Grief, Growth, and the Plastic Brain

By  Latha Thimmappa

Have you ever caught the scent of a perfume and suddenly found yourself thinking of a particular person, place, or moment from years ago? Or heard a familiar song that instantly brought back memories you thought had long faded? Many of us have experienced these unexpected moments of recall. Emotional experiences often leave traces that feel remarkably enduring, resurfacing unexpectedly and with surprising intensity. Some memories linger long after the experiences themselves have passed, quietly shaping the way we think and feel.

Last winter, I spent a few days in a friend’s room. Our conversations began with careers, education, and research, but soon drifted toward the complexities of life, love, friendship, healing, and the grief of letting go. In many ways, we were circling the emotional complexity of human relationships. Those conversations lingered with me, leaving me with a question: why do some emotional bonds remain so vivid in our minds, making them so difficult to let go of?

After the end of a long-term relationship, many people find themselves suspended between grief and healing. Well-meaning advice often follows: give it time, stay positive, practice mindfulness, and return to familiar routines. Although these suggestions are often supported by research, they rarely explain the biological changes that may underlie their effects or why they become helpful over time. To understand why such advice can be effective, we need to look at how the brain adapts to emotional experiences over time.

Neuroplasticity: How Emotional Experiences Shape the Brain

The brain possesses an intrinsic ability to adapt in response to experience, injury, or emotional stress, a property known as neuroplasticity (Radulescu et al., 2021). At its core, neuroplasticity refers to the strengthening or weakening of neural connections as our experiences, thoughts, and emotions repeatedly activate brain circuits. Although often discussed in the context of learning and recovery, these same principles also influence how emotionally significant experiences become embedded in the brain- dictating how social bonds form, persist, and eventually change.

The Neurobiology of Social Bonding

Repeated interactions with the same person lead the brain to strengthen specific neural connections gradually (Bliss and Lømo, 1973; Munakata & Plaffly, 2004). This process involves coordinated physiological changes, including the release of oxytocin, which supports social bonding, alongside neurotransmitters such as dopamine and serotonin that contribute to reward processing, motivation, emotional regulation, and memory (Johnson and Young, 2015). Acetylcholine further supports attention and learning, helping emotional experiences become embedded over time. Together with psychological tendencies such as companionship, longing, and attachment, these processes consolidate emotional bonds. Structural and functional changes can be observed in brain regions involved in emotion and memory, including the amygdala and hippocampus (Kandel et al., 2021).

Bonding is also shaped by similarity and repeated co-activation. Individuals who share values, routines, or emotional patterns are more likely to interact frequently, strengthening the same neural circuits over time. This aligns with Hebb’s principle (Munakata & Pfaffly, 2004) – “neurons that fire together wire together”, illustrating how both social closeness and neural connectivity emerge through repetition. Together, these processes help explain how particular people become deeply embedded in the brain’s systems for reward, attachment, emotion, and memory. When such a bond is later disrupted, the sudden absence of the experiences that once activated these systems can contribute to the profound distress associated with grief (Johnson and Young, 2015; Kandel et al., 2021).

From repeated interaction to lasting neural change

As conversation, shared experiences, and emotional exchanges accumulate, they gradually reinforce the underlying neural circuits, making these pathways easier to activate and strengthening the brain’s representation of the relationship (Munakata & Pfaffly, 2004). In neuroscience, one of the best-studied mechanisms underlying this process is long-term potentiation (LTP), in which repeated activation of the same neural connections makes neuronal communication more efficient over time (Kandel et al., 2021). First demonstrated by Bliss and Lømo (1973) in the rabbit hippocampus, LTP provided one of the earliest cellular explanations for how experiences can leave lasting traces in the brain. In the context of social attachment, however, repeated interactions do more than simply strengthen neural connections. Over time, the brain develops a distinctive representation of a particular person, linking their sensory and emotional cues with reward and attachment systems. Through the coordinated actions of neurotransmitters and hormones such as dopamine and oxytocin, these processes help transform repeated social experiences into a selective and enduring bond (Johnson & Young, 2015).

