Involvement of the amygdala in memory storage: Interaction with other brain systems

There is extensive evidence that the amygdala is involved in affectively influenced memory. The central hypothesis guiding the research reviewed in this paper is that emotional arousal activates the amygdala and that such activation results in the modulation of memory storage occurring in other brain regions. Several lines of evidence support this view. First, the effects of stress-related hormones (epinephrine and glucocorticoids) are mediated by influences involving the amygdala. In rats, lesions of the amygdala and the stria terminalis block the effects of posttraining administration of epinephrine and glucocorticoids on memory. Furthermore, memory is enhanced by posttraining intra-amygdala infusions of drugs that activate β-adrenergic and glucocorticoid receptors. Additionally, infusion of β-adrenergic blockers into the amygdala blocks the memory-modulating effects of epinephrine and glucocorticoids, as well as those of drugs affecting opiate and GABAergic systems. Second, an intact amygdala is not required for expression of retention. Inactivation of the amygdala prior to retention testing (by posttraining lesions or drug infusions) does not block retention performance. Third, findings of studies using human subjects are consistent with those of animal experiments. β-Blockers and amygdala lesions attenuate the effects of emotional arousal on memory. Additionally, 3-week recall of emotional material is highly correlated with positron-emission tomography activation (cerebral glucose metabolism) of the right amygdala during encoding. These findings provide strong evidence supporting the hypothesis that the amygdala is involved in modulating long-term memory storage.

Muscarinic acetylcholine receptor expression in memory circuits: Implications for treatment of Alzheimer disease

Cholinergic transmission at muscarinic acetylcholine receptors (mAChR) has been implicated in higher brain functions such as learning and memory, and loss of synapses may contribute to the symptoms of Alzheimer disease. A heterogeneous family of five genetically distinct mAChR subtypes differentially modulate a variety of intracellular signaling systems as well as the processing of key molecules involved in the pathology of the disease. Although many muscarinic effects have been identified in memory circuits, including a diversity of pre- and post-synaptic actions in hippocampus, the identities of the molecular subtypes responsible for any given function remain elusive. All five mAChR genes are expressed in hippocampus, and subtype-specific antibodies have enabled identification, quantification, and localization of the encoded proteins. The m1, m2, and m4 mAChR proteins are most abundant in forebrain regions and they have distinct cellular and subcellular localizations suggestive of various pre- and postsynaptic functions in cholinergic circuits. The subtypes are also differentially altered in postmortem brain samples from Alzheimer disease cases. Further understanding of the molecular pharmacology of failing synapses in Alzheimer disease, together with the development of new subtype-selective drugs, may provide more specific and effective treatments for the disease.

Deficits in memory and hippocampal long-term potentiation in mice with reduced calbindin D28K expression.

The influx of calcium into the postsynaptic neuron is likely to be an important event in memory formation. Among the mechanisms that nerve cells may use to alter the time course or size of a spike of intracellular calcium are cytosolic calcium binding or "buffering" proteins. To consider the role in memory formation of one of these proteins, calbindin D28K, which is abundant in many neurons, including the CA1 pyramidal cells of the hippocampus, transgenic mice deficient in calbindin D28K have been created. These mice show selective impairments in spatial learning paradigms and fail to maintain long-term potentiation. These results suggest a role for calbindin D28K protein in temporally extending a neuronal calcium signal, allowing the activation of calcium-dependent intracellular signaling pathways underlying memory function.

Lines written in memory of the late Hon. Samuel Ongley, and descriptive of his character as a sportsman /

Caption title.

An address in memory of William Seymour Tyler : delivered in the college church at Amherst, May 29, 1898 /

On cover: William Seymour Tyler.

In memory of Madeline Yale Wynne.

Lawrence J. Gutter Collection of Chicagoana.

James R. Mann. Memorial addresses delivered in the House of Representatives of the United States in memory of James R. Mann, late a representative from Illinois. Sixty-seventh Congress. January 14, 1923.

"Proceedings in the Senate": p. 109-[113]

Henry D. Flood. Memorial addresses delivered in the House of representatives of the United States in memory of Henry D. Flood, late a representative from Virginia.

Running title: Memorial addresses. Representative Flood.

Senators from Pennsylvania. Memorial addresses delivered in the Senate and House of Representatives of the United States in memory of Philander C. Knox, Boies Penrose, William E. Crow, late senators from Pennsylvania. Sixty-seventh Congress. Proceedings in the Senate, January 28, 1923. Proceedings in the House, February 18, 1923.

Running title: Memorial addresses.

The Russian military today and tomorrow : essays in memory of Mary Fitzgerald /

"July 2010."

In memory of Frank Worthing, actor, born at Edinburgh, Scotland, October 12, 1866, died at Detroit, Michigan, December 27, 1910.

"The book has been compiled and edited by Jefferson Winter, and it has been manufactured at the cost of five friends of Mr. Worthing,--Miss Blanche Bates, Miss Grace George, Tyrone Power, William Winter, and the editor."

In memory of Bert Leston Taylor (B.L.T.)

Torch Press.

In memory of Samuel Rodger Callaway. December 24, 1850, June 1, 1904

Mode of access: Internet.