INVESTIGADORES
RAMIREZ Maria Rosana
artículos
Título:
MICE DEFICIENT FOR THE VESICULAR ACETYLCHOLINE TRANSPORTER ARE MYASTHENIC AND HAVE DEFICITS IN OBJECT AND SOCIAL RECOGNITION.
Autor/es:
PRADO VF, MARTINS-SILVA C, BARROS DM, AMARAL E, RAMSEY AJ, SOTNIKOVA TD, RAMIREZ MR, KIM HG, ROSSATO JI, KOENEN J, QUAN H, COTA VR, MORAES MF, GOMEZ MV, GUATIMOSIM C, WETSEL WC, KUSHMERICK C, PEREIRA GS, GAINETDINOV RR, IZQUIERDO I, CARON MG, PRADO MA.
Revista:
NEURON
Editorial:
CELL PRESS
Referencias:
Año: 2006 vol. 51 p. 601 - 612
ISSN:
0896-6273
Resumen:
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An important step for cholinergic transmission
involves the vesicular storage of acetylcholine (ACh), a process mediated by
the vesicular acetylcholine transporter (VAChT). In order to understand the
physiological roles of the VAChT, we developed a genetically altered strain of
mice with reduced expression of this transporter. Heterozygous and homozygous
VAChT knockdown mice have a 45% and 65% decrease in VAChT protein expression,
respectively. VAChT deficiency alters synaptic vesicle filling and affects ACh
release. Whereas VAChT homozygous mutant mice demonstrate
major neuromuscular deficits, VAChT heterozygous mice appear normal in that
respect and could be used for analysis of central cholinergic function.
Behavioral analyses revealed that aversive learning
and memory are not altered in mutant mice; however, performance in cognitive
tasks involving object and social recognition is severely impaired. These observations
suggest a critical role of VAChT in the regulation of ACh release and
physiological functions
in
the peripheral and central nervous system.
