The following refs are related to the encoding of habits/instincts in dendrites - they cover recent research into
the plasticity of the dendrite spines and their 'realtime' modifications. Of particular note re 'habits' encoding
is the properties and method of NMDA receptors POST-synapse - IOW 90% of the time in dendrite spines. These receptors
are 'special' in that they require TWO prompts to elicit action, one chemical and one electrical.
The strengthening of synapses etc reflects the work of learning/memory (gets into Hebb's model of neuron etc) and
as such RESPONSES to stimuli, context can PUSH in that the dendrite areas work as filters. You can image a dendrite
'bush' as reflecting a three dimensional mandala as a 'habit' etc. These refs are all 'local', they reflect specialisations
in focus on the neuron in us and other species. When read they support the *general* transformation function. (note
that the hippocampus works to LINK events and so develop a HISTORY. The amygdala acts to COLOUR the events a la
the fight/flight dichotomy that, when applied recursively, gives us all of Plutchik's emotions and more. If I damage
the hippocampus I cannot put down NEW memories. If I ALSO damage the amydgala then all memory processing 'stops'.)
Overall we are dealing with differentiations and integrations and differentiations FROM integrations as well as
integrations FROM differentiations - all concepts focused-upon in the IDM
model where the results of specialist research leads to an emerging sense of the general patterns that influence
us as a species.
If you dont understand something or want to raise an 'issue', PLEASE DO! ;-)
==================================
from http://synapses.bu.edu/anatomy/dendrite/dendrite.stm
Perhaps the most common synaptic specialization of dendrites is that which Spanish anatomist Ramon y Cajal referred
to as "espinas", since they resembled the thorns on a flower stem. These spines are frequent on the dendrites
of the principal cells of most brain regions, notably on the pyramidal cells of cerebral cortex and the Purkinje
cells of the cerebellar cortex. For these cells, more than 90% of their excitatory synapses occur on dendritic
spines. Therefore, spines may play an important role in learning and memory.
Simple spines are very small, often less than 1 micron in diameter. This makes them difficult to study through
light microscopy. Electron microscopy must be used to determine the geometry of spines. Here are some dimensions
of simple dendritic spines as determined through serial electron microscopy. See also Comparative Morphology of
Dendritic Spines and Spine Synapses.
Adapted from:
Fiala J.C., Harris K. M. (1999) Dendrite Structure. In Dendrites (eds. G. Stuart, N. Spruston, M. Häusser),
Oxford University Press.
=====================================
also see http://www.physiol.ucl.ac.uk/research/hausser/hausser.html
also see http://www.dendrites.org/
and then...
even more on dendrites - A dendrite 'promo' off the web:
"Neuro-Scientists have recently discovered that even though neurons (brain cells) decrease with age, the dendrites
(memory storage compartments of each brain cell) can be stimulated to grow more in number. This increases memory
capacity. This growth is stimulated by "Whole Brain Learning", i.e., Albert Einstein played the violin
to establish this hemispheric balance. Scientists claim that Whole Brain Learning can be used to prevent Alzheimer's
Disease. [Life Magazine; July 1994]"
and (in http://www.psc.edu/biomed/training/workshops/1997/neuro/posters.html):
"Differential control of excitable dendrites by inhibition in neocortical pyramidal cells
Michael Beierlein and Barry Connors
Department of Neuroscience, Brown University, Providence, RI 02912
Many dendrites of pyramidal cells in neocortex express active Na+ and Ca2+ conductances, thereby altering the rules
by which synaptic inputs are transformed to generate neuronal output. Most dendrites also receive a dense inhibitory
innervation: Up to 80% of the inhibitory synapses on pyramidal cells terminate on dendrites, and various inhibitory
cell types each innervate different target regions of the pyramidal cell. GABAergic synapses can powerfully control
the somatic excitability of cortical neurons, yet the form and effects of IPSPs on dendritic spiking have not been
directly investigated in great detail.
We have recently examined the interactions between the intrinsic excitability of dendrites and synaptic inhibition
using whole cell recordings from the apical dendrites of layer V pyramidal cells. Dendritic IPSPs evoked by extracellular
stimulation were able to delay, completely block, or partially block mixed Na+/Ca2+ spikes in dendrites, critically
depending on the relative timing between inhibition and dendritic spiking. Slow, Ca2+- dependent spike components
could be blocked selectively by IPSPs.
