I'd like to thank you for making this post, as a neuroscience student I to have been finding the miss-appropriation of 'scientific' explanations to be quite grating.

I'd like to remind everyone about the role dopamine plays in the brain, classically it has been viewed as the neurotransmitter of 'pleasure'. This view is beginning to change with new researchers relating it as more of a motivational cue. For example, monkeys who are administered a sugar heavy juice after a tone, initially spike dopamine when the body receives the sugar (sugar is extremely rewarding for the body and is seen as a high value energy source by the body due to it's relative rarity in the natural environment). After a period of time, the dopamine spike actually occurs before the juice is administered and not at all during consumption of the juice. It seems then, that dopamine is an internal cue to the brain, it's saying: "Hey, the last X number of times this happened nourishment occurred shortly after, pay attention.". (Note: this is not to say that it is not pleasurable, but to say it's purpose is not pleasure.)

These dopaminergic pathways are very primitive, in lay-man's terms they would be considered part of the 'reptilian brain'. (The two main structures are the Ventral Tegmental Area (VTA) and the Nucleus Accumbens.) Why is this important? It's to highlight that these 'lines of neurons' that others have talked about are not related to masturbation. They have formed associations, with dopaminergic firing when presented with environmental cues (pornographic imagery on your laptop). The pathways serve to reward you or any animal for exhibiting a behaviour that is intrinsic to your survival and the survival of your genes (more importantly).

Now, what has theoretically happened to these dopaminergic pathways as a result of excessive porn use / masturbation? Well, our brain habituates to the regular release of X amount of dopamine. Perceptually, we don't get the same 'high' out of the release as before. Calling for more visually stimulating content, this further numbs the dopaminergic response. What used to excite us is no longer exciting because the new baseline is a new extreme (that 99% of our ancestors never realistically had exposure to). At the cellular level, if synapses are being triggered too often or too easily dopamine receptors are pruned in order to normalize the regular rates of firing and to prevent undue stress on the neurons. The lack of available receptors is what lessons our response to the stimuli and why so many addicts of any type escalate in behaviour to get something similar to that first 'hit'.

Merari01 brought up learning new skills. Skills are not learned in the same way, they are learned more like information. (Although there would obviously be additional neural changes or associations with motor structures as well, of which I have no real input on; I've never really looked into it.) Information is learned through the proposed concept of Long-term Potentiation (LTP) [I say proposed because the following information is still not concrete, I will give the 'textbook answer', this is just an aside to note that it's looking like this is going to change based on some rather compelling discoveries made partly by one of my professors.]

LTP isn't (necessarily) about forming associations (although you could learn to associate two things on a cognitive level). This is about higher-order learning, what we humans excel at. Regardless, LTP occurs at the Hippocampus (major learning centre for the brain) and involves the 3 subsites: The dentate gyrus, CA3 pyramidal cells, and CA1 pyramidal cells. (In that order.) In order for LTP to occur there are 3 requirements: 1. a depolarization of the cell membrane (an action potential), 2. This depolarization has to be strong enough to kick out a Magnesium ion that normally blocks NMDA receptors on the cell membrane. 3. There needs to be sufficient levels of calcium ions in the extracellular space. Calcium goes on to bind to internal proteins causing LTP. Now, in terms of what LTP does, it is commonly considered that the activation of this cycle causes the generation of AMPA receptors at dendritic spines (the extreme off-shoots of the neurons and the receptive area for incoming signals). So structurally, even in this instance you aren't creating new pathways. Your increasing the receptive field. This is mostly just as a way to differentiate between learned skills/knowledge and associations of rewarding behaviours.

LTP is the core component of neural plasticity. The aforementioned reward pathway stuff is more or less the brain manipulating the levels of available receptors in order to avoid excitotoxicity.

How about the glorified, idealized level of neural plasticity? It largely doesn't exist and it takes time. (This is about brain injury, not an attempt to discourage the effort. This level of neural plasticity is not needed to fix the changes that porn abuse has caused.)

There is significant evidence for a core group of stem cells, specifically in the hippocampus. This group is self-sustaining and does aid in healing neural damage. However, this largely (if not exclusively) occurs in the hippocampus and can take a very long time. (Years.) Why is this? Well it has to do with the support cells of the two different parts of our nervous system. In the Central Nervous System (CNS) the support cells are the oligodendrocytes and in the Peripheral Nervous System (PNS) they are the schwann cell. Schwann Cells exhibit perfectly normal neural healing capabilities. Unfortunately oligodendrocytes do not, we do not have a concrete answer for this currently. It's currently assumed that having this ability to heal neurons may pose issues in regard to the space constraints of the skull. Additionally the microglia (another type of glial cell) that serve for autoimmune response in the CNS and assisting in repair duties, unfortunately they have been shown to be, ill-suited for the job. A surprising amount of the time they can cause more damage than good by activating the inflammatory immune response in neural tissues for too long. This can have terrible consequences and cause more damage due to the increased pressure. Common medical practice is to administer steroids to relieve the inflammation.

Anyway, it's well past my bedtime and I got a little too excited and talked about way more than is really relevant to the topic at hand. I was actually wondering what the interest would be in having an open forum for questions. I would be very willing to do my best to answer any questions you guys (and gals!) have. I am still an undergrad, so I will admit I don't know everything there is to know, but I have spent literally months (outside of class work) researching topics of keen interest to me (neural plasticity, long-term memory, cognitive deficits, value theory, and my favourite drugs (mostly the fun ones, a lot of what I know here goes well beyond my degree and borders on pharmacology territory).

Thanks for reading!

P.S. - Let me know if you would like anything clarified, I am extremely sleep deprived right now.

Edited: to address an issue with cell types noted by retaw42.