Editing Behavioral neuroscience (section)

===Disabling or decreasing neural function===

* [[Lesions]] – A classic method in which a brain-region of interest is naturally or intentionally destroyed to observe any resulting changes such as degraded or enhanced performance on some behavioral measure. Lesions can be placed with relatively high accuracy "Thanks to a variety of brain 'atlases' which provide a map of brain regions in 3-dimensional" [[stereotactic surgery|stereotactic coordinates]].[[File:Journal.pone.0057573.g005 cropped.png|thumb|301x301px|The part of the picture emphasized shows the [[lesion]] in the brain. This type of lesion can be removed through surgery.]]
**'''Surgical''' lesions – Neural tissue is destroyed by removing it surgically.
** '''Electrolytic''' lesions – Neural tissue is destroyed through the application of electrical shock trauma.
** '''Chemical''' lesions – Neural tissue is destroyed by the infusion of a [[neurotoxin]].
** '''Temporary''' lesions – Neural tissue is temporarily disabled by cooling or by the use of [[anesthetics]] such as [[tetrodotoxin]].
* [[Transcranial magnetic stimulation]] – A new technique usually used with human subjects in which a magnetic coil applied to the scalp causes unsystematic electrical activity in nearby cortical neurons which can be experimentally analyzed as a functional lesion.
* [[Receptor activated solely by a synthetic ligand|Synthetic ligand injection]] – A receptor activated solely by a synthetic ligand (RASSL) or Designer Receptor Exclusively Activated by Designer Drugs (DREADD), permits spatial and temporal control of [[G protein]] signaling [[in vivo]]. These systems utilize G protein-coupled receptors ([[GPCR]]) engineered to respond exclusively to synthetic small molecules [[ligands]], like [[clozapine N-oxide]] (CNO), and not to their natural ligand(s). RASSL's represent a GPCR-based [[chemogenetic]] tool. These synthetic ligands upon activation can decrease neural function by G-protein activation. This can with Potassium attenuating neural activity.<ref>{{cite journal|last1=Zhu|first1=Hu|title=Silencing synapses with DREADDs|journal=Neuron|volume=82|issue=4|pages=723–725|pmc=4109642|year=2014|doi=10.1016/j.neuron.2014.05.002|pmid=24853931}}</ref>
* [[Optogenetic]] inhibition – A light activated inhibitory protein is expressed in cells of interest. Powerful millisecond timescale neuronal inhibition is instigated upon stimulation by the appropriate frequency of light delivered via fiber optics or implanted LEDs in the case of vertebrates,<ref>{{Cite journal |doi = 10.1176/appi.ajp.2008.08030444|title = Controlling Neuronal Activity|year = 2008|last1 = Schneider|first1 = M. Bret|last2 = Gradinaru|first2 = Viviana|last3 = Zhang|first3 = Feng|last4 = Deisseroth|first4 = Karl|journal = American Journal of Psychiatry|volume = 165|issue = 5|pages = 562|pmid = 18450936}}</ref> or via external illumination for small, sufficiently translucent invertebrates.<ref>{{Cite journal | doi=10.1038/nature05744| title=Multimodal fast optical interrogation of neural circuitry| year=2007| last1=Zhang| first1=Feng| last2=Wang| first2=Li-Ping| last3=Brauner| first3=Martin| last4=Liewald| first4=Jana F.| last5=Kay| first5=Kenneth| last6=Watzke| first6=Natalie| last7=Wood| first7=Phillip G.| last8=Bamberg| first8=Ernst| last9=Nagel| first9=Georg| last10=Gottschalk| first10=Alexander| last11=Deisseroth| first11=Karl| journal=Nature| volume=446| issue=7136| pages=633–639| pmid=17410168| bibcode=2007Natur.446..633Z| s2cid=4415339}}</ref> Bacterial [[Halorhodopsins]] or [[Proton pumps]] are the two classes of proteins used for inhibitory optogenetics, achieving inhibition by increasing cytoplasmic levels of halides ({{chem|Cl|-}}) or decreasing the cytoplasmic concentration of protons, respectively.<ref>Chow, B. Y. et al. "High-performance genetically targetable optical
neural silencing by light-driven proton pumps." Nature. Vol 463. 7 January 2010</ref><ref>{{Cite journal | doi=10.1007/s11068-008-9027-6| title=ENpHR: A Natronomonas halorhodopsin enhanced for optogenetic applications| year=2008| last1=Gradinaru| first1=Viviana| last2=Thompson| first2=Kimberly R.| last3=Deisseroth| first3=Karl| journal=Brain Cell Biology| volume=36| issue=1–4| pages=129–139| pmid=18677566| pmc=2588488}}</ref>