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welfare of the groups involved. A change in purity standards is shown to create winners and losers among the consumers and the suppliers of the GM and non-GM products. Our analysis provides insights on labeling policies and the position of interest groups in countries with different adoption of, and attitudes towards genetically modified products. KEYWORDS: agricultural biotechnology, AP thresholds, coexistence, genetically modified foods, labeling, purity standards, tolerances Author Notes: Konstantinos Giannakas is Professor and Co-Director, Center for Agricultural

NEUROSCIENCES LONG-TERM POTENTIATION OF INTRINSIC EXCITABILITY 313 SO pA 50 ms CS 120 min -4 Β 20 o i > J . - 2 0 Η Ε > -40- T h r - ^ - 6 0 - Control TB Ρ 0.5 s Thr-*1 v x [10 mV 10 ms Fig. 1: Three major types of intrinsic plasticity: decreased AP threshold, reduced ΑΗΡ, and decreased dendritic attenuation. A. Correlated stimulation (CS) induces LTP and LTP-IE which is expressed as a decrease in the AP threshold (Thr) and ΑΗΡ amplitude (ΑΗΡ) in hippocampal CA1 pyramidal neurons. B. Theta-burst pairing stimulation (TBP) facilitates the backpropagation of

constant (8.1 ± 4.2 ms), capacitance (0.20 ± 0.13 nF) and resistance (48.0 ± 25.4 ΜΩ). Electrophysiological properties The steady state I/V properties of the cells were linear up to AP threshold membrane potentials (Fig. 4A). The cells fired large APs in response to injection of inward current (Fig. 4B). The action potentials of these cells reached or overshot zero mV. The AP duration was 0.53 ± 0.09 ms. They had spontaneous IPSPs (Fig. 4C). The cells had a small hyperpolarization after action potential (undershoot) of about 5 mV. The small undershoot had two

and others, many independent studies have confirmed the AIS as the usual site of AP initiation in various neuron types, including hippocampal ( Meeks and Mennerick, 2007 ) and neocortical ( Palmer and Stuart, 2006 ) pyramidal cells. Further studies suggested that the AP threshold is lowest in the AIS because of its high density of voltage-gated sodium channels, up to 50 times higher than at the soma ( Kole and Stuart, 2008 ). However, subsequent studies revealed a little difference between the sodium channel density at the AIS and soma ( Fleidervish et al., 2010

repola- rizes the neuron or attenuates the impact of depolarization by shifting the membrane potential towards the potassium equilibrium potential and away from AP threshold (11). Thus, altering the conductance of these channels effectively alters the excitability of the neurons endowed with them. Voltage-gated potassium channels Although all voltage-gated potassium (KV) channels contrib- ute to stabilization of the membrane potential, two of these channels have been shown to be particularly important reg- ulators of neuronal excitability: the KV4.2 channel that con

fibers result in different AP thresholds, refractory periods, and AP durations. Consequently, any change in the amplitude and waveform of the elicited CAP amplitude can be ascribed to a change in the number of firing fibers, which is equivalent to the sum of all fibers whose thresholds are met by a given stimulus intensity, i c [ 34 ]. It is presumed that in CAP1, recorded by pair1, the Aβ-fibers and Aδ-fibers contributed the APs that fell in the region between the apex and the tail section of the bell-shaped CAP1 (see Figure 4 ) and that the Aα-fibers, if not

subthreshold depolarization and are responsible for mediating the M-current (for review see ( Brown and Passmore, 2009)). At the AIS, they control AP threshold and reduce neuronal excitability (Fig. 2B; Shah et al. 2008). They also stabilize the resting membrane potential, thereby contributing to maintenance of Nav channel availability by preventing their subthreshold, depolarization-induced inactivation ( Battefeld et al., 2014). They can thus both increase AP conduction as well as restrict neuronal excitability, demonstrating the complex role K + channels play in AP