Consolidating new memories requires the amygdala and Live chat sex men
The memory modulation is initiated, at least in part, by activation of peripheral \(\beta\)-adrenoceptors located on vagal afferents that project to the nucleus of the solitary tract (NTS) in the brain stem.
The NTS sends noradrenergic projections to forebrain regions both directly and indirectly via the locus coeruleus.
Modulation of consolidation is a common feature of animal memory, as it is found in mollusks, fish, birds and bees as well as rodents and primates (Mc Gaugh, 2000).
Such evidence suggested that memory consolidation might also be enhanced by treatments that activate brain functioning. Many stimulant drugs enhance retention when administered shortly after training (Mc Gaugh & Herz, 1972; Mc Gaugh, 1973; Jarvik & Mc Gaugh, 1978).
Research on was initially stimulated by findings that, in rats, electroconvulsive shock impairs retention of recently learned responses (Duncan, 1949; Gerard, 1949; Mc Gaugh, 1966).
Such findings of retrograde amnesia provided compelling evidence that new memory traces perseverate in a fragile state and later become consolidated (Müller & Pilzecker, 1900).
Our memories are not all created equally strong: Some experiences are well remembered and others poorly, if at all.
Understanding the neurobiological processes and systems that contribute to such differences in the strength of our memories is the special focus of research on memory modulation.