Modification by temperature of conduction and ganglionic transmission in the gastropod nervous system

The pedal ganglia of the terrestrial gastropod Ariolimax contain junctions between nerve fibers which are shown to be preferential points of fatigue and which exhibit facilitation (summation) of preganglionic impulses to produce a postganglionic spike. These characteristics in conjunction with others previously reported (reversible susceptibility to nicotine, convergence of preganglionic impulses, and inhibition of transmission through setting up a refractory state in the postganglionic fiber) are considered sufficient to indicate synaptic transmission in the pedal ganglia. The mean conduction velocity of the fastest fibers in the pedal nerves is 0.52 meter per second for preganglionic and 0.50 meter per second for postganglionic fibers at 7.56°C. The conduction rates at 21.76°C. are respectively 0.80 meter per second and 0.83 meter per second. The mean ganglionic delay is 0.033 second at 7.56°C. and 0.019 second at 21.76°C. The mean Q₁₀'s for conduction velocity are thus 1.37 for preganglionic and 1.42 for postganglionic fibers. The mean Q₁₀ for ganglionic delay is 1.49. If the assumption is made that the Q₁₀ for ganglionic delay is that of a limiting reaction, this figure then represents a value below which the Q₁₀ for synaptic delay is statistically improbable.     

The Electrical Response of the Planarian Ocellus

The planarian ocellar potential (OP), an action potential evoked from the planarian ocellus by a light flash, was recorded with microelectrodes. OP amplitude, latency, and peak delay varied as a function of stimulus intensity and state of adaptation in a manner similar to the responses of other photoreceptors. Changes in the OP that occurred with different directions of incident light are described and attributed to screening effects of the ocellar pigment cells. The temperature coefficient (Q₁₀) of OP latency was 1.5; latency decreased continuously as temperature was increased to destructive levels. The energy of activation of the rate of OP formation was calculated to approximate 10 kcal. These findings suggest dependence of OP latency on ionic diffusion and of OP formation on a biocatalytic process.     

Temperature Effect on Proximal to Distal Gradient of Quantal Release of Acetylcholine at Frog Endplate

The conduction velocity of the nerve terminal, mean quantal content, and release latencies of uniquantal endplate currents (EPCs) were recorded in proximal, central, and distal parts of the terminal by extracellular pipettes located 5, 50, and 100 mm from the end of myelinated nerve trunk. The spike conduction velocity, minimal latency, modal value of the latency histograms, and time interval during which 90% of EPCs released (P₉₀) at distal, central, and proximal part of the frog nerve terminal have different temperature dependency between 10° and 28°C. As shown by the size and time-course of reconstructed multiquantal EPCs, the secretion synchronization, which is greatest in distal parts, compensates at least partly for the progressive slowing of spike conduction velocity in the proximodistal direction, in particular at lower temperatures.     

Polymodal distribution of synaptic delays in the frog neuromuscular junction

Synaptic delay of single-quantum response with low mean quantal size (0.05–1) was measured during experiments on preparations of frog neuromuscular junctions using extracellular focal recording of presynaptic action potentials and endplate currents. It was found that distribution of these synaptic delays is of a polymodal nature and mean intermodal interval equaled 0.22±0.01 msec over 13 experiments. An increase in quantal size produced only a redistribution of mode weighting, while mean modal interval remained unchanged. A reduction in temperature induced an increase in the modal interval with the temperature coefficient Q₁₀=2.42±0.14 (n=15). The explanation is suggested that the process of quantal transmitter release is determined by interaction between the calcium-dependent mechanism for raising the likelihood of release on the one hand and the rhythmic operation of the system producing transmitter release on the other. The latter stage in the process depends on temperature, not intracellular Ca²⁺ concentration. The polymodal distribution of synaptic delay reflects the rhythmic operation of the transmitter release zone.I. M. Sechenov Institute of Evolutionary Physiology and Biochemistry, Academy of Sciences of the USSR, Leningrad. Translated from Neirofiziologiya, Vol. 18, No. 6, pp. 748–756, November–December, 1986.     

