Psychology > Faculty > Giuseppe Cataldo
Giuseppe Cataldo, PhD
Basic Information
Title: Assistant Professor
Area: Behavioral Neuroscience
PhD: CUNY
Email: gcataldo@qc.cuny.edu
Office: SB A346
Lab(phone):
Web:
Biography
Research Interests
My lab’s primary area of research focuses on the neural mechanisms and modulation of hyperalgesia and chronic pain. We use a variety of rodent models to investigate peripheral and central mechanisms that account for pain and hypersensitivity to mechanical and thermal stimuli following injury or disease. Our general approach is to examine behavioral measures of pain and hyperalgesia and correlate them to electrophysiological responses of single, identified peripheral, spinal and supraspinal neurons in vivo using the identical protocol and stimuli as used in the behavioral studies.
Current Research: Mechanisms of bivalent analgesic compounds in the treatment of cancer pain.
Pain is among the most common symptoms in patients diagnosed with cancer. While opioids are the mainstay for chronic cancer pain, they are associated with many serious side effects including tolerance, constipation, sedation, addiction, and respiratory depression-associated death. Thus, there is a requisite need to develop potent analgesics for cancer pain that are devoid of these side effects. Cisplatin and other widely employed platinum-based anticancer agents produce chemotherapy-induced peripheral neuropathy (CIPN) that often results in pain and hyperalgesia that are difficult to manage. Given my previous experience with bivalent ligands in the treatment of sickle cell disease, we investigated the efficacy of bivalent ligands for the treatment of pain arising from CIPN. It was found that MCC22 consisting of mu opioid receptor (MOR) agonist and chemokine receptor 5 (CCR5) antagonist, potently decreased CIPN hyperalgesia with a concomitant decreased inflammatory response by microglia in the spinal cord. Unlike morphine, MCC22 given daily for nine days did not exhibit tolerance to its analgesic effect and its characteristic antihyperalgesic activity was fully retained even in morphine-tolerant mice while not altering motor function or exhibiting rewarding properties. MMG22, another bivalent compound containing a MOR agonist, and a metabotropic glutamate receptor-5 antagonist tethered by a 22-atom spacer, also potently decreased CIPN pain without tolerance. Given the exceptional potency of MCC22 and MMG22 without common side effects associated with opioids, bivalent analgesics have the potential to vastly improve management of chronic pain.
Through my lab, my hope is to create a core pain research group as the foundation to bring together researchers, students and the broader community towards the shared goal of reducing the burden of pain through increased collaboration in research and education.
Selected Publications:
Selected References:
1. Cataldo, G., Rajput, S., Gupta, K. and Simone, D.A. (2015). Sensitization of nociceptive spinal neurons contributes to pain in a transgenic model of sickle cell disease. Pain, 156(4):722-730. PMID: 25630029. Received Most Cited Paper Award in PAIN for 2015.
2. Cataldo G, Lunzer MM, Olson JK, Akgun E, Belcher JD, Vercellotti GM, Portoghese PS, Simone DA. (2018). Bivalent ligand MCC22 potently attenuates nociception in a murine model of sickle cell disease. Pain, 159(7):1382-1391. PMID: 29578946.
3. (2019). The bivalent ligand MCC22 potently attenuates hyperalgesia in a mouse model of cisplatin-evoked neuropathic pain without tolerance or reward. Neuropharmacology, 158:107598. PMID: 30970233.
4. (2023) MMG22 potently blocks hyperalgesia in cisplatin-treated mice. Neuroscience, 516:54-61. PMID: 36805004
5. (2024). Opioids, Stress and Addiction: From Stress-Induced Analgesia to Opioid Heterodimers with Extraordinary Analgesic Efficacy and Without the Side Effects of Traditional Opioids. Addiction Neuroscience, 12:10016