Nature and Nurture

In chapter 11 of Animal Behavior, John Alcock postulates that the dichotomy of nature or nurture is a misconception. According to his view, the idea of a purely environmentally determined behavior makes no sense because ultimately,  in order for the environment to affect our behavior, there must be a change in our genetic material. Otherwise, what would the link between environment and our behavior be? Behavior has its substrates in our brain, so there must be a regulation of genes if we argue that the environment can affect our behavior.

He argues as well that not every environmental factor can affect our behavior. The reality is that we are sensitive to a specific range of stimuli. These environmental stimuli are the ones that we can detect using our sensory system. This idea implies that our genetic material “prepares” us to be shaped by certain environmental factors. The metamorphosis of bees is a clear example of this concept. Bees transition from being “nurses” (younger bees) to being “foragers” (older bees). Scientists discovered that nurse bees can be induced to become “foragers” if they are put in an environment where older foragers are absent. Later, it was discovered that the gene activity varies in the brains of nurse bees and foragers. Many of these genes were transcription factors, which code for proteins regulating the activity of other target genes.

Conversely, the higher the number of older foragers in a colony, the lower the number of young nurse bees that have an early transition into foragers. Scientists were puzzled by how the number of foragers in the environment could transform the behavior of younger bees. Eventually, it was discovered that foragers produce a chemical (ethyl oleate) that inhibits young bees from transitioning into foragers. Therefore, the more foragers in a colony, the less likely younger bees are to transition to foraging status because they are being inhibited by this chemical.

Alcock’s honey bee example shows that behavior, at least in this case, is not purely genetically determined because bees’ behavior is reshaped by the interaction of environmental chemicals and intrinsic genetic factors. It is important to notice that the genes that elicit the forager behavior in bees were activated only when the appropriate environmental factors were present. Gene Robinson summarized this idea by saying: “DNA is both inherited and environmentally responsive”.

In my opinion, this is an interesting concept, particularly coming from a school where I hear all the time that everything is a social construct. Is gender nothing but a purely environmentally determined behavior? What are the genetic factors that drive us here and there? The factors that make us respond in a way or another to our social experience? Will we ever find these neural substrates in our brain? What makes us female, male, or other? I share Alcock’s opinion and I think that we do not live in a mutually exclusive dichotomy of nature and nurture. Instead, we are the product of a beautiful balance of factors. Something unique that has come to be thanks to what we carry inside us and what we take from our environment. We are evolving all the time.

– H. C

Diálogo con Z sobre la distinción entre el deseo y el amor

– Z, algo extraño me sucedió anoche. Resulta que mi compañera de trabajo me confesó que ella se sentía atraída por mí al inico de año. Me ha dicho que no es lesbiana, pero que tuvo un breve deseo de estar conmigo por algun tiempo.

-Vale, ¿y tú qué le dijiste?

– No supe qué decir. No creo que fuese recíproco. Digo, a mí ella me parece muy linda, pero hasta ahí. Yo no siento nada romántico ni físico por ella. Al fin de cuentas, ¿cómo sabes si alguien te gusta?

– Si te dan ganas de besar a alguien, eso significa que te gusta la persona. A mí me ha pasado y es cierto. El deseo de un beso es el deseo de esa persona.

– No lo sé Z, pasa que a mí no siempre me dan ganas de un beso. ¿Qué si a mí me dan ganas de tomar a esa persona de la mano? Vaya, tomarse de las manos no es algo que caíga en lo sexual, pero es dulce, romántico, me apetece.

-Eso es bastante raro, no lo sé. Preguntale a S. Ella sabe de estas cosas.

-No le quiero preguntar nada a ella. Te lo digo a ti. De verdad, para mí una caricia, tomarse de las manos, un beso en la mejilla, todo eso me parece más atractivo que un intercambio feroz de saliva. Así que yo nunca estoy segura de mis sentimientos. Como te darás cuenta, soy algo así como un feto intentando entrar al mercado del noviazgo. Es por ello que sigo soltera. Nunca puedo leer las señales del deseo. Lo erótico para mí no es inmediatamente evidente. Necesito premeditarlo.

-¿Acaso no has tenido un noviazgo en el pasado? ¿No recuerdas el sentimiento que te llevó a sentirte enamorada?

-Es que yo nunca estuve segura. No fue algo de golpe, fue algo gradual. Una semillita que creció poco a poco. Recuerdo que le dije alguna vez, cuando estabamos en el proceso de ruptura, que extrañaba su piel. Se miraba tan extraviado por mi comentario. Lo cierto es que a veces aún extraño su piel. Ese contacto. Sentirlo al lado mío. Sentirnos uno. Lo mío es un poco menos érotico supongo. Una caricia me basta.

-Eres una rara, H.

Adventures in Xochimilco

Hello friends,

I want to share with you one of my favorite places around Mexico City: Xochimilco!

