17 träffar

En viktig gen har identifierats som hjälper till genom att facilitera kommunikation mellan neuroner

The gene is synaptotagmin 7 (syt7 for short), a calcium sensor that dynamically increases neurotransmitter release; each release serves to strengthen communication between neurons for about a second. These swift releases are thought to be critical for the brain’s ability to perform computations involved in short-term memory, spatial navigation and sensory perception.

“We really think one of the most important things the brain can do is change the strength of connections between neurons,” Jackman said. “Now that we have a tool to selectively turn off facilitation, we can test some long-held beliefs about its importance for thinking and working memory.”

Motståndskraft mot stress, vad är det och vart kommer det ifrån?

Nature skrev:Confronted with a life-threatening situation, hormones and neurotransmitters prep us for action. Specific stress hormones — cortisol in primates, corticosterone in most rodents — are released, some of which surge across the blood–brain barrier. Stress gets everywhere: all our cells host receptors for the hormone. “Every brain area has something happen to it,” says Kaufer. The human brain has two types of receptor for cortisol. One has a six to tenfold higher affinity for the molecule than the other, and so is activated earlier, by smaller amounts of cortisol.

The hippocampus (which is pivotal for memory) and the amygdala (the centre for emotions) contain lots of the high-affinity receptors, and are, therefore, activated by slight rises in the hormone. The frontal lobe, which is involved in executive planning and control, has only the low-affinity receptor, and is activated later, after the tide has risen. And, as Lupien and colleagues found, both memory formation and recall in adults can be influenced by cortisol1.

The existence of two receptor types means that response to stress is not linear. “The relationship between circulating stress hormone and memory is an inverted U-shape function,” Lupien explains. “Up to a certain level, stress hormones are good for your memory” — when the cortisol binds only to the high-affinity receptors, the ability to lay down and retrieve memory is enhanced. When the low-affinity receptors are activated, the relationship enters the right-hand side of the U-shape and the response shifts, she adds.

The duration of stress is also important. A transient bout of stress causes a proliferation of neural stem cells and a spike in numbers of new neurons, which take at least two weeks to mature. The brain seems to be preparing itself in case a second stressor comes calling. Chronic stress is not so beneficial. It slashes investment in new neurons, prunes the tree-like shape of existing ones, and suppresses new connections.

If stress hormones remain elevated for months or years, they can stimulate physiological changes: the hippocampus shrinks and the amygdala grows, for example. Eventually, the complex feedback system that suppresses the excess secretion of cortisol is disturbed. Once this happens, the capacity to discriminate between threat levels falls away. Either everything seems threatening (anxiety) or else nothing does (depression or burnout).

Nature skrev:Old ideas that certain individuals have an inherent 'hardiness' or an innate ability to bounce back from severe stress have fallen by the wayside. Instead, resilience and our response to trauma are recognized as being more dynamic, changing throughout life. It's a complicated milieu, but one of the main ways that stress marks the brain is through epigenetics. This does not change genes, but it can change their expression by attaching methyl groups to DNA or associated proteins.

Nature skrev:As with memory, the way that sociability changes with stress is not linear. Kaufer's lab found that rats exposed to moderate stress — in this case, being immobilized in a bag — displayed more positive social behaviour, such as huddling, resource sharing and reduced aggression4. The researchers also saw an increase in the prosocial hormone oxytocin. But if the immobilized rats were exposed to fox odour, the addition of this high-level-stress inducer caused them to lose all pro-social behaviours. Oxytocin plummeted, as did its receptors. “This is really interesting because it can start to explain the social withdrawal that you can see in some psychopathologies like PTSD and depression,” Kaufer says.

Neurobiologisk analys av olika psykossjukdomar

Vad gör egentligen D2-receptorer?

Onddruid skrev:Hittade en väldigt rolig text som använder en studie på möss för att förklara lite av the basics om gruppen D2-receptorer. Väldigt läsvärt och kanske förklarar för en del av er kunskapstörstande till exempel varför man kan bli så hungrig av antipsykotisk medicin i början av behandlingen.

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Vad gör egentligen D2-receptorer?

Bipolär sjukdom en del av ett "schizofrenispektrum"?

Ny roll för dopamin i sociala beteenden hos möss

Dynamisk reglering hos astrocyter i hjärnan kan ge nya mål för behandlingar i framtiden

Astrocytes are star-shaped cells in our brain that surround brain neurons, and neural circuits, protecting them from injury and enabling them to function properly – in essence, one of their main roles is to ‘baby-sit’ neurons. Our brain contains billions of cells, each of which need to communicate between each other in order to function properly. This communication is highly dependent on the behaviour of astrocytes. Until now, the mechanisms that create and maintain differences among astrocytes, and allow them to fulfill specialized roles, has remained poorly understood.

“It was believed that astrocytes acquired their properties during the development of the brain and then they were hardwired in their roles,” says senior study’s author Dr. Keith Murai, director of the Centre for Research in Neuroscience at the RI-MUHC, associate professor of the Department of Neurology and Neurosurgery at McGill University. “We have now discovered that astrocytes are actually incredibly flexible and potentially modifiable, which enables them to improve brain function or restore lost potential caused by disease.”

Hjärnstrukturförändringar till följd av farmakologisk behandling vid bipolär sjukdom

MRI studies comparing patients with bipolar disorder and healthy volunteers have demonstrated subtle grey matter volume deficits in patients, especially in brain regions underpinning mood regulation, as well as white matter disorganization in tracts interconnecting distributed brain regions. However studies tend to display considerable heterogeneity in their findings. In this review of in vivo neuroanatomical imaging studies of bipolar disorder to date, McDonald discusses the evidence that differential usage of psychopharmacological treatment is associated with alterations in neuroanatomy and thus an important source of this heterogeneity.

When greater weight is given to more powerful studies, with large numbers or with longitudinal design where intra-individual variation after initiation of medication is examined, substantial evidence emerges that medications used in bipolar disorder have a predominantly ameliorative affect on brain anatomy. This includes evidence that use of mood stabilizers such as lithium is associated with increased grey matter volume especially in brain regions underpinning mood regulation, as well as normalization of white matter disconnectivity.

Ny roll för dopamin i sociala beteenden hos möss

The study published today in Cell explores a group found in a particular area of the brain called the dorsal raphe nucleus.

The researchers used optogenetics to show that when this group of dopamine neurons is activated in mice this prompts the animal to interact with others. The finding could hold important clues about how isolation affects people. “Social interactions are no doubt important for our mental health and play a role in conditions such as schizophrenia and depression. Interestingly, these disorders are also associated with dysfunction of dopamine neurons,” said Ungless. “We’re less likely to be able to help with such conditions if we continue to assume that all dopamine neurons do the same thing.”

Motståndskraft mot ångest kopplat till uppmärksamhet på kroppsfunktioner

NeuroScienceNews: manliga och kvinnliga "hjärnor" en falsk dikotomi

Neurobiologisk analys av olika psykossjukdomar

Skillnader i den vita hjärnsubstansen mellen BPI och BPII?

In conclusion, we found that BD-II differs from BD-I in a localized region belonging to the right ILF while both BD-I and BD-II patients have widespread WM changes in the right cortico-spinal tract, left internal capsule and bilateral cerebellum in comparison to HC. Our data suggest that the loss of WM integrity in BD-II might be due to demyelination, whereas WM changes common to both BD subgroups could be attributable to axonal damage. Further longitudinal DTI studies focused on the different phases of the illness in balanced samples of BD-I and BD-II are essential to determine the association between the clinical course of the illness and its neurobiological underpinning.

Ett extremt low-tech test för ångest

Ett försök att undersöka kausalitet hos förändringar i hjärnan vid depression

Studie på hjärnceller från personer med bipolär sjukdom