Arthur Charles Riegel

Interests

Research

Imagine/Optical: multiphoton microscopy, intracellular uncaging (flash photolysis);Electrophysiological/Biophysical: in vitro whole-cell patch (current/voltage) clamp, in vitro cell attached recordings (omega), in vivo & in vitro extracellular recordings, focal iontophoresis, pressure applications, focal electrical stimulation;Anatomy: ballistic labeling and dynamic imaging of dendritic spines with Dil/DiO;Behavioral models of drug abuse and addiction: rat i.v. drug (cocaine and heroine) self-administration, cue/stress reinstatement, i.v. cannulations & survival surgeries, intracranial injections, neurochemical lesions, and locomotor assays;Accepted models of chronic, peripheral pain: formalin (as a model of tissue destruction), complete freund's adjuvant (CFA, as a model of inflammatory pain or rheumatoid arthritis), and spared nerve injury (SNI; model of neuropathic pain)

Courses

Scholarly Contributions

Journals/Publications

• Barber, K. R., Vizcarra, V. S., Zilch, A., Majuta, L., Diezel, C. C., Culver, O. P., Hughes, B. W., Taniguchi, M., Streicher, J. M., Vanderah, T. W., & Riegel, A. C. (2023). The Role of Ryanodine Receptor 2 in Drug-Associated Learning. bioRxiv : the preprint server for biology.
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  Type-2 ryanodine receptor (RyR2) ion channels facilitate the release of Ca from stores and serve an important function in neuroplasticity. The role for RyR2 in hippocampal-dependent learning and memory is well established and chronic hyperphosphorylation of RyR2 (RyR2P) is associated with pathological calcium leakage and cognitive disorders, including Alzheimer's disease. By comparison, little is known about the role of RyR2 in the ventral medial prefrontal cortex (vmPFC) circuitry important for working memory, decision making, and reward seeking. Here, we evaluated the basal expression and localization of RyR2 and RyR2P in the vmPFC. Next, we employed an operant model of sucrose, cocaine, or morphine self-administration (SA) followed by a (reward-free) recall test, to reengage vmPFC neurons and reactivate reward-seeking and re-evaluated the expression and localization of RyR2 and RyR2P in vmPFC. Under basal conditions, RyR2 was expressed in pyramidal cells but not regularly detected in PV/SST interneurons. On the contrary, RyR2P was rarely observed in PFC somata and was restricted to a different subcompartment of the same neuron - the apical dendrites of layer-5 pyramidal cells. Chronic SA of drug (cocaine or morphine) and nondrug (sucrose) rewards produced comparable increases in RyR2 protein expression. However, recalling either drug reward impaired the usual localization of RyR2P in dendrites and markedly increased its expression in somata immunoreactive for Fos, a marker of highly activated neurons. These effects could not be explained by chronic stress or drug withdrawal and instead appeared to require a recall experience associated with prior drug SA. In addition to showing the differential distribution of RyR2/RyR2P and affirming the general role of vmPFC in reward learning, this study provides information on the propensity of addictive drugs to redistribute RyR2P ion channels in a neuronal population engaged in drug-seeking. Hence, focusing on the early impact of addictive drugs on RyR2 function may serve as a promising approach to finding a treatment for substance use disorders.
• Urena, E. S., Diezel, C. C., Serna, M., Hala'ufia, G., Majuta, L., Barber, K. R., Vanderah, T. W., & Riegel, A. C. (2023). K 7 Channel Opener Retigabine Reduces Self-Administration of Cocaine but Not Sucrose in Rats. bioRxiv : the preprint server for biology.
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  The increasing rates of drug misuse highlight the urgency of identifying improved therapeutics for treatment. Most drug-seeking behaviors that can be modeled in rodents utilize the repeated intravenous self-administration (SA) of drugs. Recent studies examining the mesolimbic pathway suggest that K 7/KCNQ channels may contribute in the transition from recreational to chronic drug use. However, to date, all such studies used noncontingent, experimenter-delivered drug model systems, and the extent to which this effect generalizes to rats trained to self-administer drug is not known. Here, we tested the ability of retigabine (ezogabine), a K 7 channel opener, to regulate instrumental behavior in male Sprague Dawley rats. We first validated the ability of retigabine to target experimenter-delivered cocaine in a CPP assay and found that retigabine reduced the acquisition of place preference. Next, we trained rats for cocaine-SA under a fixed-ratio or progressive-ratio reinforcement schedule and found that retigabine-pretreatment attenuated the self-administration of low to moderate doses of cocaine. This was not observed in parallel experiments, with rats self-administering sucrose, a natural reward. Compared to sucrose-SA, cocaine-SA was associated with reductions in the expression of the K 7.5 subunit in the nucleus accumbens, without alterations in K 7.2 and K 7.3. Therefore, these studies reveal a reward specific reduction in SA behavior considered relevant for the study of long-term compulsive-like behavior and supports the notion that K 7 is a potential therapeutic target for human psychiatric diseases with dysfunctional reward circuitry.
• Vizcarra, V. S., Barber, K. R., Franca-Solomon, G., Majuta, L., Smith, A., Langlais, P. R., Largent-Milnes, T. M., Vanderah, T. W., & Riegel, A. C. (2022). Targeting 5-HT receptors and Kv7 channels in PFC to attenuate chronic neuropathic pain in rats using a spared nerve injury model. Neuroscience letters, 789, 136864.
