Serotonin: Human social intimacy/connection and romance

Healthy adult volunteers, whose levels of serotonin activity had been lowered, rated couples in photos as being less intimate and less romantic than volunteers with normal serotonin activity.

The approach involved giving amino acid drinks to two groups of volunteers in order to manipulate blood concentrations of the amino acid tryptophan, which is a vital ingredient in the synthesis of serotonin. One group received drinks that contained tryptophan. The other group received drinks that did not contain tryptophan. They were then asked to make judgments about sets of photographs of couples. Differences in the judgments made by the two groups reflected changes in their serotonin activity. [...]

The results raise the possibility that lower serotonin activity in people with depression and other psychiatric conditions could contribute to changes in the way they perceive personal relationships, or even in their ability to maintain positive personal relationships.

“Although this is only a small study, the same patterns may well extend to the way we perceive our own relationships,” said Professor Rogers. (via.)

Brain-Derived Neurotrophic Factor & Serotonin Effects on Aging, Plasticity & More

BDNF and 5-HT: a dynamic duo in
age-related neuronal plasticity and
neurodegenerative disorders

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 [4]. 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 [5]. In rats that had previously acquired
spatial memory by extensive training, suppression of
BDNF expression impaired both reference and working
memory [5]. Another study showed that mice lacking one
copy of the BDNF gene exhibit impaired spatial learning
in the Morris water maze [6]. 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 [7]. [...]

[A]ctivation of 5-HT1A receptors can impair learning and
memory whereas 5-HT2A and 5-HT2C receptors facilitate
memory formation [10]. [...]

5-HT can
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. [...]

Conversely, BDNF
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 [14]. (via: pdf.)

Fewer 5HT2a (serotonin) receptors in pcc & acc in autistics

The posterior cingulate cortex (PCC) is activated when normal subjects see faces or hear voices of emotionally significant people in their lives; however, in autism the level of activation is impaired. [...]

The use of selective serotonin reuptake inhibitor (SSRI) medication has been shown to be successful in the treatment of autistic behaviors in some individuals. Serotonin (5-HT) has a role in neuronal development and has been extensively studied in autism with reports of excess 5-HT in the blood (hyperserotonemia) in some people with autism. [...]

The results show that there was a significant decrease in the density of one key type of serotonin receptor, the 5HT2A receptor, in the superficial cortical layers of the PCC in the adult autistic group when compared to age-matched controls. Similar results were found recently in the anterior cingulate cortex, an area involved in social-emotional processing. Evaluated together, these findings suggest that the 5-HT2a serotonin receptor decrease occurs in widespread cortical areas and may play a central role in some of the social deficits observed in autism. (via.)

Orchid: S-allele “Depression-Risk Gene” and Potential Cognitive/Social Benefits

The reclamation of the “depression gene” proceeds apace: In a paper titled “Looking on the Bright Side of Serotonin Transporter Gene Variation,” two researchers who helped establish the “depression risk-gene” view of depression assert quite strongly that the genetic variant in question — the s-allele of the serotonin transporter gene, HTTLPR — possess greater social sensitivity than people without this variant, and have some significant cognitive advantages as well. (via.)