scholarly journals Electroconvulsive Therapy: The Role of Hippocampal Neurogenesis

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
T. Bolwig

During recent years magnetic (MRI) studies have pointed to a reduction in hippocampal volume in patients with severe depression. Volumetric changes reflect the actual number of days that individuals have been depressed (1). These findings have heightened interest in studying hippocampal structure and function in experimental animals, especially during and after electroconvulsive seizures -the most powerful of antidepressant therapies (2). Both before and after 2000, with the earliest report on hippocampal neurogenesis following seizures, findings of gliogenesis and synaptogenesis have been reported (3). During the last decade further studies of neurotropic factors have supported ideas of the role of neuroplasticity related to ECT in humans (4). All antidepressant medications, but not antipsychotics, have a similar, but weaker effect on hippocampal neurogenesis. We hypothesize that an induction of neurotropic factors leading to hippocampal neurogenesis may play a major role for the action of ECT (5).

2020 ◽  
Author(s):  
Joshua Hendrikse ◽  
Yann Chye ◽  
Sarah Thompson ◽  
Nigel C. Rogasch ◽  
Chao Suo ◽  
...  

AbstractEngaging in regular exercise has numerous benefits for brain health. In particular, a number of studies have associated exercise with improvements to the structure and function of the hippocampus, especially in older adults. This region plays a critical role in memory function, and is altered in a number of psychiatric disorders associated with memory impairments (e.g. depression and schizophrenia), as well as healthy ageing. Thus, exercise may provide an effective method of enhancing / ameliorating hippocampal integrity; however, an improved understanding of exercise-related effects in young to middle-aged adults is required. We assessed the effects of regular exercise and cardiorespiratory fitness on hippocampal structure and function in young to middle-aged adults. We recruited a sample of 40 healthy adults, comprised of individuals who self-reported as engaging in high (regular exercisers) or low (sedentary) levels of physical activity (PA) according to World Health Organisation guidelines (high PA n=20; low PA n=20). A multi-modal assessment of hippocampal structure and function was conducted using structural magnetic resonance imaging (sMRI), magnetic resonance (MR) spectroscopy, and hippocampal-dependent memory tasks. We observed evidence of increased N-acetyl-aspartate (NAA) concentration and associative memory performance in high PA individuals. However, no differences in hippocampal volume or pattern separation capacity were observed between groups. We found that cardiorespiratory fitness was positively associated with (left, right, and bilateral) hippocampal volume, NAA concentration, and pattern separation, but not associative memory. Therefore, we provide evidence that engaging in higher levels of exercise has demonstrable benefits for hippocampal integrity and function. Given that young and middle-aged adults are overrepresented in the diagnosis of psychiatric illnesses which affect hippocampal integrity (e.g. depression and schizophrenia), it is possible that exercise may provide a low-risk, effective method of remediating this dysfunction.


Brain ◽  
2019 ◽  
Vol 142 (9) ◽  
pp. 2670-2687 ◽  
Author(s):  
Lorenzo Caciagli ◽  
Britta Wandschneider ◽  
Fenglai Xiao ◽  
Christian Vollmar ◽  
Maria Centeno ◽  
...  

Abstract Juvenile myoclonic epilepsy is the most common genetic generalized epilepsy syndrome, characterized by a complex polygenetic aetiology. Structural and functional MRI studies demonstrated mesial or lateral frontal cortical derangements and impaired fronto-cortico-subcortical connectivity in patients and their unaffected siblings. The presence of hippocampal abnormalities and associated memory deficits is controversial, and functional MRI studies in juvenile myoclonic epilepsy have not tested hippocampal activation. In this observational study, we implemented multi-modal MRI and neuropsychological data to investigate hippocampal structure and function in 37 patients with juvenile myoclonic epilepsy, 16 unaffected siblings and 20 healthy controls, comparable for age, gender, handedness and hemispheric dominance as assessed with language laterality indices. Automated hippocampal volumetry was complemented by validated qualitative and quantitative morphological criteria to detect hippocampal malrotation, assumed to represent a neurodevelopmental marker. Neuropsychological measures of verbal and visuo-spatial learning and an event-related verbal and visual memory functional MRI paradigm addressed mesiotemporal function. We detected a reduction of mean left hippocampal volume in patients and their siblings compared with controls (P < 0.01). Unilateral or bilateral hippocampal malrotation was identified in 51% of patients and 50% of siblings, against 15% of controls (P < 0.05). For bilateral hippocampi, quantitative markers of verticalization had significantly larger values in patients and siblings compared with controls (P < 0.05). In the patient subgroup, there was no relationship between structural measures and age at disease onset or degree of seizure control. No overt impairment of verbal and visual memory was identified with neuropsychological tests. Functional mapping highlighted atypical patterns of hippocampal activation, pointing to abnormal recruitment during verbal encoding in patients and their siblings [P < 0.05, familywise error (FWE)-corrected]. Subgroup analyses indicated distinct profiles of hypoactivation along the hippocampal long axis in juvenile myoclonic epilepsy patients with and without malrotation; patients with malrotation also exhibited reduced frontal recruitment for verbal memory, and more pronounced left posterior hippocampal involvement for visual memory. Linear models across the entire study cohort indicated significant associations between morphological markers of hippocampal positioning and hippocampal activation for verbal items (all P < 0.05, FWE-corrected). We demonstrate abnormalities of hippocampal volume, shape and positioning in patients with juvenile myoclonic epilepsy and their siblings, which are associated with reorganization of function and imply an underlying neurodevelopmental mechanism with expression during the prenatal stage. Co-segregation of abnormal hippocampal morphology in patients and their siblings is suggestive of a genetic imaging phenotype, independent of disease activity, and can be construed as a novel endophenotype of juvenile myoclonic epilepsy.