Here, we further investigate the role of dendritic inhibition in controlling dendritic excitability with a detailed
compartmental model of a layer V pyramidal cell. In an initial set of simulations we attempt to simulate the physiology
of an intrinsically bursting cells, as these are thought to generate Ca2+ spiking in their apical dendrites. Second,
by placing inhibitory conductances at different target regions and activating them at different latencies, we investigate
possible roles of dendritic inhibition in cortical pyramidal cells."
Note the focus on 'altering the rules' in the first sentence.
ABSTRACTS
==========
These have been listed to emphasise the GENERAL perspective of encoding habits/instincts in the POST-synaptic areas
of neurons, i.e. DENDRITES. Note that a memory maps to a 'habit' in that it is a response process. The repeatition
of general experiences transfers the memory to an unconscious process, a 'habit'. (there are also links to info
on NMDA-receptors etc at the end of these abstracts)
==============
Trends Neurosci 1997 Mar;20(3):125-31 Related Articles, Cited in PMC, Books, LinkOut
Action potential initiation and backpropagation in neurons of the mammalian CNS.
Stuart G, Spruston N, Sakmann B, Hausser M.
Division of Neuroscience, John Curtin School of Medical Research, Australian National University, Canberra, Australia.
Most neurons in the mammalian CNS encode and transmit information via action potentials. Knowledge of where these
electrical events are initiated and how they propagate within neurons is therefore fundamental to an understanding
of neuronal function. While work from the 1950s suggested that action potentials are initiated in the axon, many
subsequent investigations have suggested that action potentials can also be initiated in the dendrites. Recently,
experiments using simultaneous patch-pipette recordings from different locations on the same neuron have been used
to address this issue directly. These studies show that the site of action potential initiation is in the axon,
even when synaptic activation is powerful enough to elicit dendritic electrogenesis. Furthermore, these and other
studies also show that following initiation, action potentials actively backpropagate into the dendrites of many
neuronal types, providing a retrograde signal of neuronal output to the dendritic tree.
==================
J Psychopharmacol 1998;12(3):227-38
Evidence that NMDA-dependent limbic neural plasticity in the right hemisphere mediates pharmacological stressor
(FG-7142)-induced lasting increases in anxiety-like behavior: study 3--the effects on amygdala efferent physiology
of block of NMDA receptors prior to injection of FG-7142 and its relationship to behavioral change.
Adamec RE.
Department of Psychology, Memorial University, St. John's, Newfoundland, Canada. radamec@morgan.ucs.mun.ca
The findings of this study support the hypothesis that N-methyl-D-aspartate (NMDA) receptors mediate the initiation
of long-term potentiation (LTP) and behavioral changes induced by the anxiogenic beta-carboline, FG-7142. Unlike
previous work, this study examined the effects of FG-7142 on LTP of amygdala efferents in both hemispheres. 7-amino-phosphono-heptanoic
acid (AP7), a competitive NMDA receptor blocker, given prior to administration of FG-7142, prevented LTP in amygdala
efferent transmission to the medial hypothalamus and periacqueductal gray (PAG). When given FG-7142 alone, cats
showed lasting behavioral changes accompanied by LTP in all pathways studied. Duration of LTP, and its relationship
to behavioral change, depended on the pathway and the hemisphere of the pathway. Correlation and covariance analyses
indicate that LTP in the left amygdalo-ventromedial hypothalamic pathway mediates initiation, but not maintenance,
of increased defensiveness. This finding replicates previous work. A new finding is that increased local excitability
in the right basal amygdala (reduced threshold for evoked response), and LTP in the right amygdalo-PAG pathway,
may be important for maintenance of increases in defensive behavior. Furthermore, the effects of flumazenil, a
benzodiazepine receptor antagonist, on behavior and physiology single out the importance of right amygdalo-PAG
LTP as a critical mediator of increased defensiveness. Flumazenil reversed the increase in defensiveness produced
by FG-7142 in a drug-dependent manner as described in Adamec (1998a). Moreover, flumazenil reversed LTP only in
the right amygdalo-PAG pathway. The findings of the present study suggest that response to FG-7142 may be a useful
model of the effects of traumatic stressors on limbic system function in anxiety, especially in view of the recent
data in humans implicating right hemispheric function in persisting negative affective states.