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  Chronic pain remains a disabling disease with limited therapeutic options. Pyramidal neurons in the prefrontal cortex (PFC) express excitatory G-coupled 5-HT receptors (5-HTR) and their effector system, the inhibitory Kv7 ion channel. While recent publications show these cells innervate brainstem regions important for regulating pain, the cellular mechanisms underlying the transition to chronic pain are not well understood. The present study examined whether local blockade of 5-HTR or enhanced Kv7 ion channel activity in the PFC would attenuate mechanical allodynia associated with spared nerve injury (SNI) in rats. Following SNI, we show that inhibition of PFC 5-HTRs with M100907 or opening of PFC Kv7 channels with retigabine reduced mechanical allodynia. Parallel proteomic and RNAScope experiments evaluated 5-HTR/Kv7 channel protein and mRNA. Our results support the role of 5-HTRs and Kv7 channels in the PFC in the maintenance of chronic pain.
• Vizcarra, V. S., Barber, K. R., Franca-Solomon, G., Majuta, L., Smith, A., Langlais, P. R., Milnes, T. M., Vanderah, T. W., & Riegel, A. C. (2022). Targeting 5-HT2A receptors and Kv7 channels in PFC to attenuate chronic neuropathic pain in rats using a spared nerve injury model.. Neuroscience Letters.
• Riegel, A. C., & French, E. (1997). Toluene alters rat A10 DA and non-DA neurons through a dose-dependent mechanism. NIDA monograph Series.
• Riegel, A. C., & French, E. (2001). The abused inhalant toluene has direct stimulatory effects on VTA dopamine (DA) and non-DA neurons in vitro. NIDA monograph Series.
• Buchta, W. C., Moutal, A., Hines, B., Garcia-Keller, C., Smith, A. C., Kalivas, P., Khanna, R., & Riegel, A. C. (2019). Dynamic CRMP2 Regulation of CaV2.2 in the Prefrontal Cortex Contributes to the Reinstatement of Cocaine Seeking. Molecular neurobiology, 57(1), 346-357.
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  Cocaine addiction remains a major health concern with limited effective treatment options. A better understanding of mechanisms underlying relapse may help inform the development of new pharmacotherapies. Emerging evidence suggests that collapsin response mediator protein 2 (CRMP2) regulates presynaptic excitatory neurotransmission and contributes to pathological changes during diseases, such as neuropathic pain and substance use disorders. We examined the role of CRMP2 and its interactions with a known binding partner, CaV2.2, in cocaine-seeking behavior. We employed the rodent self-administration model of relapse to drug seeking and focused on the prefrontal cortex (PFC) for its well-established role in reinstatement behaviors. Our results indicated that repeated cocaine self-administration resulted in a dynamic and persistent alteration in the PFC expression of CRMP2 and its binding partner, the CaV2.2 (N-type) voltage-gated calcium channel. Following cocaine self-administration and extinction training, the expression of both CRMP2 and CaV2.2 was reduced relative to yoked saline controls. By contrast, cued reinstatement potentiated CRMP2 expression and increased CaV2.2 expression above extinction levels. Lastly, we utilized the recently developed peptide myr-TAT-CBD3 to disrupt the interaction between CRMP2 and CaV2.2 in vivo. We assessed the reinstatement behavior after infusing this peptide directly into the medial PFC and found that it decreased cue-induced reinstatement of cocaine seeking. Taken together, these data suggest that neuroadaptations in the CRMP2/CaV2.2 signaling cascade in the PFC can facilitate drug-seeking behavior. Targeting such interactions has implications for the treatment of cocaine relapse behavior.
• Smith, A., Flohrschutz, A., Riegel, A., Largent-Milnes, T., & Vanderah, T. (2020). Functional Connectivity of Prelimic Prefrontal Cortex and Rostral Ventromedial Medulla for Descending Pain Modulation. The FASEB Journal, 34(S1), 1--1.
• Vanderah, T., Riegel, A., Flohrschutz, A., Smith, A., & Largent-Milnes, T. (2020). Functional Connectivity of Prelimic Prefrontal Cortex and Rostral Ventromedial Medulla for Descending Pain Modulation. The FASEB Journal, 34(S1), 1-1. doi:10.1096/fasebj.2020.34.s1.03633
• Mahler, S. V., Brodnik, Z. D., Cox, B. M., Buchta, W. C., Bentzley, B. S., Quintanilla, J., Cope, Z. A., Lin, E. C., Riedy, M. D., Scofield, M. D., Messinger, J., Ruiz, C. M., Riegel, A. C., España, R. A., & Aston-Jones, G. (2019). Chemogenetic Manipulations of Ventral Tegmental Area Dopamine Neurons Reveal Multifaceted Roles in Cocaine Abuse. The Journal of neuroscience : the official journal of the Society for Neuroscience, 39(3), 503-518.
