 |
ARTICLE |
Cellular/Molecular
Thermotactic Memory in C. elegans
Synaptic Activity of the AFD Neuron in Caenorhabditis
elegans Correlates with Thermotactic Memory
Aravinthan D. T. Samuel, Ruwan A. Silva, and Venkatesh N. Murthy (see pages 373-376)
It has been possible to identify synaptic transmission molecules
underlying simple behaviors in Caenorhabditis elegans
by screening mutants and working backward to identify the culprit genes. However, direct study of cellular events in C. elegans has proven difficult because of the small size of the
neurons. Samuel et al. use a clever strategy to investigate the role of the AFD neuron in thermotactic behavior (i.e., the ability of the worm
to detect spatial thermal gradients and move toward the temperature at
which it was cultivated). The worms can remember their cultivation
temperature for up to 4 hr, then they "forget." The authors used
AFD-specific promoters to restrict expression of a synaptic vesicle
protein [vesicle-associated membrane protein (VAMP)], along with a
pH-sensitive indicator (pHluorin), specifically to this neuronal type.
The 20 presynaptic terminals of AFD appeared as fluorescent puncta. The
fluorescent recovery after photobleaching (FRAP) of selected synapses
was used as a measure of synaptic release. The authors found that AFD
was active when the ambient temperature differed from the cultivation
temperature. AFD was inactive in worms that had been starved for 4 hr
(i.e., when they had forgotten the cultivation temperature). The
authors conclude that the AFD neuron is part of a comparator circuit
for temperature detection. Imaging strategies such as these may provide
a critical bridge between molecular and behavioral studies in C. elegans.
Development/Plasticity/Repair
Patterned Spontaneous Activity in Spinal Cord Development
Characterization of the Circuits That Generate Spontaneous
Episodes of Activity in the Early Embryonic Mouse Spinal Cord
M. Gartz Hanson and Lynn T. Landmesser (see pages
587-600)
Patterned neural activity, before input from the environment,
has been documented throughout the developing nervous system. Spontaneous activity, thought to play an important role in the establishment and refinement of connections, has been studied most
extensively in the visual system. In this issue, Hanson and Landmesser
used an isolated spinal cord-hindlimb preparation in the mouse to
identify the circuitry that generates local and distributed rhythmic,
patterned activity in the spinal cord. Activity was present before and
during the time at which motor neurons reach their peripheral targets
and was dependent on cholinergic and glycinergic transmission as well
as electrical coupling. AMPA/kainate or NMDA receptor-mediated
responses were not responsible for rhythmic activity. Rather, nicotinic
neurotransmission mediated by dihydro-
-erythroidine hydrobromide
(DH
E)-sensitive receptors provided the main excitatory drive.
Inhibition of glycinergic excitatory responses also completely abolished spontaneous patterned activity. Antidromic activation and
retrograde labeling of motor axons revealed an extensive network of
motor axon collaterals that arborize within motor columns, proximate
spinal cord regions, and even in developing fiber tracts of the spinal
cord. These collaterals contribute to an extensive, developing network
that can evoke both local and propagated rhythmic activity. Together,
these data provide a new conceptual framework for distinctive local and
propagating circuits in the spinal cord. In this scheme, motor neurons
are the central elements that drive the spontaneous activity that is
likely to influence the development and maturation of central and
peripheral motor function.
Behavioral/Systems/Cognitive
Trace Conditioning and Hippocampal Spine Formation
Associative Memory Formation Increases the Presence of Dendritic
Spines in the Hippocampus
Benedetta Leuner, Jacqueline Falduto, and Tracey J. Shors
(see pages 659-665)
Dendritic spines are one of the most striking structural
features of excitatory synapses on pyramidal neurons in the
hippocampus. These protuberances come in a variety of sizes and shapes
and can alter their shape within minutes to a variety of stimuli. Given
the role of the hippocampus in memory and synaptic plasticity, changes
in dendritic spine shape or number have long been considered as a
potential cause of increased synaptic efficacy. This idea has gained
support from studies of intact animals as well as in vitro
studies of synaptic plasticity. In this issue, Leuner et al. provide
additional evidence for changes in spine density in association with
learning. They analyzed hippocampal spine density on CA1 pyramidal
cells after a trace eyeblink conditioning paradigm, a task known to
require the hippocampus, and after training with delay conditioning, a
task that does not require the hippocampus but does cause increased
activity in hippocampal neurons. Both resulted in increases in spine
density. Interestingly, the increase was specific to the basal
dendrites of CA1 cells, whereas no changes occurred in the apical
dendrites. So is the increase in spines necessary for learning or does
it simply represent activity in the hippocampus? The authors argue that
the increased spine density accompanies associative memory, but that
the increase is not necessary for learning to occur.