=================
J Neurosci 2002 Aug 15;22(16):7027-44
Regulation of A-kinase anchoring protein 79/150-cAMP-dependent protein kinase postsynaptic targeting by NMDA receptor
activation of calcineurin and remodeling of dendritic actin.
Gomez LL, Alam S, Smith KE, Horne E, Dell'Acqua ML.
Department of Pharmacology, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA.
At the postsynaptic membrane of glutamatergic synapses, the cAMP-dependent protein kinase (PKA), protein kinase
C (PKC), and calcineurin (CaN) anchoring protein AKAP79/150 is recruited to NMDA and AMPA glutamate receptors by
postsynaptic density (PSD)-95 family membrane-associated guanylate kinase (MAGUK) scaffold proteins. These signaling
scaffold complexes may function to regulate receptor phosphorylation in synaptic plasticity. Thus, it is important
to understand regulation of AKAP79/150 targeting to synapses and recruitment to PSD-MAGUK complexes. AKAP79 is
targeted to the plasma membrane by an N-terminal basic domain that binds phosphatidylinositol-4,5-bisphosphate
(PI-4,5-P(2)) and is regulated by PKC phosphorylation and calmodulin binding. Here we demonstrate that this same
domain also binds F-actin in a calmodulin- and PKC-regulated manner, targets to membrane ruffles enriched in F-actin
and PI-4,5-P(2) in COS7 cells, and localizes to dendritic spines with F-actin and PSD-MAGUKs in hippocampal neurons.
Inhibition of actin polymerization disrupted AKAP79 targeting of PKA and CaN to ruffles in COS7 cells and endogenous
AKAP79/150 dendritic spine localization with PKA, CaN, and PSD-MAGUKs in neurons. AKAP79/150 postsynaptic localization
was rapidly regulated by NMDA receptors through CaN activation and F-actin remodeling, further suggesting that
AKAP79/150 signaling scaffold targeting depends on actin dynamics. NMDA receptor activation also regulated dendritic
spine localization of PKA and CaN and association of the AKAP79/150-PKA complex with PSD-MAGUKs. Because AMPA receptor
PKA phosphorylation and synaptic localization are regulated by similar NMDA receptor-CaN signaling pathways linked
to hippocampal long-term depression, this regulation of AKAP79/150 postsynaptic targeting might be important for
synaptic plasticity.
=================
Neuron 2002 Aug 1;35(3):535-45 Related Articles, Links
Polyribosomes redistribute from dendritic shafts into spines with enlarged synapses during LTP in developing rat
hippocampal slices.
Ostroff LE, Fiala JC, Allwardt B, Harris KM.
Biology Department, Program in Neuroscience, Boston University, 5 Cummington Street, Boston, MA 02215, USA.
The presence of polyribosomes in dendritic spines suggests a potential involvement of local protein synthesis in
the modification of synapses. Dendritic spine and synapse ultrastructure were compared after low-frequency control
or tetanic stimulation in hippocampal slices from postnatal day (P)15 rats. The percentage of spines containing
polyribosomes increased from 12% +/- 4% after control stimulation to 39% +/- 4% after tetanic stimulation, with
a commensurate loss of polyribosomes from dendritic shafts at 2 hr posttetanus. Postsynaptic densities on spines
containing polyribosomes were larger after tetanic stimulation. Local protein synthesis might therefore serve to
stabilize stimulation-induced growth of the postsynaptic density. Furthermore, coincident polyribosomes and synapse
enlargement might indicate spines that are expressing long-term potentiation induced by tetanic stimulation.
=============
Prog Brain Res 2002;136:135-43 Related Articles, Links
Modification of dendritic development.
Feria-Velasco A, del Angel AR, Gonzalez-Burgos I.
Division of Pathology, CIATEJ (SEP-CONACyT), Av. Normalistas 800, 44270 Guadalajara, Jal., Mexico. aferia@ciatej.net.mx
Since 1890 Ramon y Cajal strongly defended the theory that dendrites and their processes and spines had a function
of not just nutrient transport to the cell body, but they had an important conductive role in neural impulse transmission.