Voltage Gating of Shaker K+ Channels : The Effect of Temperature on Ionic and Gating Currents

Ionic (I_i) and gating currents (I_g) from noninactivating Shaker H4 K⁺ channels were recorded with the cut-open oocyte voltage clamp and macropatch techniques. Steady state and kinetic properties were studied in the temperature range 2–22°C. The time course of I_i elicited by large depolarizations consists of an initial delay followed by an exponential rise with two kinetic components. The main I_i component is highly temperature dependent (Q₁₀ > 4) and mildly voltage dependent, having a valence times the fraction of electric field (z) of 0.2–0.3 e_o. The I_g On response obtained between −60 and 20 mV consists of a rising phase followed by a decay with fast and slow kinetic components. The main I_g component of decay is highly temperature dependent (Q₁₀ > 4) and has a z between 1.6 and 2.8 e_o in the voltage range from −60 to −10 mV, and ∼0.45 e_o at more depolarized potentials. After a pulse to 0 mV, a variable recovery period at −50 mV reactivates the gating charge with a high temperature dependence (Q₁₀ > 4). In contrast, the reactivation occurring between −90 and −50 mV has a Q₁₀ = 1.2. Fluctuation analysis of ionic currents reveals that the open probability decreases 20% between 18 and 8°C and the unitary conductance has a low temperature dependence with a Q₁₀ of 1.44. Plots of conductance and gating charge displacement are displaced to the left along the voltage axis when the temperature is decreased. The temperature data suggests that activation consists of a series of early steps with low enthalpic and negative entropic changes, followed by at least one step with high enthalpic and positive entropic changes, leading to final transition to the open state, which has a negative entropic change.     

Effects of temperan a central synapse between identified motor neurons in the locust

Summary Changing the temperature from 10–40 °C modifies the transmission at an established monosynaptic connection between the fast extensor tibiae (FETi) and flexor tibiae motor neurons in the metathoracic ganglion of the locustSchistocerca gregaria (Forskål). Striking changes occur to the shape of the spikes, to membrane resistance, to the synaptic delay, and to the evoked synaptic potentials.In the presynaptic FETi motor neuron, raising the temperature reduces the amplitude of an antidromic spike recorded in the soma by a factor of 10 (40 mV to 4 mV), reduces the time taken to reach peak amplitude by 5 (3.5 to 0.7 ms) and decreases the duration at half maximum amplitude by 0.5. The conduction velocity of the spike in the axon is increased by 50% from 10 °C to 40 °C. Orthodromic spikes are affected by temperature in a similar way to the antidromic spikes.The membrane resistance of both pre- and postsynaptic motor neurons falls as the temperature is raised. The membrane resistance of FETi falls by a factor of 4 (about 4 M at 10 °C to 1 M at 40 °C). A contributory component to this fall could be the increase in the frequency of synaptic potentials generated as a result of inputs from other neurons. No temperature dependence could be demonstrated on the voltage threshold relative to resting potential for evoking orthodromic spikes, but because the resistance changes, the current needed to achieve this voltage must be increased at higher temperatures.The latency measured from the peak of the spike in the soma of FETi to the start of the EPSP in the soma of a flexor motor neuron decreases by a factor of 20 (10 ms at 10 °C to 0.5 ms at 40 °C).In a postsynaptic flexor tibiae motor neuron, the amplitude of the evoked synaptic potential increases by a factor of 3.4 (5 mV to 17 mV), its duration at half maximum amplitude decreases by 3 (7 ms at 12 °C to 2.3 ms at 32 °C) and its rate of rise increases by 3. An increased likelihood that spikes will occur in the flexor contributes to the enhanced amplitude of the compound EPSP at temperatures above 20 °C.Abbreviation FETi fast extensor tibiae motor neuron     

Parallel Changes in Structural and Functional Measures of Optic Nerve Myelination after Optic Neuritis