2020 ◽  
Vol 118 (3) ◽  
pp. 258a
Author(s):  
Laszlo Csernoch ◽  
Mónika Gönczi ◽  
Zsolt Ráduly ◽  
László Szabó ◽  
Nóra Dobrosi ◽  
...  

2021 ◽  
Vol 9 (1) ◽  
pp. 148
Author(s):  
Marius Bredon ◽  
Elisabeth Depuydt ◽  
Lucas Brisson ◽  
Laurent Moulin ◽  
Ciriac Charles ◽  
...  

The crucial role of microbes in the evolution, development, health, and ecological interactions of multicellular organisms is now widely recognized in the holobiont concept. However, the structure and stability of microbiota are highly dependent on abiotic and biotic factors, especially in the gut, which can be colonized by transient bacteria depending on the host’s diet. We studied these impacts by manipulating the digestive microbiota of the detritivore Armadillidium vulgare and analyzing the consequences on its structure and function. Hosts were exposed to initial starvation and then were fed diets that varied the different components of lignocellulose. A total of 72 digestive microbiota were analyzed according to the type of the diet (standard or enriched in cellulose, lignin, or hemicellulose) and the period following dysbiosis. The results showed that microbiota from the hepatopancreas were very stable and resilient, while the most diverse and labile over time were found in the hindgut. Dysbiosis and selective diets may have affected the host fitness by altering the structure of the microbiota and its predicted functions. Overall, these modifications can therefore have effects not only on the holobiont, but also on the “eco-holobiont” conceptualization of macroorganisms.


Author(s):  
Rachel L. Leon ◽  
Imran N. Mir ◽  
Christina L. Herrera ◽  
Kavita Sharma ◽  
Catherine Y. Spong ◽  
...  

Abstract Children with congenital heart disease (CHD) are living longer due to effective medical and surgical management. However, the majority have neurodevelopmental delays or disorders. The role of the placenta in fetal brain development is unclear and is the focus of an emerging field known as neuroplacentology. In this review, we summarize neurodevelopmental outcomes in CHD and their brain imaging correlates both in utero and postnatally. We review differences in the structure and function of the placenta in pregnancies complicated by fetal CHD and introduce the concept of a placental inefficiency phenotype that occurs in severe forms of fetal CHD, characterized by a myriad of pathologies. We propose that in CHD placental dysfunction contributes to decreased fetal cerebral oxygen delivery resulting in poor brain growth, brain abnormalities, and impaired neurodevelopment. We conclude the review with key areas for future research in neuroplacentology in the fetal CHD population, including (1) differences in structure and function of the CHD placenta, (2) modifiable and nonmodifiable factors that impact the hemodynamic balance between placental and cerebral circulations, (3) interventions to improve placental function and protect brain development in utero, and (4) the role of genetic and epigenetic influences on the placenta–heart–brain connection. Impact Neuroplacentology seeks to understand placental connections to fetal brain development. In fetuses with CHD, brain growth abnormalities begin in utero. Placental microstructure as well as perfusion and function are abnormal in fetal CHD.


Life ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 727
Author(s):  
Natalia Słabiak-Błaż ◽  
Grzegorz Piecha

The role of endogenous mammalian cardiotonic steroids (CTS) in the physiology and pathophysiology of the cardiovascular system and the kidneys has interested researchers for more than 20 years. Cardiotonic steroids extracted from toads or plants, such as digitalis, have been used to treat heart disease since ancient times. CTS, also called endogenous digitalis-like factors, take part in the regulation of blood pressure and sodium homeostasis through their effects on the transport enzyme called sodium–potassium adenosine triphosphatase (Na/K-ATPase) in renal and cardiovascular tissue. In recent years, there has been increasing evidence showing deleterious effects of CTS on the structure and function of the heart, vasculature and kidneys. Understanding the role of CTS may be useful in the development of potential new therapeutic strategies.


2006 ◽  
Vol 34 (5) ◽  
pp. 863-867 ◽  
Author(s):  
S. Mizielinska ◽  
S. Greenwood ◽  
C.N. Connolly

Maintaining the correct balance in neuronal activation is of paramount importance to normal brain function. Imbalances due to changes in excitation or inhibition can lead to a variety of disorders ranging from the clinically extreme (e.g. epilepsy) to the more subtle (e.g. anxiety). In the brain, the most common inhibitory synapses are regulated by GABAA (γ-aminobutyric acid type A) receptors, a role commensurate with their importance as therapeutic targets. Remarkably, we still know relatively little about GABAA receptor biogenesis. Receptors are constructed as pentameric ion channels, with α and β subunits being the minimal requirement, and the incorporation of a γ subunit being necessary for benzodiazepine modulation and synaptic targeting. Insights have been provided by the discovery of several specific assembly signals within different GABAA receptor subunits. Moreover, a number of recent studies on GABAA receptor mutations associated with epilepsy have further enhanced our understanding of GABAA receptor biogenesis, structure and function.


Sign in / Sign up

Export Citation Format

Share Document