Right-side olfaction Memory for shapes Stereognosis, left side Hearing (left-ear preference) Musical ability Recognition of forms, faces, and body image Left visual fieldRight visual field Mathematical ability Understanding language Hearing (right-ear preference) Motor speech Left-side olfaction Verbal memory Stereognosis, right side Right-hand skills (e.g., writing) L Left Right RLR 372 x 49 18228 •Fig. 10.9 Schematicillustrationofthefunctionalspecializationsoftheleftandrighthemispheres,asdeterminedinpatientsaftersectionofthecorpuscallosum.(ModifiedfromSiegelA,SapruHN.Essential Neuroscience. 5thed.Philadelphia:LippincottWilliams&Wilkins;2005.) paired with a significant one). In the case of habituation, the amount of transmitter released in successive responses gradually diminishes. The change involves an alteration in the Ca++ current that triggers release of neurotransmitter. The cause of this change is inactivation of presynaptic Ca++ channels by repeated action potentials. Long-term habituation can also be produced. In this case, the numbers of synaptic endings and active zones in the remaining terminals decreases.
Additional models of learning, provided by synaptic phenomena, are called long-term potentiation (LTP) and long-term depression (LTD). LTD has been studied most extensively in the cerebellum (see
Chapter 9), but it also occurs in the hippocampus and in other regions of the CNS.
LTP has been studied most intensively in slices of the hippocampus in vitro, but it has also been studied in the neocortex, cerebellum, and other parts of the CNS. Repetitive activation of an afferent pathway to the hippocampus or repetitive activation of one of the intrinsic connections increases the responses of pyramidal cells. The increased responses (the LTP) last for hours in vitro (and even days to weeks in vivo). The forms of LTP differ, depending on the particular synaptic system. The mechanism of the enhanced synaptic efficacy seems to involve both presynaptic and postsynaptic events. The neurotransmitters involved in LTP include excitatory amino acids that act on N-methyl-D-aspartate (NMDA) receptors, the responses of which are associated with an influx of Ca++ into the post-synaptic neuron. Second messenger pathways (including G proteins, Ca++/calmodulin-dependent kinase II, protein kinase G, and protein kinase C) are also involved, and these kinases cause protein phosphorylation and changes in the responsiveness of neurotransmitter receptors. A retrograde messenger, perhaps nitric oxide (or carbon monoxide), may be released from postsynaptic neurons to act on presynaptic endings in such a way that transmitter release is enhanced. Immediate-early genes are also activated during LTP. Hence, changes in gene expression may also be involved.
With regard to the stages of memory storage, a distinction between short-term memory and long-term memory is useful. Recent events appear to be stored in short-term memory by ongoing neural activity because short-term memory persists for only minutes. Short-term memory is used, for instance, to remember page numbers in a book after looking them up in the index. Long-term memory can be subdivided into an intermediate form, which can be disrupted, and a long-lasting form, which is difficult to disrupt. Memory loss, or amnesia, can be caused by a loss of memory information per se, or it can result from interference with the mechanism for accessing the information. Long-term memory probably involves structural changes because it can remain intact even after events that disrupt short-term memory.