent ovariectomy (OVX) to induce osteoporosis. Four weeks post-OVX, rats received either THC or Air treatment via inhalation for 8 weeks. A control group of age-matched rats received sham surgery. Rats were then euthanized at 38 weeks old, and hindlimb samples were collected for caliper, microCT, and biomechanical analyses. Results: OVX Air-treated rats showed significantly decreased trabecular bone volume, trabecular bone volume fraction, trabecular separation, trabecular tissue mineral density, trabecular number, and connective density compared to sham surgery controls. Compared with Air controls, OVX rats treated with THC showed increased endosteal volume (20%; p < 0.05). THC-treated rats also showed decreased trabecular bone mineral density (2%; p < 0.005) and trabecular thickness (14%; p < 0.05). Conclusions: Chronic inhaled THC worsened key aspects of trabecular bone microarchitecture. Results do not support use of THC vapor as a therapeutic agent for osteoporosis and suggest THC may adversely affect bone quality in estrogen-deficient states. Further research is needed to evaluate dose-dependent effects and to distinguish the skeletal impacts of different cannabinoid components.


  • Open Access

    Selenoprotein P in a Rodent Model of Exercise; Theorizing Its Interaction with Brain Reward Dysregulation, Addictive Behavior, and Aging

    by Patrick Mohr, Colin Hanna, Aidan Powell, Samantha Penman, Kenneth Blum, Alireza Sharafshah, Kai-Uwe Lewandrowski, Rajendra D. Badgaiyan, Abdalla Bowirrat, Albert Pinhasov, et al.

    Exercise promotes health and wellness, including its operation as a protective factor against a variety of psychological, neurological, and chronic diseases. Selenium and its biomarker, selenoprotein P (SEPP1), have been implicated in health, including cancer prevention, neurological function, and dopamine signaling. SEPP1 blood serum levels were compared with a one-way ANOVA between sedentary (SED), moderately exercised (MOD) [10 m/min starting at 10 min, increasing to 60 min], and high-intensity interval training (HIIT) exercised rats [30 min in intervals of 2-min followed by a 1-min break, speed progressively increased from 10 to 21 m/min]. HIIT rats showed significantly higher serum SEPP1 concentrations compared to MOD and SED. More specifically, HIIT exercise showed an 84% increase in SEPP1 levels compared to sedentary controls. MOD rats had greater serum SEPP1 concentrations compared to SED, a 33% increase. The results indicated that increased exercise intensity increases SEPP1 levels. Exercise-induced increases in SEPP1 may indicate an adaptive response to the heightened oxidative stress. Previous studies found a significant increase in dopamine D2 receptor (D2R) binding in these same rats, suggesting a potential association between SEPP1 and dopamine signaling during exercise. Modulating antioxidants like SEPP1 through personalized therapies, including exercise, has broad implications for health, disease, and addiction.


  • Open Access

    Fatty Acid-Binding Protein 5 Gene Deletion Enhances Nicotine-Conditioned Place Preference: Illuminating the Putative Gateway Mechanisms

    by Nicole Roeder, Brittany Richardson, Abrianna Mihalkovic, Samantha Penman, Olivia White, John Hamilton, Ashim Gupta, Kenneth Blum, Mark S. Gold, Panayotis K. Thanos

    Emerging evidence indicates that the endogenous cannabinoid system modulates the behavioral and physiological effects of nicotine. Fatty acid-binding proteins (FABPs) are among the primary intracellular trafficking mechanisms of endogenous cannabinoids, such as anandamide. To this end, changes in FABP expression may similarly impact the behavioral manifestations associated with nicotine, particularly its addictive properties. FABP5+/+ and FABP5−/− mice were tested for nicotine-conditioned place preference (CPP) at two different doses (0.1 or 0.5 mg/kg). The nicotine-paired chamber was assigned as their least preferred chamber during preconditioning. Following 8 days of conditioning, the mice were injected with either nicotine or saline. The mice were allowed to access to all the chambers on the test day, and their times spent in the drug chamber on the preconditioning versus the test days were used to examine the drug preference score. The CPP results showed that the FABP5−/− mice displayed a higher place preference for 0.1 mg/kg nicotine than the FABP5+/+ mice, while no CPP difference was observed for 0.5 mg/kg nicotine between the genotypes. In conclusion, FABP5 plays an important role in regulating nicotine place preference. Further research is warranted to identify the precise mechanisms. The results suggest that dysregulated cannabinoid signaling may impact nicotine-seeking behavior.


  • Open Access

    Effects of Δ9-Tetrahydrocannibinol (THC) on Obesity at Different Stages of Life: A Literature Review

    by Nathan Fearby, Samantha Penman, Panayotis Thanos

    The Cannabis sativa plant has historically been used for both recreational and medical purposes. With the recent surge in recreational use of cannabis among adolescents and adults in particular, there is an increased obligation to determine the short- and long-term effects that consuming this plant may have on several aspects of the human psyche and body. The goal of this article was to examine the negative effects of obesity, and how the use of Δ9-tetrahydrocannibinol (THC) or cannabidiol (CBD) can impact rates of this global pandemic at different timepoints of life. Conflicting studies have been reported between adult and adolescents, as there are reports of THC use leading to increased weight due to elevated appetite and consumption of food, while others observed a decrease in overall body weight due to the regulation of omega-6/omega-3 endocannabinoid precursors and a decrease in energy expenditure. Studies supported a positive correlation between prenatal cannabis use and obesity rates in the children as they matured. The data did not indicate a direct connection between prenatal THC levels in cannabis and obesity rates, but that this development may occur due to prenatal THC consumption leading to low birthweight, and subsequent obesity. There are few studies using animal models that directly measure the effects that prenatal THC administration on obesity risks among offspring. Thus, this is a critical area for future studies using a developmental framework to examine potential changes in risk across development.