IntroductionVisual evoked potential (VEP) latency prolongation and optic nerve lesion length after acute optic neuritis (ON) corresponds to the degree of demyelination, while subsequent recovery of latency may represent optic nerve remyelination. We aimed to investigate the relationship between multifocal VEP (mfVEP) latency and optic nerve lesion length after acute ON.MethodsThirty acute ON patients were studied at 1,3,6 and 12 months using mfVEP and at 1 and 12 months with optic nerve MRI. LogMAR and low contrast visual acuity were documented. By one month, the mfVEP amplitude had recovered sufficiently for latency to be measured in 23 (76.7%) patients with seven patients having no recordable mfVEP in more than 66% of segments in at least one test. Only data from these 23 patients was analysed further.ResultsBoth latency and lesion length showed significant recovery during the follow-up period. Lesion length and mfVEP latency were highly correlated at 1 (r = 0.94, p = <0.0001) and 12 months (r = 0.75, p < 0.001). Both measures demonstrated a similar trend of recovery. Speed of latency recovery was faster in the early follow-up period while lesion length shortening remained relatively constant. At 1 month, latency delay was worse by 1.76ms for additional 1mm of lesion length while at 12 months, 1mm of lesion length accounted for 1.94ms of latency delay.ConclusionA strong association between two putative measures of demyelination in early and chronic ON was found. Parallel recovery of both measures could reflect optic nerve remyelination.     

Effects of temperature on a moth auditory receptor

Measurements of the thoracic temperature and recordings of the spike activity of the most sensitive auditory receptor (A1 cell) were made in Empyreuma pugione (Arctiidae, Ctenuchinae). The temperature range tested (19–36 °C) is relevant for the behavior and ecology of this species. Experiments were performed during the hours of maximal flying activity in the wild: sunrise and sunset. The thoracic temperature during rest reflects that of the surrounding air; there is an increase of 3–4 °C immediately after ceasing free flying in the laboratory. The spike activity of the tympanic organ was recorded with a stainless-steelhook electrode placed beneath the tympanic nerve in the mesothorax. The A1 cell activity was studied without acoustic stimulation (spontaneous) and in response to 35-kHz acoustic pulses of 20, 40, or 100 ms duration. At all of these durations A1 cell response to saturating stimulus was analysed, while with 40-ms pulses different stimulus intensities were used (20–90 dB SPL in 10-dB steps). The number of action potentials per pulse, mean spike rate, maximal instantaneous discharge, and latency period depend strongly on air temperature, while the variation coefficients of the interspike intervals during the responses were not temperature dependent and vary non-monotonically with stimulus intensity. During responses to a saturating stimulus, the stimulus duration does not affect the activation energy, calculated from an Arrhenius plot, of different physiological features. Adaptation, studied in the responses to 100-ms pulses, is also temperature dependent. This phenomenon has two components, each of which shows different activation energies, suggesting a different membrane origin. High stimulus intensity (90 dB SPL) significantly affects the activation energy of the action potentials and mean spike rate, while the activation energy, of the maximal instantaneous discharge and latency period do not show this strong dependency. The spontaneous A1 cell spike rate varies with temperature, as does the value of the mode of the relative frequency distribution of the interspike interval. The activation energy of the spike rates measured at A1 cell responses to saturating stimuli is in good agreement with that described in amphibian innerear hair cells. It is suggested that this moth auditory receptor cell also has mechanosensitive protein channels.Abbreviations AP/p action potentials per pulse - AP/s action potentials per second - CI confidence interval - E _a activation energy - ISI interspike interval - SD standard deviation - VC variation coefficient     

Control of firing patterns by two transient potassium currents: leading spike,latency, bistability