Neural changes after a separation

When a relationship ends, the sudden absence of a partner can trigger a wave of profound distress. Individuals often experience heightened emotional sensitivity, sleep disturbances, and low mood (Cai, 2025). Research on social attachment suggests that the loss of a bonded partner can also affect stress-related hormonal systems and produce depressive-like responses, highlighting the biological impact of social loss (Johnson & Young, 2015). Changes in appetite and gastrointestinal function may also occur, reflecting the close communication between the brain and the digestive system during periods of emotional stress (Appleton, 2018).

At the neural level, this distress corresponds to a major shift: pathways that were once consistently activated by shared experiences are suddenly deprived of stimulation. Over time, the brain gradually remodels these networks, reducing the influence of pathways that are no longer reinforced while allowing new experiences to strengthen others. Memories are not erased, but the neural patterns associated with them can become less dominant, making the emotional intensity of those memories gradually fade (Kandel et al., 2021).

Imagine a well-worn footpath through a field. The more often it is used, the clearer it becomes. When it is no longer walked, the path doesn’t disappear overnight, but gradually becomes overgrown as new paths emerge elsewhere. Similarly, memories are not erased after a loss, but the neural pathways that once made them immediately and intensely accessible can become less dominant as the brain adapts to new experiences.
Understanding this adaptive nature of the brain provides a bridge to another important feature of neuroplasticity: the ability of memories themselves to change when they are recalled.

The malleability of recalled memories

When we grieve, memories of what we have lost do not simply disappear. They return repeatedly, in conversations, familiar places, photographs, songs, and unexpected moments of recall. Sometimes, revisiting these memories can briefly bring the original pain back with surprising intensity. Yet memory is not a fixed recording of the past. Each time a memory is retrieved, it briefly enters a more malleable state before being stored again, a process known as reconsolidation (Dudai, 2006). This means that recalling an emotional memory can create both vulnerability and opportunity. Memory may be reactivated with renewed emotional intensity, but it can also be updated in light of new experiences and perspectives.

The biological basis of this process was demonstrated in a landmark study by Nader et al. al (2000). In their experiments, rats first learned to associate a particular sound with a mild foot shock. When the memory was later reactivated by playing the sound again, the researchers temporarily blocked the biological processes needed to restabilize the memory. The previously learned fear response was lost, suggesting that the reactivated memory had become temporarily vulnerable to disruption before being restabilized. Although a laboratory’s fear memory in a rat is very different from the complex memories associated with human grief, the study provides an important biological insight: recalling a memory does not simply replay a fixed recording. Reactivation can briefly open the memory to change. This may help explain why the emotional intensity of grief can gradually change over time. Repeatedly ruminating on a loss can repeatedly reactivate painful memories, potentially reinforcing their emotional significance. Yet, the same malleability that makes memories vulnerable to renewed distress also creates the possibility of change. With time, new experiences, and supportive environments, memories of loss may gradually be integrated into a broader personal history rather than remaining permanently defined by their original emotional intensity.

The experiences that shape us are not erased, but neither are they permanently fixed. The brain’s capacity to revisit and update emotional memories offers one biological explanation for why healing, although often slow and nonlinear, remains possible.

BDNF and the biology of neural plasticity

Although healing is experienced emotionally, it is supported by biological processes unfolding quietly within the brain. One of the key molecules behind this remarkable adaptability is brain-derived neurotrophic factor (BDNF) (Mohandas et al., 2025), often described as the brain’s ‘fertilizer’. Just as fertilizer helps plants grow stronger roots and branches, BDNF helps neurons grow, strengthen their connections, and encourages the growth of new dendritic branches, the tree-like extensions that allow neurons to communicate with one another. The importance of BDNF is further reflected in depression research, where reduced BDNF levels are commonly observed. Some antidepressants, including selective serotonin reuptake inhibitors (SSRIs) (van der Meij et al., 2014), are thought to promote recovery partly by increasing BDNF-mediated plasticity, helping the brain strengthen and reorganize its neural connections. 

