PubMed Health⌕ Search

Biomedical subjects

C L Keenan

Publications and source records attributed to C L Keenan.

8 recordsLinked to original sources
PubMed1990

Long-term synaptic potentiation in the amygdala.

The manner in which the circuitry of the amygdala computes its suspected mnemonic functions has been a mystery, partly because the cytoarchitectual complexity of this nuclear group has impeded the necessary cellular analysis. Here we report in vitro methods and results that may help elucidate cellular learning mechanisms in amygdala neurons. The amygdala brain slice preparation was combined with the single-electrode clamp (SEC) technique for intracellular analysis of membrane properties and synaptic responses. With respect to the active and passive membrane properties, we found considerable diversity among the population of cells that were sampled in the lateral and basolateral nuclei (n = 85). Synaptic inputs to these neurons were studied by stimulating the external capsule (EC), which was shown to produce a complex response that typically consisted of an excitatory followed by an inhibitory component. Based on several criteria, the excitatory component appeared to reflect a monosynaptic connection from the EC. One immediate goal was to discover whether the excitatory component displays the phenomenon of long-term potentiation (LTP)--a persistent increase in synaptic strength that can be induced by brief periods of the appropriate synaptic stimulation. Indeed, we found that high-frequency (100 Hz) stimulation of the EC induced LTP in 80% of the cells from which suitable recordings were obtained (n = 20). This finding of LTP in the amygdala is significant in regard to current efforts to explore linkages between this use-dependent form of synaptic plasticity and rapid kinds of associative learning.

Amygdala↗
PubMed1990

Hebbian synapses: biophysical mechanisms and algorithms.

We have examined the evolution of the concept of a Hebbian synaptic modification and have suggested a contemporary definition. The biophysical mechanism demonstrated in vitro to control the induction of one type of hippocampal LTP has been shown to satisfy our definition of a Hebbian synaptic modification. Whether this biophysical mechanism is involved in the organization of behavior in the manner that Hebb originally envisioned remains to be seen. We have also summarized several modification algorithms that have been explored in theoretical studies of learning in adaptive networks. These algorithms also satisfied our definition of a Hebbian modification, but their relationships to known neurobiology require further exploration. By reviewing the biophysical mechanisms and formal algorithms together, we have exposed obvious similarities and differences. Such comparisons may help bridge the gap between computational theory and knowledge of the neurobiology of use-dependent synaptic change. Current models of LTP reveal that the activity-modification relationships are extremely sensitive to the biophysical/molecular details. The activity-modification relationships obviously can have a major influence on adaptive neurodynamics at the network level. As more accurate representations of the biological complexity and diversity are introduced into adaptive network simulations, we expect to gain new insights into the classes of computation that particular networks are capable of performing.

Algorithms↗
PubMed1988

Long-term synaptic potentiation.

Long-term synaptic potentiation (LTP) is a leading candidate for a synaptic mechanism of rapid learning in mammals. LTP is a persistent increase in synaptic efficacy that can be quickly induced. The biophysical process that controls one type of LTP is formally similar to a synaptic memory mechanism postulated decades ago by the psychologist Donald Hebb. A key aspect of the modification process involves the N-methyl-D-aspartate (NMDA) receptor-ionophore complex. This ionophore allows calcium influx only if the endogenous ligand glutamate binds to the NMDA receptor and if the voltage across the associated channel is also sufficiently depolarized to relieve a magnesium block. According to one popular hypothesis, the resulting increase in the intracellular calcium concentration activates protein kinases that enhance the postsynaptic conductance. Further biophysical and molecular understanding of the modification process should facilitate detailed explorations of the mnemonic functions of LTP.

Animals↗
PubMed1988

Videomicroscopy of acute brain slices from amygdala and hippocampus.

Video-enhanced contrast, differential-interference contrast microscopy (VEC-DICM) was used to visualize the cytoarchitecture and subcellular neuronal structure of acute brain slices from rat hippocampus and amygdala. Even at low-power magnification, the VEC-DICM system vastly improved our ability to visualize and examine the gross organization of the tissue. With medium-power magnification, the neuronal somata and proximal dendrites were clearly visible. With high-power magnification, some of the subcellular details could be clearly discerned--including cell nuclei, cell nucleoli, fine dendritic processes, and varicosities that may be synaptic expansions. We conclude that improved optical techniques should be valuable to cellular neurobiologists interested in structure-function relationships in brain slices.

Aging↗
PubMed1987

Thermosensitivity of dorsal raphe neurons in vitro.

Thermosensitivity of raphe neurons was studied in tissue slices of rat brainstems (400-500 micron). Measurement of activity of single cells in the dorsal raphe region of the slices revealed that the majority of neurons (89%) were sensitive to changes in temperature. Over the range 34 to 42 degrees C, 3 classes of thermosensitive cells were found: warm (61%), cold (15%) and biphasic type cells (13%). Many dorsal raphe neurons may be intrinsically temperature sensitive and may serve as extrahypothalamic thermodetector components in the integrative process of central thermoregulation.

Animals↗
PubMed1981

Cytoarchitecture of primitive brains: Golgi studies in flatworms.

Notoplana acticola, a free-living polyclad flatworm, has a small but well-defined brain that controls behavior of peripherally based motoneurones. This is the most primitive brain currently being studied electrophysiologicaly, but little is known of its cytoarchitecture. Using a modified rapid Golgi method, we have investigated neurone configurations within this brain. Superficially the brain resembles those of other invertebrates, but its cells also possess many vertebrate features. There is a surprising diversity of cell types with complicated branching patterns. Multipolar neurones appear to be the most common type. A few typical invertebrate monopolar cells were also stained. Bipolar cells occur in the rind. Processes resembling dendritic spines were observed. Measurements of these indicate that they fall within the range found in other vertebrates and invertebrates. Small multipolar cells that could either be glial or interneurones were found scattered through the brain.

Animals↗
PubMed1980

Neuronal repair and avoidance behavior in the flatworm, Notoplana acticola.

In Notoplana avoidance behavior is lost after bisection of the brain or removal of one of its lobes. Behavioral recovery usually occurs within 3-10 days. Recovery of individuals may be gradual or abrupt. Grouped data shows gradual linear repair of turning behavior. Most animals with all connectives between the two lobes of the brain severed recovered preoperative responses, while those with one lobe of the brain removed averaged about 60% of the preoperative level of response. Some individuals in both groups recovered completely. Histological evidence of neuronal repair was found in all animals. Where the lobes of the brain were separated, connectives between them appeared to re-form. In worms with one lobe of the brain removed, the nerves disconnected by the excision joined the remaining lobe. Action potentials are conducted across repaired tissue in both split-brain and half-brain worms in both seawater and Mg2+-rich solutions. CNS repair appears to involve functional synaptic contacts. Notoplana does not replace ganglionic tissue but does compensate adequately for CNS damage.

Action Potentials↗