Lucy G Anderson

All Publications

• Early life adversity increases striatal dopamine D1 receptor density and promotes social alcohol drinking in mice, especially males. Translational psychiatry Anderson, L. G., Tischer, A. E., Bock, R., Michaelides, M., Alvarez, V. A. 2026; 16 (1)

  Abstract

  The brain's reward-processing circuitry remains sensitive to experience throughout early life and into adulthood, allowing individuals to adapt to their unique environments. Adverse experiences early in life can increase vulnerability to substance use disorders, likely through alterations to this circuitry. Yet, the precise neurobiological mechanisms by which early life adversity acts are incompletely characterized. In this study, we used a limited bedding and nesting (LBN) paradigm as a translationally relevant model of early life adversity in isogenic C57BL/6J mice. After LBN-rearing, we assessed the lasting behavioral and neurobiological impacts of this experience in adulthood. In robust sample sizes, our results validated previous findings of increased risk avoidance, enhanced acute locomotor response to alcohol, and greater voluntary alcohol drinking in socially-housed LBN-reared mice, especially males. Further, using autoradiography, we found LBN-reared mice had increased striatal D1-like receptor binding, skewing D1- to D2-like receptor balance relative to cross-fostered controls. However, after voluntary alcohol drinking, we found a strong downregulation in D1-like, and some D2-like, receptor binding, negating pre-existing differences in striatal dopamine receptor binding. We posit that via both transcriptional and post-transcriptional mechanisms, LBN-rearing upregulates striatal D1-receptor density and alters risk avoidance and acute alcohol stimulation to promote alcohol drinking among adversity-exposed mice. Together, these findings reveal specific neurobiological mechanisms that promote alcohol consumption following early life adversity and suggest complex interactions between early life adversity, sex-related factors, and dopamine receptor regulation in contributing to alcohol use disorder (AUD) vulnerability.

  View details for DOI 10.1038/s41398-026-04033-2

  View details for PubMedID 41986313

  View details for PubMedCentralID PMC13194699

• Preexisting risk-avoidance and enhanced alcohol relief are driven by imbalance of the striatal dopamine receptors in mice. Nature communications Bocarsly, M. E., Shaw, M. J., Ventriglia, E., Anderson, L. G., Goldbach, H. C., Teresi, C. E., Bravo, M., Bock, R., Hong, P., Kwon, H. B., Khawaja, I. M., Raman, R., Murray, E. M., Bonaventura, J., Burke, D. A., Michaelides, M., Alvarez, V. A. 2024; 15 (1): 9093

  Abstract

  Alcohol use disorder (AUD) is frequently comorbid with anxiety disorders, yet whether alcohol abuse precedes or follows the expression of anxiety remains unclear. Rodents offer control over the first drink, an advantage when testing the causal link between anxiety and AUD. Here, we utilized a risk-avoidance task to determine anxiety-like behaviors before and after alcohol exposure. We found that alcohol's anxiolytic efficacy varied among inbred mice and mice with high risk-avoidance showed heightened alcohol relief. While dopamine D1 receptors in the striatum are required for alcohol's relief, their levels alone were not correlated with relief. Rather, the ratio between striatal D1 and D2 receptors was a determinant factor for risk-avoidance and alcohol relief. We show that increasing striatal D1 to D2 receptor ratio was sufficient to promote risk-avoidance and enhance alcohol relief, even at initial exposure. Mice with high D1 to D2 receptor ratio were more prone to continue drinking despite adverse effects, a hallmark of AUD. These findings suggest that an anxiety phenotype may be a predisposing factor for AUD.

  View details for DOI 10.1038/s41467-024-53414-y

  View details for PubMedID 39438478

  View details for PubMedCentralID PMC11496688

• Memory deficits and hippocampal cytokine expression in a rat model of ADHD. Brain, behavior, & immunity - health Anderson, L. G., Vogiatzoglou, E., Tang, S., Luiz, S., Duque, T., Ghaly, J. P., Schwartzer, J. J., Hales, J. B., Sabariego, M. 2024; 35: 100700