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  Ventral tegmental area (VTA) dopamine (DA) neurons perform diverse functions in motivation and cognition, but their precise roles in addiction-related behaviors are still debated. Here, we targeted VTA DA neurons for bidirectional chemogenetic modulation during specific tests of cocaine reinforcement, demand, and relapse-related behaviors in male rats, querying the roles of DA neuron inhibitory and excitatory G-protein signaling in these processes. Designer receptor stimulation of G signaling, but not G signaling, in DA neurons enhanced cocaine seeking via functionally distinct projections to forebrain limbic regions. In contrast, engaging inhibitory G signaling in DA neurons blunted the reinforcing and priming effects of cocaine, reduced stress-potentiated reinstatement, and altered behavioral strategies for cocaine seeking and taking. Results demonstrate that DA neurons play several distinct roles in cocaine seeking, depending on behavioral context, G-protein-signaling cascades, and DA neuron efferent targets, highlighting their multifaceted roles in addiction. G-protein-coupled receptors are crucial modulators of ventral tegmental area (VTA) dopamine neuron activity, but how this metabotropic signaling impacts the complex roles of dopamine in reward and addiction is poorly understood. Here, we bidirectionally modulate dopamine neuron G-protein signaling with DREADDs (designer receptors exclusively activated by designer drugs) during a variety of cocaine-seeking behaviors, revealing nuanced, pathway-specific roles in cocaine reward, effortful seeking, and relapse-like behaviors. G and G stimulation activated dopamine neurons, but only G stimulation robustly enhanced cocaine seeking. G inhibitory signaling reduced some, but not all, types of cocaine seeking. Results show that VTA dopamine neurons modulate numerous distinct aspects of cocaine addiction- and relapse-related behaviors, and point to potential new approaches for intervening in these processes to treat addiction.
• Harlan, B. A., Becker, H. C., Woodward, J. J., & Riegel, A. C. (2018). Opposing actions of CRF-R1 and CB1 receptors on VTA-GABAergic plasticity following chronic exposure to ethanol. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 43(10), 2064-2074.
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  Dopamine neurons in the ventral tegmental area (VTA) influence learned behaviors and neuropsychiatric diseases including addiction. The stress peptide corticotrophin-releasing factor (CRF) contributes to relapse to drug and alcohol seeking following withdrawal, although the cellular actions are poorly understood. In this study, we show that presynaptic CRF type 1 receptors (CRF-R1) potentiate GABA release onto mouse VTA dopamine neurons via a PKC-Ca signaling mechanism. In naive animals, activation of CRF-R1 by bath application of CRF or ethanol enhanced GABA inhibitory postsynaptic currents (IPSCs). Following 3 days of withdrawal from four weekly cycles of chronic intermittent ethanol (CIE) vapor exposure, spontaneous IPSC frequency was enhanced while CRF and ethanol potentiation of IPSCs was intact. However, withdrawal for 3 weeks or more was associated with reduced spontaneous IPSC frequency and diminished CRF and ethanol responses. Long-term withdrawal was also accompanied by decreased sensitivity to the CB1 receptor agonist WIN55212 as well as greatly enhanced sensitivity to the CB1 antagonist AM251. Inclusion of BAPTA in the internal recording solution restored the responsiveness to CRF or ethanol and reduced the potentiating actions of AM251. Together, these data suggest that GABA inhibition of VTA dopamine neurons is regulated by presynaptic actions of CRF and endocannabinoids and that long-term withdrawal from CIE treatment enhances endocannabinoid-mediated inhibition, thereby suppressing CRF facilitation of GABA release. Such findings have implications for understanding the impact of chronic alcohol on stress-related, dopamine-mediated alcohol-seeking behaviors.
• Harlan, B., Becker, H., Woodward, J., & Riegel, A. (2018). The CRF-R1 regulation of VTA-GABAergic plasticity is suppressed by CB1 receptor inhibition following chronic exposure to ethanol. BioRxiv, 272997.
• Parrilla-Carrero, J., Buchta, W. C., Goswamee, P., Culver, O., McKendrick, G., Harlan, B., Moutal, A., Penrod, R., Lauer, A., Ramakrishnan, V., & others, . (2018). Restoration of Kv7 channel-mediated inhibition reduces cued-reinstatement of cocaine seeking. Journal of Neuroscience, 38(17), 4212--4229.
• Buchta, W. C., Mahler, S. V., Harlan, B., Aston-Jones, G. S., & Riegel, A. C. (2017). Dopamine terminals from the ventral tegmental area gate intrinsic inhibition in the prefrontal cortex. Physiological reports, 5(6), e13198.
• Buchta, W. C., Mahler, S. V., Harlan, B., Aston-Jones, G. S., & Riegel, A. C. (2017). Dopamine terminals from the ventral tegmental area gate intrinsic inhibition in the prefrontal cortex. Physiological reports, 5(6).