Together, these biological processes help explain how the brain adapts to emotional experiences. While they cannot fully capture the complexity of grief, they offer one window into how healing gradually becomes possible.

Beyond the wiring

The brain is not rigid; it remains plastic across the lifespan. As neural connections reorganize over time, emotions, perspectives, and ways of relating to others also evolve. This is evident when we compare how relationships and responsibilities are understood in childhood versus adulthood. What is often described as “maturity” reflects changes in underlying thought patterns, shaped, in part, by neuroplastic processes.

Neuroscience offers valuable insights into how the brain adapts to love, loss, and recovery, but these experiences are not defined by biology alone. While research helps explain the mechanisms and evidence behind emotional change, the course of a relationship is shaped by choices, shared experiences, individual needs, and timing. In this space between neural wiring and lived experience, the deeply human aspects of bonding and letting go continue to unfold.

Do you think understanding how the brain changes during grief can help people heal? Tell us in the comments!

What would you like to read about next? Let us know here!

~~~

Written by Latha Thimmappa

Illustrated by Ava Piper

Edited by Sneha Mathur, Tony Nguyen, Janie Oberhauser, Monserrat Orozco, and Rohma Syed

~~~

Become a Patron!

References:

Appleton J. (2018). The Gut-Brain Axis: Influence of Microbiota on Mood and Mental Health. Integrative Medicine: A Clinician’s Journal, 17(4):28–32. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6469458/

Bliss, T. V. P., & Lømo, T. (1973). Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path. The Journal of Physiology, 232(2), 331–356. https://doi.org/10.1113/jphysiol.1973.sp010273

Cai, S. (2025). Factors influencing post-breakup recovery: A review of relationship dynamics, individual differences, and therapeutic interventions. SHS Web of Conferences, 222, 02023. https://doi.org/10.1051/shsconf/202522202023

Dudai, Y. (2006). Reconsolidation: the advantage of being refocused. Current Opinion in Neurobiology, 16(2):174-178. https://doi.org/10.1016/j.conb.2006.03.010

Johnson, Z. V., & Young, L. J. (2015). Neurobiological mechanisms of social attachment and pair bonding. Current opinion in behavioral sciences, 3, 38–44. 10.1016/j.cobeha.2015.01.009

Kandel, E. R., Koester, J., Mack, S. H., & Siegelbaum, S. A. (Eds.). (2021). Principles of neural science (6th ed). McGraw Hill https://neurology.mhmedical.com/book.aspx?bookID=3024

Mohandas, K., Rishikesh, R., Balan, Y. M., Deepti, A., Hosseini, S., Korte, M., & Sasidharan, B. C. P. (2025). BDNF signaling in glutamatergic neurons during long-term potentiation (LTP): A spatio-temporal exploration of events. Molecular Neurobiology, 62(12), 16261–16279.https://doi.org/10.1007/s12035-025-05238-0

Munakata, Y., & Pfaffly, J. (2004). Hebbian learning and development. Developmental Science, 7(2), 141–148. https://doi.org/10.1111/j.1467-7687.2004.00331.x

Nader, K., Schafe, G. E., & LeDoux, J. E. (2000). Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval. Nature, 406(6797), 722–726. https://doi.org/10.1038/35021052

Radulescu, I., Dragoi, A. M., Trifu, S. C., & Cristea, M. B. (2021). Neuroplasticity and depression: Rewiring the brain’s networks through pharmacological therapy (Review). Experimental and Therapeutic Medicine, 22(4), 1131. https://doi.org/10.3892/etm.2021.10565

Van der Meij, A., Comijs, H. C., Dols, A., Janzing, J. G. E., & Oude Voshaar, R. C. (2014). BDNF in late-life depression: Effect of SSRI usage and interaction with childhood abuse. Psychoneuroendocrinology, 43, 81–89. https://doi.org/10.1016/j.psyneuen.2014.02.001