“There has been occasional talk of “sensory cells” located in particular regions, or of sensitive or sensorial “special cells”. People have invented acoustic or optic special cells and even a “memory” (*12) cell, and have not shied away from the fantastic “psychic cell”. Apart from the fact that such so-called “special cells” have only been described in young or foetal brain with the Golgi method and mainly only in animals, and therefore lack confirmation in the adult human brain, and quite apart from the fact that no attempt has been made to determine the precise regional location of the zone within which such cells appear exclusively, it seems to me that to pose this problem is wrong.” [emphasis added]
And here is a news item from a couple of years ago:
Psychic cells indeed! Or perhaps we should call them zombie cells.
(Zombie concepts keep coming back from the dead to eat our brains. Other examples include ‘selfish genes’ and ‘pleasure molecules’.)
This is a potentially controversial issue, since there is no consensus yet on the evolution of the brain, beyond a very coarse-grained chronology. Broadly speaking, neocortical areas are new, hence the term “neo-cortex”. But among cortical areas, there is still some disagreement about which areas emerged most recently in primates.
Based on what we know about development in the womb, along with structural findings, my labmates, who are neuroanatomists, suggest that the “eulaminate” areas — the ones that have sharply defined layers — may be the most recent, evolutionarily, compared to the “agranular” and “dysgranular” cortices, which have less sharply defined layers. These less sharply defined areas are also labeled as “limbic”.
Acetaminophen (a.k.a) relieves some types of headache. But this does not mean that these headaches are caused by acetaminophen deficiency. The brain doesn’t even produce acetaminophen.
The point of this analogy is to make clear that a medicine can work even if it is not acting on the cause of the symptom. In many cases a medicine can work even when the cause of the symptom is completely unknown.
While reading a paper on the neuroscience of dreaming I came across a reference to a 1940 paper by Donald Hebb and Wilder Penfield. It’s a neurosurgery case study that is quite stunning. It shows that in some cases, removal of prefrontal brain tissue can actually cause improvements in intelligence and personality. So basically it’s the opposite of the Phineas Gage story.
Here are some excerpts from the paper:
I was asked this question on Quora:
From an evolutionary standpoint, why would the early years of brain development be paramount in determining life-long neurological patterns, when those patterns can often be detrimental to long-term success in life?
Good question. We can restate it as follows:
Why would natural selection allow animals to be so sensitive to negative early experience?
I was interviewed by the excellentfor his . Check it out if you want to know about my research… and also my take on the question of Life, the Universe, and Everything. 😛
There’s also a shorter excerpt where we speculate about schizophrenia and “hyperrealities”:
My latest modeling paper has been published in Computational Psychiatry.
Here’s the abstract:
“Schizophrenia is associated with diverse cognitive deficits, including disorders of attention-related oculomotor behavior. At the structural level, schizophrenia is associated with abnormal inhibitory control in the circuit linking cortex and thalamus. We developed a spiking neural network model that demonstrates how dysfunctional inhibition can degrade attentive gaze control. Our model revealed that perturbations of two functionally distinct classes of cortical inhibitory neurons, or of the inhibitory thalamic reticular nucleus, disrupted processing vital for sustained attention to a stimulus, leading to distractibility. Because perturbation at each circuit node led to comparable but qualitatively distinct disruptions in attentive tracking or fixation, our findings support the search for new eye movement metrics that may index distinct underlying neural defects. Moreover, because the cortico-thalamic circuit is a common motif across sensory, association, and motor systems, the model and extensions can be broadly applied to study normal function and the neural bases of other cognitive deficits in schizophrenia.”
Here’s Figure 1, which shows the circuit we modeled.
A very important point about dopamine (DA) and reward, from a recent review paper:
“The DA hypothesis of reward is a ubiquitous feature of the scientific literature, as well as popular media, the internet, and film. Yet, despite the almost automatic tendency of some to explain virtually any aspect of DA function as somehow being dependent on reward, there are critical theoretical and empirical problems with this, many of which have been reviewed in detail elsewhere (Salamone et al., 1997, 2007; Salamone and Correa, 2002, 2012; Floresco, 2015; Nicola, 2016). First and foremost, the term reward has no consistent scientific meaning (Salamone et al., 2005; Salamone and Correa, 2012), and, depending upon the paper, or even the paragraph, this term is used variously to refer to subjective pleasure or hedonic reactivity, appetite, preference, and even reinforcement learning. Given the slippery and imprecise nature of this term, it is wholly inadequate to attribute specific effects in experiments simply to reward without any qualification or explication.” [Emphasis added]
Salamone, J. D., Correa, M., Ferrigno, S., Yang, J. H., Rotolo, R. A., & Presby, R. E. (2018). The psychopharmacology of effort-related decision making: Dopamine, adenosine, and insights into the neurochemistry of motivation. Pharmacological Reviews, 70(4), 747-762.
This post, which mostly provides useful citations, was originally written as an answer to the following Quora question: