Peripartum buprenorphine and oxycodone exposure impair maternal behavior and increase neuroinflammation in new mother rats.

7 % of pregnant people use opioids. Opioid use during pregnancy can negatively impact maternal and offspring health. Medications for opioid use disorder (MOUD), commonly buprenorphine, are the recommended treatment for opioid use disorder during pregnancy to prevent cycles of withdrawal and relapse.

The transition to motherhood: linking hormones, brain and behaviour.

We are witnessing a stark increase in scientific interest in the neurobiological processes associated with pregnancy and maternity. Convergent evidence suggests that around the time of labour, first-time mothers experience a specific pattern of neuroanatomical changes that are associated with maternal behaviour. Here we provide an overview of the human neurobiological adaptations of motherhood, focusing on the interplay between pregnancy-related steroid and peptide hormones, and neuroplasticity in the brain.

Microglia depletion facilitates the display of maternal behavior and alters activation of the maternal brain network in nulliparous female rats.

The peripartum period is accompanied by peripheral immune alterations to promote a successful pregnancy. We and others have also demonstrated significant neuroimmune changes that emerge during late pregnancy and persist postpartum, most prominently decreased microglia numbers within limbic brain regions. Here we hypothesized that microglial downregulation is important for the onset and display of maternal behavior.

Multiparity Differentially Affects Specific Aspects of the Acute Neuroinflammatory Response to Traumatic Brain Injury in Female Mice.

Pregnancy is associated with profound acute and long-term physiological changes, but the effects of such changes on brain injury outcomes are unclear. Here, we examined the effects of previous pregnancy and maternal experience (parity) on acute neuroinflammatory responses to lateral fluid percussion injury (FPI), a well-defined experimental traumatic brain injury (TBI) paradigm. Multiparous (2-3 pregnancies and motherhood experiences) and age-matched nulliparous (no previous pregnancy or motherhood experience) female mice received either FPI or sham injury and were euthanized 3 days post-injury (DPI).

GABA System Modifications During Periods of Hormonal Flux Across the Female Lifespan.

The female lifespan is marked by periods of dramatic hormonal fluctuation. Changes in the ovarian hormones estradiol and progesterone, in addition to the progesterone metabolite allopregnanolone, are among the most significant and have been shown to have widespread effects on the brain. This review summarizes current understanding of alterations that occur within the GABA system during the major hormonal transition periods of puberty, the ovarian cycle, pregnancy and the postpartum period, as well as reproductive aging.

Immune System Alterations and Postpartum Mental Illness: Evidence From Basic and Clinical Research.

The postpartum period is a time associated with high rates of depression and anxiety as well as greater risk for psychosis in some women. A growing number of studies point to aberrations in immune system function as contributing to postpartum mental illness. Here we review evidence from both clinical and animal models suggesting an immune component to postpartum depression, postpartum anxiety, and postpartum psychosis.

Less can be more: Fine tuning the maternal brain.

PAWLUSKI, J.L., Hoekzema, E.

GABA in the medial prefrontal cortex regulates anxiety-like behavior during the postpartum period.

The postpartum period is commonly accompanied by emotional changes, which for many new mothers includes a reduction in anxiety. Previous research in rodents has shown that the postpartum attenuation in anxiety is dependent on offspring contact and has further implicated enhanced GABAergic neurotransmission as an underlying mechanism. However, the specific brain regions where GABA acts to regulate the offspring-induced reduction in postpartum anxiety requires further investigation.

Pregnancy, postpartum and parity: Resilience and vulnerability in brain health and disease.

Risk and resilience in brain health and disease can be influenced by a variety of factors. While there is a growing appreciation to consider sex as one of these factors, far less attention has been paid to sex-specific variables that may differentially impact females such as pregnancy and reproductive history. In this review, we focus on nervous system disorders which show a female bias and for which there is data from basic research and clinical studies pointing to modification in disease risk and progression during pregnancy, postpartum and/or as a result of parity: multiple sclerosis (MS), depression, stroke, and Alzheimer's disease (AD).

Sex differences in the effects of early life stress exposure on mast cells in the developing rat brain.

Early life stress leads to long lasting effects on behavior. Neuroimmune cells have been implicated as key mediators of experience-induced changes in brain and behavioral development, in that they are highly responsive to stress. Mast cells are one such type of neuroimmune cell, but little is known about their role in brain development or following early life stress.

The long and short term effects of motherhood on the brain.

Becoming a mother is associated with dramatic changes in physiology, endocrinology, immune function, and behaviour that begins during pregnancy and persists into the postpartum. Evidence also suggests that motherhood is accompanied by long-term changes in brain function. In this review, we summarize the short (pregnancy and postpartum) and long-term (beyond the postpartum and into middle age) effects of pregnancy and motherhood on cognition, neuroplasticity, and neuroimmune signalling.

The maternal reward system in postpartum depression.

The experience of motherhood is most often emotionally positive and rewarding, but for many new mothers suffering from postpartum depression (PPD), this is not the case. Preclinical and clinical research has sought to uncover brain changes underlying PPD in order to gain a better understanding of how this disorder develops. This review focuses on the mesolimbic dopamine system, particularly the ventral tegmental area-nucleus accumbens pathway which has been implicated in the regulation of critical functions disrupted in PPD including mood, motivation, and mothering.

Oxytocin in the medial prefrontal cortex attenuates anxiety: Anatomical and receptor specificity and mechanism of action.

Numerous studies in animals and humans have established that oxytocin (OT) reduces anxiety. In rats, the prelimbic (PL) subregion of the medial prefrontal cortex (mPFC) is among the brain areas implicated in the anxiolytic actions of OT. However, questions remain about the anatomical and receptor specificity of OT and its mechanism of action.

The influence of offspring, parity, and oxytocin on cognitive flexibility during the postpartum period.

Pregnancy and the postpartum period are times of profound behavioral change including alterations in cognitive function. This has been most often studied using hippocampal-dependent tasks assessing spatial learning and memory. However, less is known about the cognitive effects of motherhood for tasks that rely on areas other than the hippocampus.

A survey of neuroimmune changes in pregnant and postpartum female rats.

During pregnancy and the postpartum period, the adult female brain is remarkably plastic exhibiting modifications of neurons, astrocytes and oligodendrocytes. However, little is known about how microglia, the brain's innate immune cells, are altered during this time. In the current studies, microglial density, number and morphological phenotype were analyzed within multiple regions of the maternal brain that are known to show neural plasticity during the peripartum period and/or regulate peripartum behavioral changes.

The birth of new neurons in the maternal brain: Hormonal regulation and functional implications.

The maternal brain is remarkably plastic and exhibits multifaceted neural modifications. Neurogenesis has emerged as one of the mechanisms by which the maternal brain exhibits plasticity. This review highlights what is currently known about peripartum-associated changes in adult neurogenesis and the underlying hormonal mechanisms.

The effects of gestational stress and Selective Serotonin reuptake inhibitor antidepressant treatment on structural plasticity in the postpartum brain--A translational model for postpartum depression.

This article is part of a Special Issue "Parental Care". Postpartum depression (PPD) is a common complication following childbirth experienced by one in every five new mothers. Although the neural basis of PPD remains unknown, previous research in rats has shown that gestational stress, a risk factor for PPD, induces depressive-like behavior during the postpartum period.

Elevated levels of kynurenic acid during gestation produce neurochemical, morphological, and cognitive deficits in adulthood: implications for schizophrenia.

The levels of kynurenic acid (KYNA), an endogenous negative modulator of alpha7 nicotinic acetylcholine receptors (α7nAChRs), are elevated in the brains of patients with schizophrenia (SZ). We reported that increases of brain KYNA in rats, through dietary exposure to its precursor kynurenine from embryonic day (ED)15 to postnatal day (PD) 21, result in neurochemical and cognitive deficits in adulthood. The present experiments focused on the effects of prenatal exposure to elevated kynurenine on measures of prefrontal excitability known to be impaired in SZ.

Gestational stress induces persistent depressive-like behavior and structural modifications within the postpartum nucleus accumbens.

Postpartum depression (PPD) is a common complication following childbirth experienced by one in every five new mothers. Pregnancy stress enhances vulnerability to PPD and has also been shown to increase depressive-like behavior in postpartum rats. Thus, gestational stress may be an important translational risk factor that can be used to investigate the neurobiological mechanisms underlying PPD.