He extensively discussed and supported this theory in the Volume 1 of his extraordinary book Textura del Sistema
Nervioso del Hombre y de los Vertebrados. Also, Don Santiago significantly contributed to a detailed description
of the various neural components of the hippocampus and cerebral cortex during development. Extensive investigation
has been done in the last Century related to the functional role of these complex brain regions, and their association
with learning, memory and some limbic functions. Likewise, the organization and expression of neuropsychological
qualities such as memory, exploratory behavior and spatial orientation, among others, depend on the integrity and
adequate functional activity of the cerebral cortex and hippocampus. It is known that brain serotonin synthesis
and release depend directly and proportionally on the availability of its precursor, tryptophan (TRY). By using
a chronic TRY restriction model in rats, we studied their place learning ability in correlation with the dendritic
spine density of pyramidal neurons in field CA1 of the hippocampus during postnatal development. We have also reported
alterations in the maturation pattern of the ability for spontaneous alternation and task performance evaluating
short-term memory, as well as adverse effects on the density of dendritic spines of hippocampal CA1 field pyramidal
neurons and on the dendritic arborization and the number of dendritic spines of pyramidal neurons from the third
layer of the prefrontal cortex using the same model of TRY restriction. The findings obtained in these studies
employing a modified Golgi method, can be interpreted as a trans-synaptic plastic response due to understimulation
of serotoninergic receptors located in the hippocampal Ammon's horn and, particularly, on the CA1 field pyramidal
neurons, as well as on afferences to the hippocampus which needs to be further investigated.
=============
Neuron 2002 Jul 3;35(1):91-105 Related Articles, Links
Depolarization drives beta-Catenin into neuronal spines promoting changes in synaptic structure and function.
Murase S, Mosser E, Schuman EM.
Caltech/HHMI, Division of Biology, 216-76, 1200 East California Boulevard, Pasadena 91125, USA.
Activity-induced changes in adhesion molecules may coordinate presynaptic and postsynaptic plasticity. Here, we
demonstrate that beta-catenin, which mediates interactions between cadherins and the actin cytoskeleton, moves
from dendritic shafts into spines upon depolarization, increasing its association with cadherins. beta-catenin's
redistribution was mimicked or prevented by a tyrosine kinase or phosphatase inhibitor, respectively. Point mutations
of beta-catenin's tyrosine 654 altered the shaft/spine distribution: Y654F-beta-catenin-GFP (phosphorylation-prevented)
was concentrated in spines, whereas Y654E-beta-catenin-GFP (phosphorylation-mimic) accumulated in dendritic shafts.
In Y654F-expressing neurons, the PSD-95 or associated synapsin-I clusters were larger than those observed in either
wild-type-beta-catenin or also Y654E-expressing neurons. Y654F-expressing neurons exhibited a higher minifrequency.
Thus, neural activity induces beta-catenin's redistribution into spines, where it interacts with cadherin to influence
synaptic size and strength.
===============
Neuron 2002 Jul 3;35(1):1-3 Related Articles, Links
Comment on:
Neuron. 2002 Jul 3;35(1):77-89.
Cadherins communicate structural plasticity of presynaptic and postsynaptic terminals.
Goda Y.
MRC Cell Biology Unit and Laboratory for Molecular Cell Biology, University College London, Gower Street, United
Kingdom.
Synapse adhesion molecules play a key role in specifying and facilitating the recognition of axodendritic contacts.
New studies by and reported in this issue of Neuron reveal multiple functions for the cadherin-catenin complex.
This adhesion complex regulates synaptogenesis and coordinates synaptic strength with presynaptic and postsynaptic
organization, including the shape of dendritic spines.
=========
Synapse 2002 Jul;45(1):10-24 Related Articles, Links
Differentiation of spinous synapses in the mouse organ of corti.
Sobkowicz HM, Slapnick SM, August BK.