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  Spike frequency adaptation (SFA or accommodation) and calcium-activated potassium channels that underlie after-hyperpolarization potentials (AHP) regulate repetitive firing of neurons. Precisely how neuromodulators such as dopamine from the ventral tegmental area (VTA) regulate SFA and AHP (together referred to as ) in the prefrontal cortex (PFC) remains unclear. Using whole cell electrophysiology, we measured intrinsic inhibition in prelimbic (PL) layer 5 pyramidal cells of male adult rats. Results demonstrate that bath application of dopamine reduced intrinsic inhibition (EC: 25.0 mol/L). This dopamine action was facilitated by coapplication of cocaine (1 mol/L), a blocker of dopamine reuptake. To evaluate VTA dopamine terminals in PFC slices, we transfected VTA dopamine cells of rats in vivo with Cre-dependent AAVs to express channelrhodopsin-2 (ChR2) or designer receptors exclusively activated by designer drugs (DREADDS). In PFC slices from these animals, stimulation of VTA terminals with either blue light to activate ChR2 or bath application of clozapine-N-oxide (CNO) to activate Gq-DREADDs produced a similar reduction in intrinsic inhibition in PL neurons. Electrophysiological recordings from cells expressing retrograde fluorescent tracers showed that this plasticity occurs in PL neurons projecting to the accumbens core. Collectively, these data highlight an ability of VTA terminals to gate intrinsic inhibition in the PFC, and under appropriate circumstances, enhance PL neuronal firing. These cellular actions of dopamine may be important for dopamine-dependent behaviors involving cocaine and cue-reward associations within cortical-striatal circuits.
• Goswamee, P., Parrilla-Carrero, J., Buchta, W., Kalivas, P. W., & Riegel, A. C. (2017). Chronic Cocaine Self-Administration Potentiates the Dopamine-Induced Hyperexcitability Gated by Inhibition of KCNQ/Kv7 Channels. Biophysical Journal, 112(3), 445a.
• Buchta, W. C., & Riegel, A. C. (2015). Chronic cocaine disrupts mesocortical learning mechanisms. Brain research, 1628(Pt A), 88-103.
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  The addictive power of drugs of abuse such as cocaine comes from their ability to hijack natural reward and plasticity mechanisms mediated by dopamine signaling in the brain. Reward learning involves burst firing of midbrain dopamine neurons in response to rewards and cues predictive of reward. The resulting release of dopamine in terminal regions is thought to act as a teaching signaling to areas such as the prefrontal cortex and striatum. In this review, we posit that a pool of extrasynaptic dopaminergic D1-like receptors activated in response to dopamine neuron burst firing serve to enable synaptic plasticity in the prefrontal cortex in response to rewards and their cues. We propose that disruptions in these mechanisms following chronic cocaine use contribute to addiction pathology, in part due to the unique architecture of the mesocortical pathway. By blocking dopamine reuptake in the cortex, cocaine elevates dopamine signaling at these extrasynaptic receptors, prolonging D1-receptor activation and the subsequent activation of intracellular signaling cascades, and thus inducing long-lasting maladaptive plasticity. These cellular adaptations may account for many of the changes in cortical function observed in drug addicts, including an enduring vulnerability to relapse. Therefore, understanding and targeting these neuroadaptations may provide cognitive benefits and help prevent relapse in human drug addicts.
• Buchta, W. C., & Riegel, A. C. (2015). Chronic cocaine disrupts mesocortical learning mechanisms. Brain research, 1628, 88--103.
• Harlan, B., Wooodward, J., Becker, H., & Riegel, A. (2015). BLOCKADE OF CB1 RECEPTORS RESTORES THE PRESYNAPTIC REGULATION OF VTA-GABA SYNAPSES FOLLOWING CHRONIC EXPOSURE TO ETHANOL: 103. Alcoholism: Clinical & Experimental Research, 39.
• Williams, C. L., Buchta, W. C., & Riegel, A. C. (2014). CRF-R2 and the heterosynaptic regulation of VTA glutamate during reinstatement of cocaine seeking. The Journal of neuroscience : the official journal of the Society for Neuroscience, 34(31), 10402-14.
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  Stress can reinstate cocaine seeking through an interaction between the stress hormone corticotropin releasing factor (CRF) and glutamate release onto dopamine neurons in the ventral tegmental area (VTA). To better understand the underlying causes, synaptic mechanisms were investigated in brain slices from rats. In control tissue, EPSCs displayed concentration-dependent, bimodal responses to CRF potentiation at low concentrations (3-100 nm) and attenuation at higher concentrations (300 nm). EPSC potentiation and attenuation were mediated by CRF-R1 and CRF-R2 receptor subtypes, respectively, localized to presynaptic terminals. The CRF-R2 attenuation was blocked by the GABA-B receptor antagonist CGP55843. Additional recordings of GABA-A IPSCs showed CRF-R2 activation-facilitated presynaptic release of GABA, suggesting that CRF-R2 may regulate glutamate release via heterosynaptic facilitation of GABA synapses. After chronic cocaine self-administration and extinction training, the sensitivity of glutamate and GABA receptors was unchanged. However, the ability of CRF-R2 agonists to depress EPSCs and potentiate IPSCs was diminished. After yohimbine plus cue reinstatement, the actions of CRF-R2 on GABA and glutamate release were reversed. CRF-R2 activation increased EPSCs as a result of a reduction of tonic GABA-dependent inhibition. After reinstatement, application of the A1 adenosine antagonist 1,3-dipropyl-8-cyclopentylxanthine increased GABA tone to inhibit the CRF-R2 action. Blockade of GABA-B receptors prevented both the CRF-R2 increase in EPSCs and the attenuation produced by 1,3-dipropyl-8-cyclopentylxanthine. These studies demonstrate that presynaptic CRF-R1/R2 tightly regulate glutamate transmission in the VTA via a concerted, heterosynaptic manner that may become altered by stress-related pathologies, such as addiction.
