Editing Behavioral neuroscience (section)

=== Enhancing neural function ===

* Electrical stimulation – A classic method in which neural activity is enhanced by application of a small electric current (too small to cause significant cell death).
* '''Psychopharmacological''' manipulations – A chemical [[receptor antagonist]] induces neural activity by interfering with [[neurotransmission]]. Antagonists can be delivered systemically (such as by intravenous injection) or locally (intracerebrally) during a surgical procedure into the ventricles or into specific brain structures. For example, [[NMDA]] [[antagonist]] [[AP5]] has been shown to inhibit the initiation of [[long term potentiation]] of excitatory synaptic transmission (in rodent fear conditioning) which is believed to be a vital mechanism in learning and memory.<ref>{{Cite journal |last1=Kim |first1=Jeansok J. |last2=Decola |first2=Joseph P. |last3=Landeira-Fernandez |first3=Jesus |last4=Fanselow |first4=Michael S. |year=1991 |title=N-methyl-D-aspartate receptor antagonist APV blocks acquisition but not expression of fear conditioning |journal=Behavioral Neuroscience |volume=105 |issue=1 |pages=126–133 |doi=10.1037/0735-7044.105.1.126 |pmid=1673846}}</ref>
* Synthetic Ligand Injection – Likewise, G<sub>q</sub>-DREADDs can be used to modulate cellular function by innervation of brain regions such as Hippocampus. This innervation results in the amplification of γ-rhythms, which increases motor activity.<ref>{{cite journal|last1=Ferguson|first1=Susan|title=Grateful DREADDs: Engineered Receptors Reveal How Neural Circuits Regulate Behavior|journal= Neuropsychopharmacology|date=2012|volume=37|issue=1|pages=296–297|doi=10.1038/npp.2011.179|pmid=22157861|pmc=3238068}}</ref>
* [[Transcranial magnetic stimulation]] – In some cases (for example, studies of [[motor cortex]]), this technique can be analyzed as having a stimulatory effect (rather than as a functional lesion).
* [[Optogenetic]] excitation – A light activated excitatory protein is expressed in select cells. [[Channelrhodopsin]]-2 (ChR2), a light activated cation channel, was the first bacterial opsin shown to excite neurons in response to light,<ref>{{Cite journal |doi = 10.1038/nmeth936|title = Channelrhodopsin-2 and optical control of excitable cells|year = 2006|last1 = Zhang|first1 = Feng|last2 = Wang|first2 = Li-Ping|last3 = Boyden|first3 = Edward S.|last4 = Deisseroth|first4 = Karl|journal = Nature Methods|volume = 3|issue = 10|pages = 785–792|pmid = 16990810|s2cid = 15096826}}</ref> though a number of new excitatory optogenetic tools have now been generated by improving and imparting novel properties to ChR2.<ref>{{Cite journal |doi = 10.1016/j.cell.2010.02.037|title = Molecular and Cellular Approaches for Diversifying and Extending Optogenetics|year = 2010|last1 = Gradinaru|first1 = Viviana|last2 = Zhang|first2 = Feng|last3 = Ramakrishnan|first3 = Charu|last4 = Mattis|first4 = Joanna|last5 = Prakash|first5 = Rohit|last6 = Diester|first6 = Ilka|last7 = Goshen|first7 = Inbal|last8 = Thompson|first8 = Kimberly R.|last9 = Deisseroth|first9 = Karl|journal = Cell|volume = 141|issue = 1|pages = 154–165|pmid = 20303157|pmc = 4160532}}</ref>