question about brains of newborns

[gib65]

Here's a passage from a paper I'm writing:

 

In the newborn' date=' the brain begins completely devoid of any social and intellectual programming. The interconnections between neurons are all more or less the same - every neuron reaches out to as many other neurons as possible, forging connections that have yet to be programmed with specific receptor types - that is, either inhibitory or excitatory.

[/quote']

 

Can anyone tell me if this is accurate? I would also like to know how neural connections get programmed to be inhibitory or excitatory.

 

Thanks.

[iNow]

My studies are too rusty for me to explain why and where, but I will say your premise appears false at first glance. The neural connections are NOT equally distributed. All of those months during gestation result in the growth of neural webs which are denser in some areas and more dispersed in others.

 

Think of it this way. Neural connections to the stomach are more important than neural connections to the toes when a kid is born, therefore, it would be inaccurate to say that the brain is "completely devoid of programming" or that the "interconnections are all more or less the same."

 

 

For your inhibitory/excitatory question, a quick google gives me this:

 

 

http://childstudycenter.yale.edu/faculty/vaccarino.html

We have shown that in the developing cerebral cortex, genes of Fibroblast Growth Factors (FGF) family are crucial for attaining the proper number of excitatory projection neurons with respect to that of inhibitory interneurons. Gain or loss of function for FGF2 cause increases or decreases, respectively, in the number of cortical pyramidal neurons that are generated during development, without any change in inhibitory neurons. However, conditional loss-of-function for the FGF receptors affects both excitatory and inhibitory neuron types in different proportions

 

 

http://www.nature.com/neuro/journal/v9/n6/abs/nn1706.html

 

Ascl1 and Gsh1/2 control inhibitory and excitatory cell fate in spinal sensory interneurons

 

 

Sensory information from the periphery is integrated and transduced by excitatory and inhibitory interneurons in the dorsal spinal cord. Recent studies have identified a number of postmitotic factors that control the generation of these sensory interneurons. We show that Gsh1/2 and Ascl1 (Mash1), which are expressed in sensory interneuron progenitors, control the choice between excitatory and inhibitory cell fates in the developing mouse spinal cord. During the early phase of neurogenesis, Gsh1/2 and Ascl1 coordinately regulate the expression of Tlx3, which is a critical postmitotic determinant for dorsal glutamatergic sensory interneurons. However, at later developmental times, Ascl1 controls the expression of Ptf1a in dILA progenitors to promote inhibitory neuron differentiation while at the same time upregulating Notch signaling to ensure the proper generation of dILB excitatory neurons. We propose that this switch in Ascl1 function enables the cogeneration of inhibitory and excitatory sensory interneurons from a common pool of dorsal progenitors.

[gib65]

My studies are too rusty for me to explain why and where, but I will say your premise appears false at first glance. The neural connections are NOT equally distributed. All of those months during gestation result in the growth of neural webs which are denser in some areas and more dispersed in others.

 

Think of it this way. Neural connections to the stomach are more important than neural connections to the toes when a kid is born, therefore, it would be inaccurate to say that the brain is "completely devoid of programming" or that the "interconnections are all more or less the same."

 

Yes, I suspected as much. I was being overly simplistic in my first statement (somewhat on purpose, admittedly). I'll be cleaning that up accordingly.

 

But it's really the next part I'm interested in:

 

For your inhibitory/excitatory question, a quick google gives me this:

 

 

http://childstudycenter.yale.edu/faculty/vaccarino.html

 

We have shown that in the developing cerebral cortex, genes of Fibroblast Growth Factors (FGF) family are crucial for attaining the proper number of excitatory projection neurons with respect to that of inhibitory interneurons. Gain or loss of function for FGF2 cause increases or decreases, respectively, in the number of cortical pyramidal neurons that are generated during development, without any change in inhibitory neurons. However, conditional loss-of-function for the FGF receptors affects both excitatory and inhibitory neuron types in different proportions

 

http://www.nature.com/neuro/journal/v9/n6/abs/nn1706.html

 

Ascl1 and Gsh1/2 control inhibitory and excitatory cell fate in spinal sensory interneurons

 

 

Sensory information from the periphery is integrated and transduced by excitatory and inhibitory interneurons in the dorsal spinal cord. Recent studies have identified a number of postmitotic factors that control the generation of these sensory interneurons. We show that Gsh1/2 and Ascl1 (Mash1), which are expressed in sensory interneuron progenitors, control the choice between excitatory and inhibitory cell fates in the developing mouse spinal cord. During the early phase of neurogenesis, Gsh1/2 and Ascl1 coordinately regulate the expression of Tlx3, which is a critical postmitotic determinant for dorsal glutamatergic sensory interneurons. However, at later developmental times, Ascl1 controls the expression of Ptf1a in dILA progenitors to promote inhibitory neuron differentiation while at the same time upregulating Notch signaling to ensure the proper generation of dILB excitatory neurons. We propose that this switch in Ascl1 function enables the cogeneration of inhibitory and excitatory sensory interneurons from a common pool of dorsal progenitors.

 

Since I posted this, I also found the wiki article on Hebbian Theory quite valuable, especially this quote:

 

If the inputs to a system cause the same pattern of activity to occur repeatedly, the set of active elements constituting that pattern will become increasingly strongly interassociated. That is, each element will tend to turn on every other element and (with negative weights) to turn off the elements that do not form part of the pattern.

[Sayonara]

Don't take this is a criticism, I'm just curious... shouldn't you research things you state as fact before you write the paper?

[gib65]

Don't take this is a criticism, I'm just curious... shouldn't you research things you state as fact before you write the paper?

 

Maybe I should, but this isn't a professional paper. It's a personal/recreational paper on my philosophies of mind and brain.

 

Technically, I could cite not a single soure if I really wanted to, although that probably wouldn't go over well with others.

 

But I'm not that lazy. I plan to add sources and documentation as I come across them on a casual basis. I'm fairly certain about the things I say (remembering that I learnt it elsewhere but can't put my finger on when or where). If I learn that anything I say is dreadfully wrong, I'll rewrite it, of course, but most of the stuff that should have sources is more to support the major philosophical points I'm making, but these points aren't totally dependent on them.

 

It's a casual thing.

[Sayonara]

Fair enough!

 

Was worried you were going to get whacked by the Peer Review Mafia or something.

[iNow]

Since I posted this, I also found the wiki article on Hebbian Theory quite valuable, especially this quote:

That's very cool. Thank you for sharing it.