Transient potassium currents distinctively affect firing properties, particularly in regulating the latency before repetitive firing. Pyramidal cells of the dorsal cochlear nucleus (DCN) have two transient potassium currents, I _Kif and I _Kis, fast and slowly inactivating, respectively, and they exhibit firing patterns with dramatically variable latencies. They show immediate repetitive firing, or only after a long latency with or without a leading spike, the so-called pauser and buildup patterns. We consider a conductance-based, ten-variable, single-compartment model for the DCN pyramidal cells (Kanold and Manis 2001). We develop and analyze a reduced three-variable integrate-and-fire model (KM-LIF) which captures the qualitative firing features. We apply dynamical systems methods to explain the underlying biophysical and mathematical mechanisms for the firing behaviors, including the characteristic firing patterns, the latency phase, the onset of repetitive firing, and some discontinuities in the timing of latency duration (e.i. first spike latency and first inter spike interval). Moreover, we obtain new insights associated with the leading spike by phase plane analysis. We further demonstrate the effects of possible heterogeneity of I _Kis. The latency before repetitive firing can be controlled to cover a large range by tuning of the relative amounts of I _Kif and I _Kis. Finally, we find for the full system robust bistability when enough I _Kis is present.     

Temperature dependence of multiple high voltage activated Ca2+ channels in chick sensory neurones

The temperature dependence of high voltage activated Ca²⁺ channels has been investigated in cultured dorsal root ganglion neurones from chick embryos, using the cell-attached patch-clamp technique. The dihydropyridine sensitive L-type Ca²⁺ channel had a conductance of 23 pS, with 110 mM Ba²⁺ as charge carrier and in the presence of 3 M Bay K 8644. When the temperature was raised from 15 to 30 °C, the unitary channel current amplitude increased, with Q₁₀ value equal to 1.4. The rising phase of the averaged single-channel current became faster, with Q₁₀ value 2.7, whereas the decay phase showed a lower temperature sensitivity. Channel open probability decreased according to an exponential distribution of open and closed times. A second type of Ca²⁺ channel was identified, which was DHP-insensitive and had a lower conductance with a mean value equal to 13 pS. For the current amplitude, the Q₁₀ value was 1.3. Both activation and inactivation kinetics were strongly accelerated by an increase in temperature. The corresponding time constants gave Q₁₀ values equal to 5.9 for activation, and 2.0 for inactivation. Peak channel open probability was highly sensitive to a change in temperature, with a Q₁₀ value of 1.6. Finally, in -conotoxin GVIA pre-treated neurones, a non-inactivating DHP-insensitive Ca²⁺ channel with the lowest unitary conductance (10 pS) and a much lower temperature dependence was recorded. Single-channel current was increased by heating, with Q₁₀ value 1.3, whereas the channel kinetics were almost unaffected by temperature. Our data are consistent with the assumption that the different temperature dependence of the Ca²⁺ channel behaviours may be explained by separate gating processes of three types of Ca²⁺ channels.     

Decrease in excitability of LG following habituation of the crayfish escape reaction

Crayfish escapes from threatening stimuli to the abdomen by tailflipping upwards and forwards. This lateral giant (LG)-mediated escape reaction habituates readily upon repetitive sensory stimulation. Using an isolated abdominal nerve cord preparation, we have analyzed the change in LG activity by applying additional sensory stimulation after different periods following habituation to characterize the retention of LG habituation. Results show that the LG mediated response habituates more quickly, but the retention time is shorter, as repetitive sensory stimulation is applied at progressively shorter inter-stimulus time intervals. The spike response of LG recovers quickly, within several minutes after habituation, but they fail to spike when an additional stimulus is applied after specific long periods following habituation. The critical period of the delay for this decrease in excitability of LG is dependent on the inter-stimulus time interval of the initial repetitive stimulus. As the inter-stimulus interval became longer, the delay needed for decrease in excitability became shorter. Furthermore, the local injection of 10^–6 mol l^–1 octopamine into the neuropil just following habituation promotes the achievement of decrease in excitability. No effects were observed when 10^–6 mol l^–1 serotonin and tyramine were injected. These results suggested octopamine promotes decrease in excitability of LG following habituation.     