Neurology Department, University of Wisconsin, Madison, Wisconsin 53706, USA. hmsobkow@facstaff.wisc.edu
The inner hair cells, the primary auditory receptors, are perceived only as a means for transfer of sound signals
via the auditory nerve to the central nervous system. During initial synaptogenesis, they receive relatively few
and mainly somatic synapses. However, around the onset of hearing (10-14 postnatal days in the mouse), a complex
network of local spinous synapses differentiates, involving inner hair cells, their afferent dendrites, and lateral
olivocochlear terminals. Inner hair cell spines participate in triadic synapses between olivocochlear terminals
and afferent dendrites. Triadic synapses have not yet been confirmed in the adult. Synaptic spines of afferent
dendrites form axodendritic synapses with olivocochlear terminals and somatodendritic synapses with inner hair
cells. The latter are of two types: ribbon-dendritic spines and stout dendritic spines surrounded only by a crown
of synaptic vesicles. Formation of spinous afferent synapses results from sprouting of dendritic filopodia that
intussuscept inner hair cell cytoplasm. This process continues in the adult, indicating ongoing synaptogenesis.
Spinous processes of olivocochlear synaptic terminals contact adjacent afferent dendrites, thus integrating their
connectivity. They develop about 14 postnatal days, but their presence in the adult has yet to be confirmed. Differentiation
of spinous synapses in the organ of Corti results in a total increase of synaptic contacts and in a complexity
of synaptic arrangements and connectivity. We propose that spinous synapses provide the morphological substrate
for local processing of initial auditory signals within the cochlea. Copyright 2002 Wiley-Liss, Inc.
==============
Brain Res Brain Res Rev 2002 Jun;39(1):29-54 Related Articles, Links
Dendritic spine pathology: cause or consequence of neurological disorders?
Fiala JC, Spacek J, Harris KM.
Department of Biology, Boston University, 5 Cummington Street, MA 02215, USA. fiala@bu.edu
Altered dendritic spines are characteristic of traumatized or diseased brain. Two general categories of spine pathology
can be distinguished: pathologies of distribution and pathologies of ultrastructure. Pathologies of spine distribution
affect many spines along the dendrites of a neuron and include altered spine numbers, distorted spine shapes, and
abnormal loci of spine origin on the neuron. Pathologies of spine ultrastructure involve distortion of subcellular
organelles within dendritic spines. Spine distributions are altered on mature neurons following traumatic lesions,
and in progressive neurodegeneration involving substantial neuronal loss such as in Alzheimer's disease and in
Creutzfeldt-Jakob disease. Similarly, spine distributions are altered in the developing brain following malnutrition,
alcohol or toxin exposure, infection, and in a large number of genetic disorders that result in mental retardation,
such as Down's and fragile-X syndromes. An important question is whether altered dendritic spines are the intrinsic
cause of the accompanying neurological disturbances. The data suggest that many categories of spine pathology may
result not from intrinsic pathologies of the spiny neurons, but from a compensatory response of these neurons to
the loss of excitatory input to dendritic spines. More detailed studies are needed to determine the cause of spine
pathology in most disorders and relationship between spine pathology and cognitive deficits.
==============
Annu Rev Neurosci 2002;25:127-49 Related Articles, Links
Molecular control of cortical dendrite development.
Whitford KL, Dijkhuizen P, Polleux F, Ghosh A.
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
Dendritic morphology has a profound impact on neuronal information processing. The overall extent and orientation
of dendrites determines the kinds of input a neuron receives. Fine dendritic appendages called spines act as subcellular
compartments devoted to processing synaptic information, and the dendritic branching pattern determines the efficacy
with which synaptic information is transmitted to the soma. The acquisition of a mature dendritic morphology depends
on the coordinated action of a number of different extracellular factors. Here we discuss this evidence in the
context of dendritic development in the cerebral cortex. Soon after migrating to the cortical plate, neurons extend
an apical dendrite directed toward the pial surface. The oriented growth of the apical dendrite is regulated by
Sema3A, which acts as a dendritic chemoattractant. Subsequent dendritic development involves signaling by neurotrophic
factors and Notch, which regulate dendritic growth and branching. During postnatal development the formation and
stabilization of dendritic spines are regulated in part by patterns of synaptic activity. These observations suggest
that extracellular signals play an important role in regulating every aspect of dendritic development and thereby
exert a critical influence on cortical connectivity.