  Abstract

  Attention-deficit/hyperactivity disorder (ADHD) is a complex behavioral disorder characterized by hyperactivity, impulsivity, inattention, and deficits in working memory and time perception. While animal models have advanced our neurobiological understanding of this condition, there are limited and inconsistent data on working and elapsed time memory function. Inflammatory signaling has been identified as a key factor in memory and cognitive impairments, but its role in ADHD remains unclear. Additionally, the disproportionate investigation of male subjects in ADHD research has contributed to a poor understanding of the disorder in females. This study sought to investigate the potential connections between memory, neuroimmunology, and ADHD in both male and female animals. Specifically, we utilized the spontaneously hypertensive rat (SHR), one of the most extensively studied animal models of ADHD. Compared to their control, the Wistar-Kyoto (WKY) rat, male SHR are reported to exhibit several behavioral phenotypes associated with ADHD, including hyperactivity, impulsivity, and poor sustained attention, along with impairments in learning and memory. As the hippocampus is a key brain region for learning and memory, we examined the behavior of male and female SHR and WKY rats in two hippocampal-dependent memory tasks. Our findings revealed that SHR have delay-dependent working memory deficits that were similar to, albeit less severe than, those seen in hippocampal-lesioned rats. We also observed impairments in elapsed time processing in female SHR, particularly in the discrimination of longer time durations. To investigate the impact of inflammatory signaling on memory in these rats, we analyzed the levels of several cytokines in the dorsal and ventral hippocampus of SHR and WKY. Although we found some sex and genotype differences, concentrations were generally similar between groups. Taken together, our results indicate that SHR exhibit deficits in spatial working memory and memory for elapsed time, as well as some differences in hippocampal cytokine concentrations. These findings contribute to a better understanding of the neurobiological basis of ADHD in both sexes and may inform future research aimed at developing effective treatments for the disorder. Nonetheless, the potential mediating role of neuroinflammation in the memory symptomatology of SHR requires further investigation.

  View details for DOI 10.1016/j.bbih.2023.100700

  View details for PubMedID 38107021

  View details for PubMedCentralID PMC10724493

• Musical groove shapes children's free dancing DEVELOPMENTAL SCIENCE Kragness, H. E., Anderson, L., Chow, E., Schmuckler, M., Cirelli, L. K. 2023; 26 (1): e13249

  Abstract

  The drive to move to music is evident across a variety of contexts, from the simple urge to tap our toe to a song on the radio, to massive crowds dancing in time at a rock concert. Though seemingly effortless, beat synchronization is difficult to master and children are often poor beat synchronizers. Nevertheless, auditory-motor integration is fundamental for many daily processes, such as speech. A topic that has been relatively understudied concerns how stimulus properties affect young children's movement in responses to auditory stimuli. In the present study, we examined how musical groove (adult-rated desire to move) affected 3.0- to 6.9-year-old children's free dancing in the comfort of their home (n = 78). In the high groove conditions, children danced more and with more energy compared to the low groove conditions. Moreover, in the high groove condition, children's movement tempos corresponded better with the tempos of the music. Results point to early childhood sensitivity to the musical features that motivate adults to move to music. High groove music may therefore prove especially effective at facilitating early auditory-motor integration. A video abstract of this article can be viewed at https://youtu.be/vli0-6N12Ts.

  View details for DOI 10.1111/desc.13249

  View details for Web of Science ID 000762848600001

  View details for PubMedID 35175668

• Medial entorhinal cortex lesions produce delay-dependent disruptions in memory for elapsed time. Neurobiology of learning and memory Vo, A., Tabrizi, N. S., Hunt, T., Cayanan, K., Chitale, S., Anderson, L. G., Tenney, S., White, A. O., Sabariego, M., Hales, J. B. 2021; 185: 107507

  Abstract

  Our memory for time is a fundamental ability that we use to judge the duration of events, put our experiences into a temporal context, and decide when to initiate actions. The medial entorhinal cortex (MEC), with its direct projections to the hippocampus, has been proposed to be the key source of temporal information for hippocampal time cells. However, the behavioral relevance of such temporal firing patterns remains unclear, as most of the paradigms used for the study of temporal processing and time cells are either spatial tasks or tasks for which MEC function is not required. In this study, we asked whether the MEC is necessary for rats to perform a time duration discrimination task (TDD), in which rats were trained to discriminate between 10-s and 20-s delay intervals. After reaching a 90% performance criterion, the rats were assigned to receive an excitotoxic MEC-lesion or sham-lesion surgery. We found that after recovering from surgery, rats with MEC lesions were impaired on the TDD task in comparison to rats with sham lesions, failing to return to criterion performance. Their impairment, however, was specific to the longer, 20-s delay trials. These results indicate that time processing is dependent on MEC neural computations only for delays that exceed 10 s, perhaps because long-term memory resources are needed to keep track of longer time intervals.

  View details for DOI 10.1016/j.nlm.2021.107507

  View details for PubMedID 34474155