Relationships Among Cognition, Emotion, and Motivation: Implications for Intervention and Neuroplasticity in Psychopathology.

Relationships among cognition, emotion, and motivation: implications for intervention and neuroplasticity in psychopathology.

Front Hum Neurosci. 2013; 7: 261
Crocker LD, Heller W, Warren SL, O’Hare AJ, Infantolino ZP, Miller GA

Emotion-cognition and motivation-cognition relationships and related brain mechanisms are receiving increasing attention in the clinical research literature as a means of understanding diverse types of psychopathology and improving biological and psychological treatments. This paper reviews and integrates some of the growing evidence for cognitive biases and deficits in depression and anxiety, how these disruptions interact with emotional and motivational processes, and what brain mechanisms appear to be involved. This integration sets the stage for understanding the role of neuroplasticity in implementing change in cognitive, emotional, and motivational processes in psychopathology as a function of intervention. HubMed – depression


Genetic and pharmacological manipulations of the serotonergic system in early life: neurodevelopmental underpinnings of autism-related behavior.

Front Cell Neurosci. 2013; 7: 72
Kinast K, Peeters D, Kolk SM, Schubert D, Homberg JR

Serotonin, in its function as neurotransmitter, is well-known for its role in depression, autism and other neuropsychiatric disorders, however, less known as a neurodevelopmental factor. The serotonergic system is one of the earliest to develop during embryogenesis and early changes in serotonin levels can have large consequences for the correct development of specific brain areas. The regulation and functioning of serotonin is influenced by genetic risk factors, such as the serotonin transporter polymorphism in humans. This polymorphism is associated with anxiety-related symptoms, changes in social behavior, and cortical gray and white matter changes also seen in patients suffering from autism spectrum disorders (ASD). The human polymorphism can be mimicked by the knockout of the serotonin transporter in rodents, which are as a model system therefore vital to explore the precise neurobiological mechanisms. Moreover, there are pharmacological challenges influencing serotonin in early life, like prenatal/neonatal exposure to selective serotonin reuptake inhibitors (SSRI) in depressed pregnant women. There is accumulating evidence that this dysregulation of serotonin during critical phases of brain development can lead to ASD-related symptoms in children, and reduced social behavior and increased anxiety in rodents. Furthermore, prenatal valproic acid (VPA) exposure, a mood stabilizing drug which is also thought to interfere with serotonin levels, has the potency to induce ASD-like symptoms and to affect the development of the serotonergic system. Here, we review and compare the neurodevelopmental and behavioral consequences of serotonin transporter gene variation, and prenatal SSRI and VPA exposure in the context of ASD. HubMed – depression


Effects of interactions between intestinal microbiota and intestinal macrophages on health.

Anticancer Res. 2013 Jul; 33(7): 2849-53
Nakata K, Yamamoto M, Inagawa H, Soma G

Macrophages reside in every tissue of the body and play an important role in maintaining homeostasis. The intestinal mucosa is the largest immune organ and harbors macrophages in abundance. Dysfunction of intestinal macrophages is characteristic of patients with certain inflammatory bowel diseases. Although intestinal macrophages exhibit hyporesponsiveness to foreign substances, including various bacterial products, their physiological functions are unknown, but may be related to the contribution of intestinal bacteria to the maintenance of various physiological functions of the host. Moreover, recent reports suggest that there are associations between intestinal microbiota and the onset of pathologies, such as diverse metabolic syndromes, depression, and cancer. Evidence indicates that the host’s immune response to intestinal microbiota may be etiologically-linked to these diseases; however, the mechanisms are poorly understood. In the present review, we discuss the possibility that intestinal microbiota influence health through the function of intestinal macrophages. HubMed – depression


Characterization of cardiac lesions in calves after ingestion of Japanese yew (Taxus cuspidata).

J Vet Diagn Invest. 2013 Jun 18;
Sula MJ, Morgan S, Bailey KL, Schumpert M, Njaa BL

Plants of the genus Taxus are common ornamental shrubs that contain cardiotoxic alkaloids. Gross lesions consistent with heart failure are frequently reported in fatal cases; however, microscopic lesions in the heart have not been well characterized. The current report describes 2 related outbreaks in which 7 of 30, 250-kg calves died after confirmed exposure to clippings of Japanese yew (Taxus cuspidata). Three calves died 24 hr after initial exposure, with no significant gross or histologic lesions. Leaves of the yew plant were identified within the rumen contents, and Taxus alkaloids were confirmed by gas chromatography-mass spectrometry. Following the initial diagnosis, the yew clippings were burned. Two days later, the remaining calves were reintroduced to the enclosure. Within 24 hr, 3 additional calves began to show clinical signs of depression (3/3) or labored breathing (1/3), and by the fourth day, these 3 calves and an additional calf were found dead. Partially burnt yew leaves were found during close inspection of the enclosure. Two of 3 calves submitted for necropsy were severely autolyzed; the third had pulmonary edema and mild fibrinous pleural effusion. Histologic lesions in the latter included multifocal cardiac myocyte hypereosinophilia, sarcolemma fragmentation, pyknosis, karyolysis, myocyte loss, and a mild interstitial lymphoplasmacytic infiltrate with edema. Moderate fibrinosuppurative interstitial pneumonia was the only other significant finding. Cardiac changes were attributed to damage from the initial exposure to Taxus 6 days prior to death. HubMed – depression