=============
Neuroscience 2002;111(4):853-62 Related Articles, Links
Dendritic spine plasticity in hippocampus.
Gazzaley A, Kay S, Benson DL.
Fishberg Research Center for Neurobiology and Program in Cell Adhesion, The Mount Sinai School of Medicine, P.O.
Box 1065/Neurobiology, 1425 Madison Avenue, New York, NY 10029, USA.
Most excitatory input in the hippocampus and cerebral cortex impinges on dendritic spines. Alterations in dendritic
spine density or shape are suspected to be morphological manifestations of changes in physiology or behavior. The
links between spine plasticity and physiological responses have probably been best studied in the hippocampus in
the context of changes in the circulating levels of steroid hormones or long-term potentiation. Here we review
and present data which indicate that both the age of the preparation and the timing of the analysis can dramatically
effect the results obtained. Collectively the data suggest that different cellular and morphological strategies
may be utilized at different ages and under different circumstances to effect similar physiological responses or
behaviors.
============
Recent Prog Horm Res 2002;57:357-84 Related Articles, Links
Estrogen actions throughout the brain.
McEwen B.
Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, The Rockefeller University, New York, New
York 10021, USA. mcewen@rockefeller.edu
Besides affecting the hypothalamus and other brain areas related to reproduction, ovarian steroids have widespread
effects throughout the brain, on serotonin pathways, catecholaminergic neurons, and the basal forebrain cholinergic
system as well as the hippocampal formation, a brain region involved in spatial and declarative memory. Thus, ovarian
steroids have measurable effects on affective state as well as cognition, with implications for dementia. Two actions
are discussed in this review; both appear to involve a combination of genomic and nongenomic actions of ovarian
hormones. First, regulation of the serotonergic system appears to be linked to the presence of estrogen- and progestin-sensitive
neurons in the midbrain raphe as well as possibly nongenomic actions in brain areas to which serotonin neurons
project their axons. Second, ovarian hormones regulate synapse turnover in the CA1 region of the hippocampus during
the 4- to 5-day estrous cycle of the female rat. Formation of new excitatory synapses is induced by estradiol and
involves N-methyl-D-aspartate (NMDA) receptors, whereas downregulation of these synapses involves intracellular
progestin receptors. A new, rapid method of radioimmunocytochemistry has made possible the demonstration of synapse
formation by labeling and quantifying the specific synaptic and dendritic molecules involved. Although NMDA receptor
activation is required for synapse formation, inhibitory interneurons may play a pivotal role as they express nuclear
estrogen receptor-alpha (ERa). It is also likely that estrogens may locally regulate events at the sites of synaptic
contact in the excitatory pyramidal neurons where the synapses form. Indeed, recent ultrastructural data reveal
extranuclear ERalpha immunoreactivity within select dendritic spines on hippocampal principal cells, axons, axon
terminals, and glial processes. In particular, the presence of ER in dendrites is consistent with a model for synapse
formation in which filopodia from dendrites grow out to find new synaptic contacts and estrogens regulate local,
post-transcriptional events via second messenger systems.
=============
: Neurosci Lett 2002 May 24;324(3):209-12 Related Articles, Links
Drebrin, a dendritic spine protein, is manifold decreased in brains of patients with Alzheimer's disease and Down
syndrome.
Shim KS, Lubec G.
Department of Pediatrics, University of Vienna, Waehringer Guertel 18, A-1090 Vienna, Austria.
Drebrin, located in the dendritic spines of the neuron, plays a role in the synaptic plasticity together with actin
filaments. Although drebrin regulates the morphological changes of spines in neurodegenerative disease such as
Alzheimer's disease (AD), drebrin in Down syndrome (DS) showing AD-like neuropathology has not been studied. We
used Western blotting to determine protein levels of drebrin and F-actin in frontal, temporal cortex and cerebellum
from patients with DS and AD as compared to controls. A monoclonal antibody against drebrin and F-actin was used.