Regulation of somatic firing dynamics by backpropagating dendritic spikes

Pyramidal cells of the apteronotid ELL have been shown to display a characteristic mechanism of burst discharge, which has been shown to play an important role in sensory coding. This form of bursting depends on a reciprocal dendro-somatic interaction, in which discharge of a somatic spike causes a dendritic spike, which in turn contributes a dendro-somatic current flow to create a depolarizing afterpotential (DAP) in the soma. We review here our recent work showing how the timing of this DAP influences the somatic firing dynamics, and how the degree of inactivation of dendritic Na⁺ currents can cause an increased delay between somatic and dendritic spikes. This ultimately allows the DAP to become more effective at increasing the excitability of the somatic spike generating mechanism. Further, this delay between dendritic and somatic spiking can be regulated by strongly hyperpolarizing GABA_B mediated dendritic inhibition, allowing the burst dynamics to fall under synaptic regulation. In contrast, a weaker, shunting inhibition due to GABA_A mediated dendritic inhibition can regulate the dendritic spike waveform to decrease the dendro-somatic current flow and the resulting DAP. We therefore show that the qualitative behaviour of an individual cell can depend on the degree of synaptic input, and the exact timing of events across the spatial extent of the neuron. Thus, our results serve to illustrate the complex dynamics that can be observed in cells with significant dendritic arborisation, a nearly ubiquitous adaptation amongst principal neurons.     

Temperature dependence of proton permeation through a voltage-gated proton channel

Voltage-gated proton channels are found in many different types of cells, where they facilitate proton movement through the membrane. The mechanism of proton permeation through the channel is an issue of long-term interest, but it remains an open question. To address this issue, we examined the temperature dependence of proton permeation. Under whole cell recordings, rapid temperature changes within a few milliseconds were imposed. This method allowed for the measurement of current amplitudes immediately before and after a temperature jump, from which the ratios of these currents (I_ratio) were determined. The use of I_ratio for evaluating the temperature dependence minimized the contributions of factors other than permeation. Temperature jumps of various degrees (ΔT, −15 to 15°C) were applied over a wide temperature range (4–49°C), and the Q₁₀s for the proton currents were evaluated from the I_ratios. Q₁₀ exhibited a high temperature dependence, varying from 2.2 at 10°C to 1.3 at 40°C. This implies that processes with different temperature dependencies underlie the observed Q₁₀. A novel resistivity pulse method revealed that the access resistance with its low temperature dependence predominated in high temperature ranges. The measured temperature dependence of Q₁₀ was decomposed into Q₁₀ of the channel and of the access resistances. Finally, the Q₁₀ for proton permeation through the voltage-gated proton channel itself was calculated and found to vary from 2.8 at 5°C to 2.2 at 45°C, as expected for an activation enthalpy of 64 kJ/mol. The thermodynamic features for proton permeation through proton-selective channels were discussed for the underlying mechanism.     

Noise-induced burst and spike synchronizations in an inhibitory small-world network of subthreshold bursting neurons

We are interested in noise-induced firings of subthreshold neurons which may be used for encoding environmental stimuli. Noise-induced population synchronization was previously studied only for the case of global coupling, unlike the case of subthreshold spiking neurons. Hence, we investigate the effect of complex network architecture on noise-induced synchronization in an inhibitory population of subthreshold bursting Hindmarsh–Rose neurons. For modeling complex synaptic connectivity, we consider the Watts–Strogatz small-world network which interpolates between regular lattice and random network via rewiring, and investigate the effect of small-world connectivity on emergence of noise-induced population synchronization. Thus, noise-induced burst synchronization (synchrony on the slow bursting time scale) and spike synchronization (synchrony on the fast spike time scale) are found to appear in a synchronized region of the J–D plane (J: synaptic inhibition strength and D: noise intensity). As the rewiring probability p is decreased from 1 (random network) to 0 (regular lattice), the region of spike synchronization shrinks rapidly in the J–D plane, while the region of the burst synchronization decreases slowly. We separate the slow bursting and the fast spiking time scales via frequency filtering, and characterize the noise-induced burst and spike synchronizations by employing realistic order parameters and statistical-mechanical measures introduced in our recent work. Thus, the bursting and spiking thresholds for the burst and spike synchronization transitions are determined in terms of the bursting and spiking order parameters, respectively. Furthermore, we also measure the degrees of burst and spike synchronizations in terms of the statistical-mechanical bursting and spiking measures, respectively.     

