Here are more citations on the ability of the brain to rewire itself from addiction.

Research has shown that after a stroke, for motor deficits, notable recovery takes place within 30 days for mild, moderate, and moderate-severe severity with additional recovery up to 90 days for severe strokes (Duncan, P., Goldstein, L., Matchar, D., Divine, G. and Feussner, J., 1992). (Reyst)

Even if axons are destroyed, the brain may be able to recover lost function through alternate white matter pathways that can reconnect relevant gray matter regions.

(Terayama et al., 1993 ; Alexander, 1997 ; Johansen-Berg et al., 2010 ).

Filley, Christopher (2012-05-18). The Behavioral Neurology of White Matter (Page 376). Oxford University Press. Kindle Edition.

  • Increase or decrease in myelin sheath (white matter): Covers nerve fibers to increase the speed of nerve impulses.

•Increase or decrease in number of dendrites (gray matter): These branch-like fibers are where nerve cells communicate.

•Increase or decrease in the number of synapses: Helps to determine strength of pathways, information flow, learning and memories.

•Increase or decrease in the strength of a synapse: Same as above

The above mechanisms are at work during brain development, learning, memory formation, and the development of addiction. Neuroplasticity works in two directions: it can weaken or delete old connections as well as strengthen or create new connections. In a very simplified model, the major addiction-related brain changes include:

0.Desensitization: Weakening of circuits related to natural rewards (e.g. food, sex, etc.)

0.Sensitization: Formation of Pavlovian memory circuits related to the addiction

0.Hypofrontality: Weakening of the impulse control circuits

0.Altered stress systems: CRF, Amygdala, and HPA axis

http://www.yourbrainonporn.com/rewire-your-brain-using-ocd-neuroscience

In fact, synaptic plasticity occurs throughout the brain, including in excitatory and inhibitory neurons (Kullmann and Lamsa 2007). Moreover, dendritic spines can grow 4-fold within 2 min of forming a new memory (Lang et al., 2004) which in turn would effect neural transmission and increase the number of interconnections between neurons.

Excitatory synapses stimulate neurotransmitters while inhibitory synapses inhibit them.

Read more: http://www.differencebetween.net/science/difference-between-inhibitory-and-excitatory/#ixzz4Ek4H62V7

Joseph, R.  (2011-11-10). Memory, Amnesia, Amygdala, Hippocampus, Neural Networks, Long Term Potentiation, Dissociation, Confabulation, False Memories, Traumatic Stress (Kindle Locations 79-81). University Press. Kindle Edition.

Neurobiological Changes after Acquired Brain Injury

After injury to the brain, the processes of neuroplasticity are thought to be the underpinnings of recovery (Carmichael, 2010). To begin, research has found a variety of neuroplastic changes which occur after injury, including:

1.Increases or changes to synapses:
• This includes synaptogenesis and synaptic plasticity (Chen, Epstein and Stern; 2010; Nudo, 2011)• Dendrite changes including increased arborization, dendritic growth and spine growth (Nudo, 2011)• Axonal changes including axonal sprouting (Nudo, 2011; Charmichael, 2010)

2.Increased neuron growth:
• Neurogenesis in specific brain areas like the hippocampus subgranular zone of the dentate gyrus and subventricular zone in some areas (Schoch, Madathil and Saatman, 2012), substantia nigra and perinfarcted areas (Font, Arboix & Krupinski, 2010).

3.Angiogenesis
• Angiogenesis is the process through which new blood vessels form from pre-existing vessels.

4.Excitability changes:
• Excitability refers to the ability of a neuron to generate action potentials, which is a short-term change in the electrical potential on the surface of a cell. It is an all or nothing proposition as it either fires or does not fire depending on the strength of the potential.

Neuroplasticity After Aquired Brain Injury

By Heidi Reyst, Ph.D., CBIST
Rainbow Rehabilitation Centers

As our experiences change, at a neurobiological level, we either increase or decrease the numbers of synapses, dendrites and axons. If we stop a function, we lose synapses, etc., and if we increase an activity we proliferate synapses, etc., resulting in experience-dependent learning.

Neuroplasticity After Aquired Brain Injury

By Heidi Reyst, Ph.D., CBIST
Rainbow Rehabilitation Centers