• Deignan, J., Luj'an, R., Bond, C., Riegel, A., Watanabe, M., Williams, J. T., Maylie, J., & Adelman, J. P. (2012). SK2 and SK3 expression differentially affect firing frequency and precision in dopamine neurons. Neuroscience, 217, 67--76.
• Moussawi, K., Riegel, A., Nair, S., & Kalivas, P. W. (2011). Extracellular glutamate: functional compartments operate in different concentration ranges. Frontiers in systems neuroscience, 5, 94.
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  Extracellular glutamate of glial origin modulates glial and neuronal glutamate release and synaptic plasticity. Estimates of the tonic basal concentration of extracellular glutamate range over three orders of magnitude (0.02-20 μM) depending on the technology employed to make the measurement. Based upon binding constants for glutamate receptors and transporters, this range of concentrations translates into distinct physiological and pathophysiological roles for extracellular glutamate. Here we speculate that the difference in glutamate measurements can be explained if there is patterned membrane surface expression of glutamate release and transporter sites creating extracellular subcompartments that vary in glutamate concentration and are preferentially sampled by different technologies.
• Riegel, A. C., & Kalivas, P. W. (2010). Lack of inhibition leads to abuse. Nature, 463(7282), 743--744.
• Riegel, A. C., & Williams, J. T. (2008). CRF facilitates calcium release from intracellular stores in midbrain dopamine neurons. Neuron, 57(4), 559--570.
• Riegel, A. C., Zapata, A., Shippenberg, T. S., & French, E. D. (2007). The abused inhalant toluene increases dopamine release in the nucleus accumbens by directly stimulating ventral tegmental area neurons. Neuropsychopharmacology, 32(7), 1558--1569.
• Lupica, C., & Riegel, A. (2006). ACTIVITY-DEPENDENT ENDOCANNABINOID RELEASE FROM MIDBRAIN DA NEURONS: 44. Alcoholism: Clinical & Experimental Research, 30(6).
• Lupica, C. R., & Riegel, A. C. (2005). Endocannabinoid release from midbrain dopamine neurons: a potential substrate for cannabinoid receptor antagonist treatment of addiction. Neuropharmacology, 48(8), 1105--1116.
• Lupica, C. R., Riegel, A. C., & Hoffman, A. F. (2004). Marijuana and cannabinoid regulation of brain reward circuits. British journal of pharmacology, 143(2), 227--234.
• Riegel, A. C., & Lupica, C. R. (2004). Independent presynaptic and postsynaptic mechanisms regulate endocannabinoid signaling at multiple synapses in the ventral tegmental area. Journal of Neuroscience, 24(49), 11070--11078.
• Riegel, A. C., Ali, S. F., Torinese, S., & French, E. D. (2004). Repeated exposure to the abused inhalant toluene alters levels of neurotransmitters and generates peroxynitrite in nigrostriatal and mesolimbic nuclei in rat. Annals of the New York Academy of Sciences, 1025(1), 543--551.
• Hoffman, A. F., Riegel, A. C., & Lupica, C. R. (2003). Functional localization of cannabinoid receptors and endogenous cannabinoid production in distinct neuron populations of the hippocampus. European Journal of Neuroscience, 18(3), 524--534.
• Riegel, A. C., Ali, S. F., & French, E. D. (2003). Toluene-induced locomotor activity is blocked by 6-hydroxydopamine lesions of the nucleus accumbens and the mGluR2/3 agonist LY379268. Neuropsychopharmacology, 28(8), 1440--1447.
• Riegel, A. C., & French, E. D. (2002). Abused inhalants and central reward pathways: electrophysiological and behavioral studies in the rat. Annals of the New York Academy of Sciences, 965(1), 281--291.
• Riegel, A. C. (2001). The abused inhalant toluene is a potent activator of the rat mesolimbic dopamine system: Extracellular studies in brain slices with neurobehavioral correlates.
• Riegel, A. C., & French, E. D. (1999). Acute toluene induces biphasic changes in rat spontaneous locomotor activity which are blocked by remoxipride. Pharmacology Biochemistry and Behavior, 62(3), 399--402.
• Riegel, A. C., & French, E. D. (1999). An electrophysiological analysis of rat ventral tegmental dopamine neuronal activity during acute toluene exposure. Pharmacology & toxicology, 85(3), 37--43.
• Riegel, A. C., & French, E. D. (1999). The susceptibility of rat non-dopamine ventral tegmental neurones to inhibition during toluene exposure. Pharmacology & toxicology, 85(1), 44-6.
• Riegel, A. C., & French, E. D. (1999). The susceptibility of rat non-dopamine ventral tegmental neurones to inhibition during toluene exposure. Pharmacology & toxicology, 85(3), 44--46.

Proceedings Publications

• Harlan, B. J., Woodward, J. J., Becker, H. C., & Riegel, A. C. (2018). CHRONIC INTERMITTENT EXPOSURE TO ETHANOL CAUSES PERSISTENT CHANGES IN THE CB1 AND CRF REGULATION OF GABA RELEASE ONTO VTA DOPAMINE NEURONS. In ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH, 42.
• Gioia, D. A., Wayman, W. N., Xu, M., Riegel, A. C., Reichel, C. M., & Woodward, J. J. (2017). EFFECTS OF DRUGS OF ABUSE ON CHANNELRHODOPSIN-2 CURRENTS AND KINETICS. In ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH, 41.
• Lupica, C., Riegel, A., & Hoffman, A. (2004). Cellular substrates of Delta (9)-THC and endogenous cannabinoid effects on brain drug reward circuitry. In NEUROPSYCHOPHARMACOLOGY, 29.

Presentations

• Riegel, A. C. (2009). Max Planck Institute for Biophysical Chemistry, Göttingen Germany. “CRF regulates calcium release – implications for the excitability of dopamine neurons.”. Max Planck Institute for Biophysical Chemistry, Göttingen Germany.
• Riegel, A. C. (2022). Faculty Data Blitz, University of Arizona —Tucson Arizona  . Faculty Data Blitz, University of Arizona —Tucson Arizona.
• Riegel, A. C. (2020). Committee on Neuroscience Community Data Blitz, University of Arizona —Tucson . Committee on Neuroscience Community Data Blitz.
• Riegel, A. C. (2020). UBRP Conversations with Faculty Data Blitz, University of Arizona —Tucson Arizona  . UBRP Conversations with Faculty Data Blitz.
• Riegel, A. C. (2019). Committee on Neuroscience Community Data Blitz, University of Arizona —Tucson Arizona  . Committee on Neuroscience Community Data Blitz.
• Riegel, A. C. (2019). Department of Neuroscience, University of Arizona —Tucson Arizona  . Department of Neuroscience.
• Riegel, A. C. (2019). Graduate Interdisciplinary Program, University of Arizona —Tucson Arizona  . Graduate Interdisciplinary Program.
• Riegel, A. C. (2016). University of Puerto Rico, San Juan PR. University of Puerto Rico, San Juan PR.
• Riegel, A. C. (2016). University of Texas at San Antonio (UTSA), Neurosciences Institute—San Antonio Texas . University of Texas at San Antonio (UTSA), Neurosciences Institute.
• Riegel, A. C. (2015). Integrative Neuroscience Research Center, Marquette University—Milwaukee Wisconsin. Integrative Neuroscience Research Center, Marquette University.
• Riegel, A. C. (2014). Department of Pharmacology, University of Arizona —Tucson, Arizona . Department of Pharmacology.
• Riegel, A. C. (2014). International Narcotics Research Conference (INRC), Hot topics —Montreal Canada  . International Narcotics Research Conference (INRC), Hot topics.
• Riegel, A. C. (2013). Ernest Gallo Clinic and Research Center, UCSF —San Francisco California. Ernest Gallo Clinic and Research Center.
• Riegel, A. C., & Riegel, A. C. (2012). Center for Excellence in the Neurosciences, UNE—Biddeford & Portland, Maine. Center for Excellence in the Neurosciences.
• Riegel, A. C., & Riegel, A. C. (2012). Medical Science Training Program (MSTP) Seminar Series, MUSC —Charleston SC. Medical Science Training Program (MSTP) Seminar Series.
• Riegel, A. C. (2008). Symposia on CRF & Dopamine Neurons, 42^nd Winter Conference on Brain Research, “CRF effects on midbrain dopamine neurons – implications for psychostimulant actions.”. Symposia on CRF & Dopamine Neurons, 42nd Winter Conference on Brain Research.

Poster Presentations

• Riegel, A. C. (2021). Cue-induced recall for cocaine or morphine self-administration increases ryanodine 2 (RyR2) phosphorylation in the prefrontal cortex. Society for Neuroscience Annual Meeting. Chicago, IL..
• Riegel, A. C. (2021). RNAscope to Quantify Transcription of 5HT2A Receptor in Prefrontal Cortex of Rats with Spared Nerve Injury. Annual Biomedical Research Conference for Minority Students (ABRCMS).
• Riegel, A. C. (2021). Retigabine reduces the Self-administration of Cocaine but not Sucrose. Annual Biomedical Research Conference for Minority Students (ABRCMS).
• Riegel, A. C. (2022). RNAscope to Quantify Transcription of 5HT2A Receptor in Prefrontal Cortex of Rats with Spared Nerve Injury. Undergraduate Biology Research Program (UBRP) & MARC.
• Riegel, A. C. (2022). Retigabine Produces Dose-Dependent Changes in the Self- administration of Cocaine but not on Sucrose. . Undergraduate Biology Research Program (UBRP).
• Riegel, A. C. (2023). Characterizing the Role of RyR2 and its Phosphorylation in  Learning and Drug Relapse. Health Frontiers, Arizona Health Sciences.
• Riegel, A. C. (2023). The effects of Retigabine on Self-Administration of Fentanyl in Rats. Annual Biomedical Research Conference for Minority Students (ABRCMS).
• Riegel, A. C. (2024). CRISPR Knockout of RYR2 in the Prefrontal Cortex Potentiates Seeking Behavior in Rats with a History of Cocaine Self-administration. Molecular and Cellular Biology Program, University of Arizona.
• Bailes, C., Pavlinchak, B., Riegel, A. C., & William, B. (2014, Aug). Increased intracellular Ca2+ signaling in the prefrontal cortex contributes to cocaine sensitization. MUSC Research Day Meeting.
• Barber, K., Lopez, B., Culver, P., Majuta, L., Vizcarra, S., Parmarr, R., & Riegel, A. C. (2021, April). Exploring the Role of Ryanodine 2 (RyR2) Phosphorylation in Addictive Drugs. Discover BIO5 Research to Innovation Showcase 2021.
• Barber, K., Ochoa, R., Majuta, L., Aryeh, K., Vizcarra, S., & Riegel, A. C. (2020, August). Using immunohistochemistry to analyze CFOS and RYR2P coexpression in the infralimbic and prelimbic cortex of the medical prefontal cortex after acute morphine exposure. Annual Biomedical Research Conference for Minority Students (ABRCMS).
• Buchta, W., & Riegel, A. C. (2013, Aug). VTA Dopamine terminals regulate neuronal excitability in the PFC via inhibition of the slow afterhyperpolarization. MUSC Student Research Day.
• Buchta, W., & Riegel, A. C. (2014, Aug). Regulation of prefrontal cortex activity by VTA dopamine terminals following Chronic Cocaine Self-Administration & Cue-Reinstatement: an electrophysiological analysis using optogenetics & DREADDs. American College of Neuropsychopharmacology (ACNP).
• Buchta, W., & Riegel, A. C. (2014, Aug). Superactivation of dopamine-D1 receptor signaling in the prefrontal cortex following chronic cocaine self-administration. Gordon Conference on Synaptic Transmission.
• Buchta, W., & Riegel, A. C. (2014, Nov). Ventral tegmental area regulation of the prefrontal cortex is superactivated by chronic cocaine self-administration. Society for Neuroscience Meeting (Washington, DC).
• Buchta, W., & Riegel, A. C. (2015, Oct). Superactivation of dopamine-D1 receptor signaling in the prefrontal cortex following chronic cocaine self-administration. Society for Neuroscience Meeting (Chicago, IL).
• Buchta, W., Harlan, B., Kalivas, P., & Riegel, A. C. (2012, Aug). Chronic cocaine self-administration induces hyperexcitability in cortical neurons via cellular adaptations in KCNQ (Kv7) but not SK channels. Annual Meeting for the Society of Neuroscience.
• Buchta, W., Harlan, B., Kalivas, P., & Riegel, A. C. (2013, Aug). Cocaine potentiates dopamine regulation of calcium activated K+ channels in the prefrontal cortex. Annual Society for Neuroscience Scientific Meeting.
• Buchta, W., Harlan, B., Kalivas, P., & Riegel, A. C. (2013, Aug). Dopamine Signaling Regulates Spike-Frequency Adaptation in the Prefrontal Cortex. The Neuroscience Institute of the Medical University of South Carolina's 14th Annual Frontiers in Neuroscience Research Day.
• Buchta, W., Quattlebaum, A., Harlan, B., & Riegel, A. C. (2011, Aug). Plasticity of Prefrontal Cortex Pyramidal Neurons after Cocaine Self-Administration. Neuropalooza, MUSC.
• Butcha, W., Mahler, S., Aston-Jones, G., & Riegel, A. C. (2015, Aug). Mesocortical dopamine encodes cocaine cues after chronic cocaine self-administration via enduring inhibition of Kv7 channels. American College of Neuropsychopharmacology Conference.
• Feltenstein, M., Shippenburg, T., Zapata, A., See, R., & Riegel, A. C. (2010, Aug). Pain during heroin self-administration enhances relapse of heroin-seeking in rats. College on Problems of Drug Dependence.
• Goswamee, P., Parrilla-Carrero, J., Butcha, W., Kalivas, P., & Riegel, A. C. (2016, Aug). Chronic Cocaine Self-Administration Potentiates the Dopamine-induced Hyperexcitability by Inhibition of Kv7/KCNQ Channels. 2015 MUSC Research Day Meeting.
• Harlan, B., Buchta, W., Hughes, H., Shippenburg, T., & Riegel, A. C. (2012, Aug). dmPFC neurons as biomarkers to study the affective component of neuropathic pain. Annual Meeting for the Society of Neuroscience.
• Harlan, B., Griffin, W., Lopez, M., Becker, H., & Riegel, A. C. (2011, Aug). CRF Regulates GABA release onto Ventral Tegmental Area Dopamine Neurons: Persistent Cellular Adaptations During Protracted Withdrawal From Exposure to Chronic Intermittent Ethanol. Annual Meeting of Frontiers in Neuroscience.
• Harlan, B., Hughes, H., & Riegel, A. C. (2011, Aug). Annual Meeting of Frontiers in Neuroscience Chronic Cocaine Induces Lasting Changes in mGluR/sK Mediated Inhibitory Postsynaptic Currents in Midbrain Dopaminergic Neurons. Annual Meeting of Frontiers in Neuroscience.
• Harlan, B., Hughes, H., & Riegel, A. C. (2013, Aug). Intercellular Calcium Stores in PFC Pyramidal Neurons are Dysregulated by Neuropathic Pain. The Neuroscience Institute of the Medical University of South Carolina's 14th Annual Frontiers in Neuroscience Research Day.
• Harlan, B., Hughes, H., Buchta, W., Wang, R., Shippenburg, T., & Riegel, A. C. (2013, Aug). Cellular adaptations in dmPFC neurons: mechanisms underlying the affective component of neuropathic pain. American Pain Society's 32nd Annual Scientific Meeting.
• Harlan, B., Hughes, H., Buchta, W., Wang, R., Shippenburg, T., & Riegel, A. C. (2014, Aug). The Functional Rewiring of Cortical Synapses in a Translational Model of Neuropathic Pain. International Narcotics Research Conference.
