Question: How can antisense RNA bind to mRNA?
About the article "RNA", section "Regulatory RNAs".

Candidate passages:
Antisense RNA is an RNA transcript that is complementary to endogenous mRNA.
In other words, it is a non-coding strand complementary to the coding sequence of RNA; this is similar to negative-sense viral RNA.
Introducing a transgene coding for antisense RNA is a technique used to block expression of a gene of interest.
Radioactively-labelled antisense RNA can be used to show the level of transcription of genes in various cell types.
Some alternative antisense structural types are being experimentally applied as antisense therapy, with at least one antisense therapy approved for use in humans.
When mRNA forms a duplex with a complementary antisense RNA sequence, translation is blocked.
This process is related to RNA interference.
Antisense nucleic acid molecules have been used experimentally to bind to mRNA and prevent expression of specific genes.
Antisense therapies are also in development; in the USA, the Food and Drug Administration (FDA) has approved phosphorothioate antisense oligos fomivirsen (Vitravene) and mipomersen (Kynamro) for human therapeutic use.
Cells can produce antisense RNA molecules naturally, which interact with complementary mRNA molecules and inhibit their expression. 
sRNAs can either bind to protein targets, and modify the function of the bound protein, or bind to mRNA targets and regulate gene expression.
Antisense sRNAs can be categorised as "cis"-encoded sRNAs, where there is an overlap between the antisense sRNA and the target gene, and "trans"-encoded sRNAs, where the antisense sRNA gene is separate from the target gene. 
 methods used in research.
Antisense oligonucleotides.
Antisense oligonucleotides were discovered in 1978 by Paul Zamecnik and Mary Stephenson.
Oligonucleotides, which are short nucleic acid fragments, bind to complementary target mRNA molecules when added to the cell.
These molecules can be composed of single-stranded DNA or RNA and are generally 13-25 nucleotides long.
The antisense oligonucleotides can affect gene expression in two ways: by using an RNase H-dependent mechanism or by using a steric blocking mechanism.
RNase H-dependent oligonucleotides cause the target mRNA molecules to be degraded, while steric-blocker oligonucleotides prevent translation of the mRNA molecule.
The majority of antisense drugs function through the RNase H-dependent mechanism, in which RNase H hydrolyzes the RNA strand of the DNA/RNA heteroduplex.
This mechanism is thought to more efficient, resulting in an approximately 80% to 95% decrease in the protein and mRNA expression. 
Antisense oligonucleotides (single strands of DNA or RNA that are complementary to a chosen sequence) against hippocampal CREB mRNA can lower levels of CREB within 6 hours of infusion and impair spatial memory.
Tests given immediately after training showed that the antisense oligonucleotides against CREB do not disrupt short-term memory. 
Antisense RNA-type addiction modules use a regulatory strand of RNA which is at least partially "antisense" (having complimentary base pair encoding) to bind to toxin RNA, and thus prevent toxin transcription.
This antisense RNA molecule plays the role of antitoxin, similar to the proteic equivalent described above, and is similarly degraded at a faster rate than the toxin mRNA it inhibits.
In addition, the transcription of the antitoxin RNA is heavily upregulated by a strong promoter which ensures excess antitoxin in cells which have a functioning addiction module.