Publications by authors named "Izabela Panek"

Background: The REGAIN (Regional versus General Anesthesia for Promoting Independence after Hip Fracture) trial found similar ambulation and survival at 60 days with spinal versus general anesthesia for hip fracture surgery. Trial outcomes evaluating pain, prescription analgesic use, and patient satisfaction have not yet been reported.

Objective: To compare pain, analgesic use, and satisfaction after hip fracture surgery with spinal versus general anesthesia.

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Our movements are shaped by our perception of the world as communicated by our senses. Perception of sensory information has been largely attributed to cortical activity. However, a prior level of sensory processing occurs in the spinal cord.

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Motor systems must be responsive to the environment in which the organism moves. Accordingly, there are many sensory systems that affect intrinsic motor programs. In this mini review, we will discuss the effects that inputs from cutaneous low-threshold mechanoreceptors have on motor function, focusing on locomotion and hand grasp.

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G-protein-coupled octopamine (OA) receptors mediate their effects by Ca²(+) signaling or adjusting intracellular cAMP levels. Depending on OA concentration and cell type, activation of OA receptors in excitable cells triggers excitatory or inhibitory effects, but the mechanisms by which Ca²(+) or cAMP mediates these effects are not well understood. We investigated signaling mechanisms that are potentially activated by OA, and OA effects on excitability and frequency sensitivity in mechanosensory neurons innervating the VS-3 slit sensilla on the patella of the spider Cupiennius salei.

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gamma-Aminobutyric acid type A (GABA(A)) receptor activation inhibits many primary afferent neurons by depolarization and increased membrane conductance. Deterministic (step and sinusoidal) functions are commonly used as stimuli to test such inhibition. We found that when the VS-3 mechanosensory neurons innervating the spider lyriform slit-sense organ were stimulated by randomly varying white-noise mechanical or electrical signals, their responses to GABA(A) receptor agonists were more complex than the inhibition observed during deterministic stimulation.

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Activation of ionotropic gamma-aminobutyric acid type A (GABA(A)) receptors depolarizes neurons that have high intracellular [Cl(-)], causing inhibition or excitation in different cell types. The depolarization often leads to inactivation of voltage-gated Na channels, but additional ionic mechanisms may also be affected. Previously, a simulated model of spider VS-3 mechanosensory neurons suggested that although voltage-activated Na(+) current is partially inactivated during GABA-induced depolarization, a slowly activating and inactivating component remains and may contribute to the depolarization.

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Afferent neurons entering the central nervous systems of vertebrates and invertebrates receive presynaptic inhibition on their axon terminals. This usually involves an increase in membrane conductance (shunting) and depolarization (primary afferent depolarization, PAD). In arachnids and crustaceans the peripherally located parts of afferent neurons also receive efferent synapses.

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Peripherally located parts of spider mechanosensory neurons are modulated by several neurotransmitters released from apposed efferent fibers. Activities of acetylcholine (ACh) synthesizing enzyme choline acetyltransferase (ChAT) and ACh degrading enzyme acetylcholine esterase (AChE) were previously found in some efferent fibers. ChAT activity was also present in all the mechanosensory neurons, while AChE activity was only found in some.

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Most mechanosensory neurons are inhibited by GABAergic efferent neurons. This inhibition is often presynaptic and mediated by ionotropic GABA receptors at the axon terminals. GABA receptor activation opens Cl- channels, leading to membrane depolarization and an increase in membrane conductance.

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GABAergic inhibition of mechanosensory afferent axon terminals is a widespread phenomenon in vertebrates and invertebrates. Spider mechanoreceptor neurons receive efferent innervation on their peripherally located axons, somata and sensory dendrites, and the dendrites have recently been shown to be excitable. Excitability of the spider sensory neurons is inhibited by muscimol and GABA, agonists of ionotropic GABA receptors.

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The mechanosensilla in spider exoskeleton are innervated by bipolar neurons with their cell bodies close to the cuticle and dendrites attached to it. Numerous efferent fibers synapse with peripheral parts of the mechanosensory neurons, with glial cells surrounding the neurons, and with each other. Most of these efferent fibers are immunoreactive to gamma-aminobutyric acid (GABA), and the sensory neurons respond to agonists of ionotropic GABA receptors with a rapid and complete inhibition.

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Arthropod mechanosensory afferents have long been known to receive efferent synaptic connections onto their centrally located axon terminals. These connections cause presynaptic inhibition by attenuating the action potentials arriving at the axon terminals, thus reducing the synaptic potentials in the postsynaptic neurons. This type of inhibition can specifically reduce the excitation of selected postsynaptic neurons while leaving others unaffected.

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Many neurons of the vertebrate and invertebrate central nervous system (CNS) exhibit rhythmic oscillations of membrane potentials in absence of external stimuli. Spontaneous firing of these cells generates the activity in various areas of CNS. Firing patterns produced by autoactive neurons and role of several ionic conductances in driving membrane potential to the threshold of action potential generation is described.

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Spider mechanosensory neurons receive an extensive network of efferent synapses onto their sensory dendrites, somata and distal axonal regions. The function of these synapses is unknown. Peripheral synapses are also found on crustacean stretch-receptor neurons but not on mechanosensory afferents of other species, although inhibitory GABAergic synapses are a common feature of centrally located axon terminals.

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