• Harlan, B., Hughes, H., Wang, R., Shippenburg, T., & Riegel, A. C. (2011, Aug). Neuroplasticity of pyramidal neurons in the dmPFC following chronic neuropathic pain. Neuropalooza.
• Lopez, B., Millard, S., Barber, K., Majuta, L., Vizcarra, S., & Riegel, A. C. (2021, May). Targeted Analysis of Ryanodine Receptor 2 in the Prefrontal Cortex and Nuceleus Accumbens in Cocain-Seeking Rats. UArizona College of Medicine Research Day.
• McKendrick, G., Anderson, M., Parrilla-Carrero, J., Goswamee, P., & Riegel, A. C. (2016, Aug). Characterization of Circuit-specific Responses of Mesolimbic Dopamine Neuron Projections to Stress. Perry V. Halushka MUSC Research Day.
• Mustafa, S., Barber, K., Lopez, B., Parmar, R., Vizcarra, S., Aryeh, K., & Riegel, A. C. (2020, Aug). Targeting 5HT2AR to Attenuate Cocaine Related Behaviors. Annual Biomedical Research Conference for Minority Students (ABRCMS).
• Parrilla, J., Pavlinchak, B., Bailes, C., & Riegel, A. C. (2015, Aug). Disruption of mGluR/SK inhibition in VTA dopamine neurons by exposure to stress potentiates the responsiveness to cocaine. 2015 MUSC Research Day Meeting.
• Parrilla-Carrero, J., & Riegel, A. C. (2016, Aug). Relapse to cocaine seeking disrupts KCNQ channel inhibition in the prefrontal cortex. 2016 MUSC Research Day Meeting.
• Parrilla-Carrero, J., Goswamee, P., Bailes, C., Pavlinchak, B., & Riegel, A. C. (2016, Aug). Acute Stress Exposure Mediates Circuit-Specific, Neuroadaptations in Glutamate Inhibition in VTA Dopaminergic Neuron. Society for Neuroscience.
• Parrilla-Carrero, J., Goswamee, P., Butcha, W., & Riegel, A. C. (2017, Aug). Cocaine self-administration causes a persistent reduction of Kv7 channel mediate intrinsic inhibition in the prefrontal cortex. Society for Neuroscience.
• Potapenko, E., Bailes, C., & Riegel, A. C. (2014, Aug). Repeated Exposure to Cocaine or Environmental Stressor Unmasks SMOCs in VTA Dopamine Neurons. MUSC Research Day Meeting.
• Quaranto, N., Zapata, A., Shippenburg, T., & Riegel, A. C. (2009, Aug). Peripheral pain produces superactivates mesolimbic dopamine neurons. Frontiers in Neuroscience.
• Quattlebaum, A., & Riegel, A. C. (2011, Aug). Desensitization of Burst-Pause Firing Patterns in VTA Dopamine Neurons During Reinstatement to Cocaine-Seeking. Annual Meeting of Frontiers in Neuroscience.
• Riegel, A. C., & Butcha, W. (2015, Aug). Cocaine self-administration and cue-reinstatement disrupt Kv7 (KCNQ) channel inhibition in the prefrontal cortex. 2015 MUSC Research Day Meeting.
• Riegel, A. C., Pavlinchak, B., Bailes, C., & Buchta, W. (2015, Aug). Intracellular Ca2+ signaling in the prefrontal cortex regulates cocaine sensitization. SYNAPSE - University of North Carolina - Asheville, Reuter Center.
• Smith, A., Flohrschutz, A., Riegel, A. C., Largent-Milnes, T., & Vanderah, T. (2020, Aug). Functional Connectivity of Prelimbic Prefrontal Cortez and Rostral Ventromedial Medulla for Descending Pain Modulation. Experimental Biology.
• Vizcarra, V. S., Barber, K. R., Franca-Solomon, G., Smith-Flint, A., Majuta, L., Langlais, P. R., Milnes, T. M., Vanderah, T. W., & Riegel, A. C. (2021, November). Targeted manipulation of PFC 5HT2A receptors and KV7 channels attenuates chronic neuropathic pain in rats.. Society for Neuroscience.
• William, C., & Riegel, A. C. (2010, Aug). Stress, addiction, and relapse: the cellular circuitry underlying the stress regulation of brain reward pathways. College of Charleston (Charleston, SC).
• Williams, C., & Riegel, A. C. (2010, Aug). Cocaine self-administration dysregulates the actions of glutamate on VTA dopamine neurons. Frontiers in Neuroscience.
• Williams, C., & Riegel, A. C. (2010, Aug). Corticotrophin-Releasing Factor Reduces GABA Release onto Ventral Tegmental Area Dopamine Neurons: Neuroadaptations after chronic cocaine self-administration. The Annual Perry Halushka Research Conference.
• Williams, C., & Riegel, A. C. (2015, Aug). Changes in Kv7 channel inhibition after neuropathic pain. International Narcotics Research Conference (INRC).
• Harlan, B., Riegel, A., Hughes, H., Buchta, W., Wang, R., & Shippenberg, T. (2013). Cellular adaptations in dmPFC neurons: mechanisms underlying the affective component of neuropathic pain. The Journal of Pain.