Shared effects of electroconvulsive shocks and ketamine on neuroplasticity: A systematic review of animal models of depression.
Jesca E De Jager, Rutger Boesjes, Gijs H J Roelandt, Ilektra Koliaki, Iris E C Sommer, Robert A Schoevers, Jasper O Nuninga
Neuroscience and biobehavioral reviews September 1, 2024 DOI: 10.1016/j.neubiorev.2024.105796 via PubMed
Summary
AI-generated from the abstractElectroconvulsive shocks (ECS) and ketamine are fast-acting antidepressant treatments whose shared neurobiological mechanisms are explored in this systematic review of animal models of depression. Both interventions consistently increase hippocampal neurogenesis and brain-derived neurotrophic factor (BDNF) levels. They also positively affect glutamatergic neurotransmission, astrocyte and neuronal morphology, synaptic density, vasculature, and functional plasticity. Restoration of neuroplasticity may be a common mechanism underlying their antidepressant efficacy. Fewer studies have examined these processes after ECS. Understanding these shared fundamental mechanisms could help develop novel therapeutic approaches for severe depression.
Study at a glance
| Characteristics | Systematic review Peer reviewed |
|---|---|
| Population | Animal models of depression |
| Interventions | Electroconvulsive shocks Ketamine |
| Topics | Depression Ketamine Neuroplasticity |
| Keywords | Electroconvulsive shocks Ltp/ltd Antidepressants Electroconvulsive therapy Glutamate receptors |
| Citations | 13 |
| Key finding | Hippocampal neurogenesis and BDNF levels are consistently increased after both ECS and ketamine, and both interventions positively affect glutamatergic neurotransmission, astrocyte and neuronal morphology, synaptic density, vasculature, and functional plasticity. |
Abstract
Electroconvulsive shocks (ECS) and ketamine are antidepressant treatments with a relatively fast onset of therapeutic effects compared to conventional medication and psychotherapy. While the exact neurobiological mechanisms underlying the antidepressant response of ECS and ketamine are unknown, both interventions are associated with neuroplasticity. Restoration of neuroplasticity may be a shared mechanism underlying the antidepressant efficacy of these interventions. In this systematic review, literature of animal models of depression is summarized to examine the possible role of neuroplasticity in ECS and ketamine on a molecular, neuronal, synaptic and functional level, and specifically to what extent these mechanisms are shared between both interventions. The results highlight that hippocampal neurogenesis and brain-derived neurotrophic factor (BDNF) levels are consistently increased after ECS and ketamine. Moreover, both interventions positively affect glutamatergic neurotransmission, astrocyte and neuronal morphology, synaptic density, vasculature and functional plasticity. However, a small number of studies investigated these processes after ECS. Understanding the shared fundamental mechanisms of fast-acting antidepressants can contribute to the development of novel therapeutic approaches for patients with severe depression.