Temperature dependence of acetylcholine receptor channels activated by different agonists

The temperature dependence of agonist binding and channel gating were measured for wild-type adult neuromuscular acetylcholine receptors activated by acetylcholine, carbamylcholine, or choline. With acetylcholine, temperature changed the gating rate constants (Q₁₀ ≈ 3.2) but had almost no effect on the equilibrium constant. The enthalpy change associated with gating was agonist-dependent, but for all three ligands it was approximately equal to the corresponding free-energy change. The equilibrium dissociation constant of the resting conformation (K_d), the slope of the rate-equilibrium free-energy relationship (Φ), and the acetylcholine association and dissociation rate constants were approximately temperature-independent. In the mutant αG153S, the choline association and dissociation rate constants were temperature-dependent (Q₁₀ ≈ 7.4) but K_d was not. By combining two independent mutations, we were able to compensate for the catalytic effect of temperature on the decay time constant of a synaptic current. At mouse body temperature, the channel-opening and -closing rate constants are ∼400 and 16 ms⁻¹. We hypothesize that the agonist dependence of the gating enthalpy change is associated with differences in ligand binding, specifically to the open-channel conformation of the protein.     

ACTIVE UPTAKE OF [3H]5-HT BY SYNAPTIC VESICLES FROM RAT BRAIN

The question of whether synaptic vesicles accumulate [³H]5-HT by an active process was investigated in a mixed population of vesiclcs from whole rat brain. The temperature dependence and the effect of metabolic inhibitors were studied in synaptosomal suspensions and vesicular fractions. Arrhenius plots for synaptosomes differed from those for vesicles as did the temperature coefficients for these two fractions. For synaptosomes the Q₁₀ was 7 and for vesicles 1.6. However, if ATP was added to the incubation, the temperature dependence of vesicular amine accumulation became manifest; the Arrhenius plot resembled that of synaptosomes and the Q₁₀ was greater than 20 indicating strong temperature dependence. In the presence of ATP, vesicular uptake was stimulated approx 8-fold. Ouabain, dinitrophenol and NEM inhibited synaptosomal uptake but failed to affect [³H]5-HT accumulation by vesicles in the absence of ATP. When ATP was added, vesicular uptake was also blocked by NEM but was unaffected by either ouabain or DNP. Total observed uptake consisted of two components, one ATP-dependent and one nonsaturable and ATP-independent. The active process had a K_m= 1.25 × 10^?7 M and could be completely blocked by either 10^?3 M or 10^?7 M-reserpine. Active vesicular [³H]5-HT uptake was magnesium dependent and was inhibited by sodium and potassium. Cation effects on uptake were specific and could not be accounted for by either changes in osmotic pressure or ionic strength. It was concluded that synaptic vesicles from whole rat brain accumulate [³H]5-HT by an active process.     

Repetitive spikes in photoreceptor axons of the scorpion eye. Invertebrate eye structure and tetrodotoxin

A graded depolarization accompanied by nerve impulses can be recorded from the scorpion lateral and median eyes in response to light. Electron microscopy shows that axons forming the optic nerve arise directly from the photoreceptors. Thus, photoreceptors must respond both by the generation of a slow receptor potential and the initiation of spikes. The latency of the first spike, and the maximal and mean discharge frequencies were a function of light intensity. Spikes were abolished by tetrodotoxin. Repetitive firing to light therefore appears to be a normal response of scorpion photoreceptors and is the result of regenerative Na influx in the cell membrane.     

