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Federico Casares

Publications and source records attributed to Federico Casares.

4 recordsLinked to original sources
PubMed2004

Nitric oxide modulates microglial activation.

BACKGROUND: Nitric oxide (NO) has important physiological regulatory roles, i.e, vasodilation, neurotransmitter release, etc. Little is known about the processes in neural tissues, which stabilize microglia. This study attempts to answer this question by demonstrating a role for basal NO in maintaining microglia juxtaposed to neurons. MATERIAL/METHODS: Mytilus edulis (a marine bivalve), were used to examine microglia egress from excised pedal ganglia microscopically. Nitric oxide is measured in excised pedal ganglia amperometrically in real-time. RESULTS: Pedal ganglia exhibit basal NO release (1 nM range). Inhibition of basal NO release by L-NAME results in greater numbers of microglia in the incubation medium. This process appears to involve two phases of egress. The first involves a slow egress of microglia, whereas the second, occurring 18 hours later, involves a more rapid release of these cells. Low levels of the NO donor SNAP (1 nM) does not interrupt microglial egress, whereas in the presence of L-NAME it does. Exposing the ganglia to high NO levels for a short period of time inhibits their egress. CONCLUSIONS: Spontaneous ganglionic NO release maintains/stabilizes microglia juxtaposed to neurons. Excised ganglia at the various observation periods reveals a transition of constitutive nitric oxide synthase (NOS) to inducible NOS derived NO. It also appears that the microglia in some unknown manner become insensitive to iNOS derived NO since they exhibit enhanced migration during this last phase of the ganglionic NO response. Taken together, NO is involved with regulating microglial activation.

Animals↗
PubMed2002

The blueprint for stress can be found in invertebrates.

Through an extremely complicated equilibrium called homeostasis, all living organisms maintain their survival in the face of both externally and internally generated "stimuli". This apparent harmony is constantly challenged. Survival through successful adaptation is maintained as close to steady state as possible by adaptive responses, which may also be called perturbation responses since they have a constitutively defined dynamic capacity, i.e., an immediate limit, in a series of balancing and feedback activities reflecting an astounding array of biological, psychological and sociological behaviors. The broad spectrum of stimuli capable of engaging this protective response is remarkable. We define stress as a type of stimulation that is stronger and lasts for a longer duration, upsetting a typical perturbation response given its dynamic parameters. The stress response, which evolves out of the perturbation response, involves inducible signal molecules, i.e., cytokines. We surmise that the ability to exist in an ever-changing environment was a requirement for all life forms, including invertebrates and single celled organisms. It would be expected that these organisms exhibit both perturbation and stress responses. In this regard, we demonstrate that these organisms have mammalian-like signal molecule systems, i.e., opioid, and corresponding behaviors that are similar to those found in mammals with regard to both perturbation and stress responses. Thus, it would appear that these responses evolved first in simpler organisms and were then maintained and enhanced during evolution.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Immunocytes modulate ganglionic nitric oxide release which later affects their activity level.

Pedal ganglia excised and maintained in culture for up to 2 h, release NO at low levels. The range can vary between 0 to 1.1 nM. Non-stimulated immunocytes do not significantly stimulate ganglionic NO release when incubated with pedal ganglia. However, ganglia exposed to immunocytes that had been previously activated by a 30 min incubation with interleukin 1 beta, release NO significantly above basal levels. In these experiments, 91 +/- 2.5% of the non-stimulated immunocytes exhibited form factors in the 0.72 to 0.89 range (sampled prior to ganglionic addition), whereas 62 +/- 10.3% of the interleukin 1 beta stimulated immunocytes had form factors in the 0.39 to 0.49 range, demonstrating activation. Addition of the nitric oxide synthase inhibitor, L-NAME (10(-4) M), inhibited basal ganglionic NO release as well as that initiated by exposing the ganglia to activated immunocytes. Interestingly, non activated immunocytes, following ganglionic exposure, exhibited activity levels in the 13% range, representing a non significant increase. Cells exposed to interleukin 1 beta had a 65% activity level at the beginning of the experiment, followed by a drop of activity to 19 +/- 3.2% after ganglionic exposure. Repeating this last observation in the presence of L-NAME (10(-4) M), brought the activity level of the immunocytes back to the pre-ganglionic exposure level of activity, demonstrating that ganglionic NO was involved in down regulating immunocyte activity.

Animals↗