Drebrin levels were significantly decreased in frontal (means +/- standard deviation; DS 0.24 +/- 0.52; AD 0.16
+/- 0.14; controls 2.56 +/- 3.48) and temporal cortex (DS 0.07 +/- 0.11; AD 0.07 +/- 0.15; controls 1.71 +/- 1.51)
and drebrin was also decreased when normalized with F-actin. No changes were observed in cerebellum. Decreased
drebrin could not simply be due to cell loss (F-actin) or neuronal loss (comparable neuron-specific enolase between
groups). Reduced drebrin could be responsible for or representing the loss of spine plasticity in DS and may be
a useful indicator for the impaired arborization in neurodegenerative disorders.
================
Hippocampus 2002;12(2):186-205 Related Articles, Links
Projections from the lateral, basal, and accessory basal nuclei of the amygdala to the entorhinal cortex in the
macaque monkey.
Pitkanen A, Kelly JL, Amaral DG.
A.I. Virtanen Institute, University of Kuopio, Finland.
We used the anterograde tracers Phaseolus vulgaris-leucoagglutinin (PHA-L) and biotinylated dextran amine (BDA)
to examine the projections from the lateral, basal, and accessory basal nuclei of the amygdaloid complex to the
entorhinal cortex in Macaca fascicularis monkeys. The heaviest amygdaloid projections originate in the lateral
nucleus, which innervates the rostrally situated entorhinal fields but does not project to the caudal entorhinal
cortex. The most extensive projections originate in the ventral division of the lateral nucleus. Injections in
this subdivision lead to moderate to heavy fiber and terminal labeling in the entorhinal cortex, rostral levels
of the rostral intermediate El (ER) and lateral fields, (ELr), and light labeling in the olfactory field EO. The
projections from all portions of the lateral nucleus terminate most heavily in layer III. Layer II of EO and ER
also receives a substantial input from the ventral division of the lateral nucleus. Layer II of ELr receives light
innervation from all portions of the lateral nucleus that project to layer III. Projections from the basal nucleus
arise mainly from the parvicellular division and are light to moderate in density. Fibers terminate predominantly
in ELr, ER, EO, and the caudal portion of the lateral field (Elc); only the most rostral portion of El receives
projections. While fibers from the basal nucleus innervate the same layers as the projections from the lateral
nucleus, they tend to have a more vertical or radial orientation within the entorhinal cortex. Electron microscopic
analysis of these fibers and terminals indicates that they overwhelmingly form asymmetrical synapses onto dendrites
and dendritic spines. The accessory basal nucleus provides a light projection to the same regions of the entorhinal
cortex innervated by the lateral and basal nuclei.
==================
Neuron 2002 Apr 11;34(2):265-73 Related Articles, Links
Formation of dendritic spines with GABAergic synapses induced by whisker stimulation in adult mice.
Knott GW, Quairiaux C, Genoud C, Welker E.
Institut de Biologie Cellulaire et Morphologie, Universite de Lausanne, Rue du Bugnon 9, CH 1005, Lausanne, Switzerland.
During development, alterations in sensory experience modify the structure of cortical neurons, particularly at
the level of the dendritic spine. Are similar adaptations involved in plasticity of the adult cortex? Here we show
that a 24 hr period of single whisker stimulation in freely moving adult mice increases, by 36%, the total synaptic
density in the corresponding cortical barrel. This is due to an increase in both excitatory and inhibitory synapses
found on spines. Four days after stimulation, the inhibitory inputs to the spines remain despite total synaptic
density returning to pre-stimulation levels. Functional analysis of layer IV cells demonstrated altered response
properties, immediately after stimulation, as well as four days later. These results indicate activity-dependent
alterations in synaptic circuitry in adulthood, modifying the flow of sensory information into the cerebral cortex.
=======================
note in all of these the tie to memory and so habits where context will 'set off' associations and, in well versed
memories, responses to the context.
In all of these is the thread of (a) post synaptic modifications and (b) the influence on context to 'push' once
you have the modifications. The linking process is in the hippocampus, the 'emotionalisation' is derived from the
amygdala. Both of these feed into the associations areas of the frontal cortex etc.
===============
MORE ON NMDA receptor etc:
http://bioinformatics.weizmann.ac.il/hotmolecbase/entries/nmda.htm
and http://web.sfn.org/content/Publications/BrainBriefings/nmda.html
and http://www.biopsychiatry.com/nmdarew.htm
and http://aidscience.org/neuroaids/zones/articles/2000/11/NMDA/index.asp
================