As you may know, Mexico City was established on top of a lake LOL. That’s why earthquakes suck. Anyway, only a few lakes remain around the city and Xochimilco is one of them. It’s relatively inexpensive to travel all the canals in Xochimilco in those lovely trajineras (rafts). The entire tour lasts around 5 hours, but we decided to go only half-way (3hrs) up to this place where you get to see the famous “axolotl” aka the Mexican salamander. This beautiful amphibian can regenerate and it’s sooo smushy. You can take a closer look as you watch the video below. Finally, if you ever get to go to Xochimilco, don’t forget to buy some quesadillas, bring your own music, and a good group of friends!


Sex Steroid Receptors Cheat Sheet

This is a cheat sheet I made to understand the role of estrogen and progestin receptors in sexual behavior. If you are studying basic neuroendocrinology, this might be a useful resource.






Results in rodents



Estrogen receptor (ER)

Knock-out (KO) ERa gene Completely eliminates hormonal induction of feminine sexual behavior
ERb KO ERb gene §  No apparent effect in ovariectomized (OVX) hormone-injected mice

§  Extends the period of behavioral estrus

§  Enhances receptivity in estrous-cycling mice


double knockout

§  Infertile

§  Decreased levels of sexual receptivity




Results in rodents


Progestin receptor (PR)

PRAKO mice §  Showed minimal progesterone (P) -facilitated lordosis in the presence of males

§  dominant PR-B isoform alone was incapable of mediating the effects of P on sexual behavior


§  Essential role in progesterone-facilitated sexual behavior

PR-B PRKBKO §  Improved PR-A-dependent receptivity with experience

§  Lesser role



  Experiment Result
Dopamine (DA) agonists DA agonist + P antagonists DA facilitates sexual behavior by indirectly activating PRs

(acts on both isoform)


(PKA activator)



Protein kinase A =cAMP-dependent protein kinase

Primarily mediated via PR-A isoform


  • Each isoform of PR may be involved in signaling routes leading to facilitation of sexual behavior, but PR-A seems to have the dominant role in most situations, and PR-B involvement seems to depend upon the mode of activation of the receptor.
  • ER down regulates alpha-ER in most neuroanatomical areas
  • Downregulation of PRs leads to estrous termination and the refractory period
  • Progesterone downregulates its own receptors
  • Functional participation of both the isoforms is critical for P-mediated effects on sexual receptivity
  • Thus, both isoforms of PR, probably via heterodimerization, appear to be required in the RU38486 effects on ligand-independent PR-mediated lordosis.


Ligand-Independent Activation of PRs

  • DA agonists can also activate PRs== blocked by P antagonists
  • Facilitation by dopaminergic agonists was blocked by progesterone antagonists, antisense oligonucleotides directed at the PR mRNA or in PRKO mice
  • SKF 81297= DA agonist


Russian spy: Novichok. How does this nerve agent work?

Apparently, this week, the Russian government poisoned a former spy and his daughter using Novichok in the UK. As a response, many countries have decided to expel Russian diplomats. I was curious to know more about the nerve agent that was used in this poisoning, so I am writing a short post about the mechanism of action of Novichok.

Novichok acts on the cholinergic system. Acetylcholine (ACh) is involved in a diverse number of functions both in the central (CNS) and peripheral nervous system (PNS). In the PNS, acetylcholine is vital for muscular function because it is released by motor neurons at the neuromuscular junction to activate the muscles. In addition, acetylcholine works in the autonomic nervous system, which controls functions not consciously directed such as our breathing, heartbeat, and digestive system. In the CNS, acetylcholine is a neuromodulator that participates in cognitive functions (Fig. 1). Fun fact: cholinergic neurons die in the hippocampus in Alzheimer’s disease, so some drugs (e.g., galantamine) target AChE in order to increase acetylcholine and alleviate memory problems.

The major cholinergic pathways in the brain. Source:

Novichok inhibits the enzyme acetylcholinesterase (AChE). This enzyme is responsible for the breakdown of the neurotransmitter acetylcholine. As a result, there is a build-up of ACh in our system. In the PNS, the muscles are hyperactivated because ACh depolarizes the postsynaptic muscle fibers and puts them in a sort of “pause” state because the cells enter a refractory period. Ultimately, the build-up of ACh leads to neuromuscular paralysis. Because we need muscles to breath, our breathing is messed up. Moreover, acetylcholine acts on a different type of receptors in the heart, which cause a decrease in the heart rate as ACh builds up. In the case of the CNS, the major result of ACh build-up is convulsions, loss of consciousness, and coma. Finally, our pupils’ size is modulated by acetylcholine. In fact, some antagonists of acetylcholine are used to dilate the pupils and make them look “pretty”. In this case, because Novichok increases acetylcholine, the pupils are constricted.

Novichok inhibits the enzyme that breaks down acetylcholine (AChE). As a result, ACh builds up in the system. Source:

The antidote for Novichok and other nerve agents is a combination of anticholinergic drugs. This type of drugs prevent acetylcholine from acting on its receptors, so they allow our system to recover from the toxicity of ACh build-up. Unfortunately, Novichok and other similar nerve agents are very potent and they act very fast. If you have ever seen an insect dying from an insecticide, you might understand how these nerve agents work. In fact, insecticides and pesticides use the same concept of attacking the cholinergic system to kill animals.

Final note: I think it is crazy how a single neurotransmitter can have such a drastic effect on our system. It’s almost like if it were our Achilles heel.


Further readings: