Three to four years later, however, the researchers found an increase in gray matter in the posterior hippocampi, or the back part of the hippocampus, among the 39 trainees who ultimately qualified as taxi drivers. This change was not observed in the non-taxi drivers or trainees who had failed the exams. [...]
Qualified taxi drivers showed better memory performance for London-based information during the follow-up testing than controls or those who failed the test; however, they displayed “surprisingly poorer learning and memory for certain types of new visual information,” compared with controls, the researchers write online today in the journal Current Biology, “suggesting there might be a price to pay for the acquisition of their spatial knowledge.” (via.)
BDNF and 5-HT: a dynamic duo in
age-related neuronal plasticity and
Brain-derived neurotrophic factor (BDNF) and serotonin (5-hydroxytryptamine, 5-HT) are known to regulate synaptic plasticity, neurogenesis and neuronal survival in the adult brain. These two signals co-regulate one another such that 5-HT stimulates the expression of BDNF, and BDNF enhances the growth and survival of 5-HT neurons. Impaired 5-HT and BDNF signaling is central to depression and anxiety disorders, but could
also play important roles in the pathogenesis of several age-related disorders, including insulin resistance syndrome, Alzheimer’s disease and Huntington’s disease.
Enhancement of BDNF signaling may be a key mechanism whereby cognitive stimulation, exercise, dietary restriction and antidepressant drugs preserve brain function during aging. Behavioral and pharmacological manipulations that enhance 5-HT and BDNF signaling
could help promote healthy brain aging. [...]
By promoting neurogenesis,
synaptic plasticity and cell survival, BDNF plays a pivotal
role in the development and plasticity of the brain. During
development of the cerebral cortex and hippocampus,
BDNF induces the differentiation of neural stem cells into
neurons and promotes the survival of newly generated
neurons [1–3]. BDNF signaling at synapses enhances
long-term potentiation (LTP), a process of synaptic
strengthening associated with learning and memory;
the effect of BDNF on LTP is apparently mediated by
cAMP-response-element-binding protein (CREB), which
regulates the expression of genes involved in LTP and
memory formation . Levels of BDNF are increased in
the hippocampus of rats during and after performance
of a spatial learning task (a radial-arm maze), and both
acquisition and maintenance of spatial memory are
impaired when BDNF levels are decreased using antisense
methods . In rats that had previously acquired
spatial memory by extensive training, suppression of
BDNF expression impaired both reference and working
memory . Another study showed that mice lacking one
copy of the BDNF gene exhibit impaired spatial learning
in the Morris water maze . BDNF also plays an important
role in preventing death of neurons during development,
and promotes cell survival during stressful conditions
such as ischemia and trauma in the adult brain . [...]
[A]ctivation of 5-HT1A receptors can impair learning and
memory whereas 5-HT2A and 5-HT2C receptors facilitate
memory formation . [...]
also promote the survival of neurons in the adult brain, as
demonstrated by the abilities of a 5-HT receptor agonist
and SSRI to protect neurons against excitotoxic and
ischemic injury in animal models [12,13]. There are therefore
several commonalities of function in the CNS for
BDNF and 5-HT in terms of their effects on synaptic
plasticity, neurogenesis and cell survival. [...]
can stimulate the growth and sprouting of 5-HT neuron
axons innervating the cerebral cortex, thereby presumably
increasing the number of 5-HT synapses in this brain
region . (via: pdf.)
Abuse of anabolic androgenic steroids (AASs) is frequently associated with changes in mood, including depression. [...] We used male adult rats injected for 4 weeks with either nandrolone or stanozolol at daily doses (5 mg/kg, s.c.) that are considered equivalent to those abused by humans [...] AAS treatment reduced levels of brain-derived neurotrophic factor in the hippocampus and prefrontal cortex, reduced the expression of low-affinity glucocorticoid receptors in the hippocampus, and increased morning trough basal plasma corticosterone levels. All these changes have been related to the pathophysiology of major depressive disorder. Accordingly, rats treated with nandrolone or stanozolol showed an increased immobility time in the forced swim test, which is widely used for the screening of antidepressant drugs. All effects produced by AASs were prevented by co-administration with the classical antidepressant, chlorimipramine. (via.)
Just some loosely connected neuro-things I wanted to save somewhere.
- Notably without citation, Wikipedia claims BDNF is also expressed in the retina, the central nervous system, motor neurons, the kidneys, and the prostate (aside from just the hippocampus and cerebral cortex). (via.)
- BDNF knockingout in mice affects coordination, balance, hearing, taste, and breathing. “Knockout mice also exhibit cerebellar abnormalities and an increase in the number of sympathetic neurons.” (via.)
- BDNF is increased by prolonged seizures, and important to GABA pathways. (via.)
- Hypergraphia, a condition which afflicts individuals with a compulsive desire to write, is associated with temporal lobe epilepsy… and quite a few interesting characters have had it. (via.)
- Hyperlexia, the extreme variety of a compulsion to read, may be caused by a “cerebral infarction in the left anterior cingulate cortex and corpus callosum.” (via.)
- Temporal lobe epileptics are often hyposexual. (via.)
Certain personality traits heighten susceptibility to psychiatric disorders. Therefore a research team at Umeå University wanted to study whether this patient group had any susceptibility factors that could explain the development of their disorder. The patient group is distinguished by being anxious and pessimistic, with a weak sense of self, which is common in many psychiatric disorders. What was special about this group was that they stood out as persistent, ambitious, and pedantic individuals.
Being ambitious, fastidious, and overachieving also appears to make a person more prone to exhaustion syndrome. According to Agneta Sandström’s dissertation, individuals with exhaustion syndrome demonstrate impaired memory and attention capacity as well as reduced brain activity in parts of the frontal lobes. Regulation of the stress hormone cortisol is also impacted in the group, with altered sensitivity in the hypothalamic-pituitary-adrenal axis (HPA axis). [...]
The HPA axis in the patient group shows reduced sensitivity in the pituitary, with less secretion of adrenocorticotropic hormone (ACTH) following stimulation with corticotropin (CRH), as well as heightened sensitivity in the adrenal cortex, with increased release of cortisol in relation to the amount of ACTH secreted. There is also a difference in the diurnal rhythm of cortisol, with the patients presenting a flatter secretion curve than the other two groups. The researchers could not detect any reduction in the volume of the hippocampus in the patient group. The proportion of individuals with measurable levels of the pro-inflammatory cytokine interleukin 1 is higher in the patient group. (via.)
Researchers found that female Siberian hamsters exposed to dim light every night for eight weeks showed significant changes in a part of the brain called the hippocampus.
This is the first time researchers have found that light at night, by itself, may be linked to changes in the hippocampus.
These alterations may be a key reason why the researchers also found that the hamsters exposed to dim light at night showed more depressive symptoms when compared to hamsters in a standard light-dark cycle.
“Even dim light at night is sufficient to provoke depressive-like behaviors in hamsters, which may be explained by the changes we saw in their brains after eight weeks of exposure,” said Tracy Bedrosian, co-author of the study and doctoral student in neuroscience at Ohio State University. [...]
The results are significant because the night-time light used in the study was not bright: 5 lux, or the equivalent of having a television on in a darkened room, said Randy Nelson, co-author of the study and professor of neuroscience and psychology at Ohio State. (via.)
Exercise can ameliorate anxiety and depression-like behaviours induced by an adverse early-life environment by altering the chemical composition in the hippocampus – the part of the brain that regulates stress response, researchers from UNSW have found. [...]
“What’s exciting about this is that we are able to reverse a behavioural deficit that was caused by a traumatic event early in life, simply through exercise,” said Professor of Pharmacology Margaret Morris, who will present the findings this week at the International Congress of Obesity in Stockholm.
In the study, rats were divided into groups and either isolated from their mothers for controlled periods of time to induce stress or given normal maternal contact. Half were given access to a running wheel.
In addition to being more anxious, animals that were subjected to stress early in life had higher levels of stress hormones and fewer steroid receptors in the part of the brain controlling behaviour.
“Both the anxious behaviour and the levels of hormones in these rats were reversed with access to the exercise wheel,” Professor Morris said.
“We know that exercise can elevate mood, but here we are seeing chemical changes that may underpin this improvement. One of these is increases in brain-derived neurotrophic factor (BDNF), which helps nerve cells grow. (via.)
In other news…
Morphine found to decrease testosterone in the brain, as well as liver, and testis. Which is interesting in light of the fact that a stressed/anxious phenotype of rat would have fewer steroid receptors in their brain.