Metabolic uniformity over the environmental temperature range in Brachionus plicatilis (rotifera)

Organisms inhabiting small water bodies frequently encounter radical, short-term fluctuations in temperature. The population of Brachionus plicatilis that was used in this study encounters temperature changes as great as 12°C in 24 hours. In this paper we describe the metabolic response to temperature change in this eurythermal rotifer population. Metabolism was determined over the environmental range (15°C to 32°C) in intervals of 2°C. Utilization of such narrow temperature intervals allowed us to approximate the instantaneous Q₁₀, which we define as the Q₁₀ over an infinitely small temperature interval. Our results show the existence of a plateau in the curve of respiration against temperature (Q₁₀ > 1) over the range 20–28°C. The plateau is bounded on either side by temperature ranges over which metabolism is temperature sensitive (Q₁₀ values from 3.4 to 4.8). It is significant that the plateau occurs over the environmental temperature range for the major portion of the growing season. This population is thus programmed to hold a constant (preferred?) metabolic rate in spite of diel temperature fluctuations when the environment is otherwise favorable.     

Temperature effects on the tympanal membrane and auditory receptor neurons in the locust

Poikilothermic animals are affected by variations in environmental temperature, as the basic properties of nerve cells and muscles are altered. Nevertheless, insect sensory systems, such as the auditory system, need to function effectively over a wide range of temperatures, as sudden changes of up to 10 °C or more are common. We investigated the performance of auditory receptor neurons and properties of the tympanal membrane of Locusta migratoria in response to temperature changes. Intracellular recordings of receptors at two temperatures (21 and 28 °C) revealed a moderate increase in spike rate with a mean Q10 of 1.4. With rising temperature, the spike rate–intensity–functions exhibited small decreases in thresholds and expansions of the dynamic range, while spike durations decreased. Tympanal membrane displacement, investigated using microscanning laser vibrometry, exhibited a small temperature effect, with a Q10 of 1.2. These findings suggest that locusts are affected by shifts in temperature at the periphery of the auditory pathway, but the effects on spike rate, sensitivity, and tympanal membrane displacement are small. Robust encoding of acoustic signals by only slightly temperature-dependent receptor neurons and almost temperature-independent tympanal membrane properties might enable locusts and grasshoppers to reliably identify sounds in spite of changes of their body temperature.     

Temperature Dependence of Photosynthesis in Agropyron smithii Rydb. : I. FACTORS AFFECTING NET CO(2) UPTAKE IN INTACT LEAVES AND CONTRIBUTION FROM RIBULOSE-1,5-BISPHOSPHATE CARBOXYLASE MEASURED IN VIVO AND IN VITRO

As part of an extensive analysis of the factors regulating photosynthesis in Agropyron smithii Rydb., a C₃ grass, we have examined the response of leaf gas exchange and ribulose-1,5-bisphosphate (RuBP) carboxylase activity to temperature. Emphasis was placed on elucidating the specific processes which regulate the temperature response pattern. The inhibitory effects of above-optimal temperatures on net CO₂ uptake were fully reversible up to 40°C. Below 40°C, temperature inhibition was primarily due to O₂ inhibition of photosynthesis, which reached a maximum of 65% at 45°C. The response of stomatal conductance to temperature did not appear to have a significant role in determining the overall temperature response of photosynthesis. The intracellular conductance to CO₂ increased over the entire experimental temperature range, having a Q₁₀ of 1.2 to 1.4. Increases in the apparent Michaelis constant (K_c) for RuBP carboxylase were observed in both in vitro and in vivo assays. The Q₁₀ values for the maximum velocity (V_max) of CO₂ fixation by RuBP carboxylase in vivo was lower (1.3-1.6) than those calculated from in vitro assays (1.8-2.2). The results suggest that temperature-dependent changes in enzyme capacity may have a role in above-optimum temperature limitations below 40°C. At leaf temperatures above 40°C, decreases in photosynthetic capacity were partially dependent on temperature-induced irreversible reductions in the quantum yield for CO₂ uptake.