Role of Glutamate in the Mechanisms of Adaptation of the System of Respiratory Control in Rats to Intermittent Hypoxia

In experiments on Wistar rats, we studied the role of changes in the state of glutamatergic transmission in the course of adaptation of the system of respiratory control to intermittent hypoxia. The volume/temporal parameters of respiration were estimated according to characteristics of EMG activity (amplitude, integral intensity of EMG discharges) recorded from the diaphragmatic muscle. Changes in EMG activity of the diaphragm induced by acute hypoxia (breathing a 12% О₂-containing gas mixture) were estimated before and after of a 14-day-long course of intermittent hypoxia trainings and before and after inductions of a blocker of NMDA receptors, МK-801. The results prove that the glutamatergic transmitter system is significantly involved in the reaction of the respiratory system to presentation of a hypoxic stimulus within all stages of formation of the ventilatory response, both before and after the action of intermittent hypoxia. Blocking of NMDA receptors under conditions of adaptation to intermittent hypoxia exerted a more intense influence on the amplitude of respiratory EMG discharges of the diaphragm than on their frequency.     

Adenosine A2A Receptors Activation Facilitates Neuromuscular Transmission in the Pre-Symptomatic Phase of the SOD1(G93A) ALS Mice,but Not in the Symptomatic Phase

Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative disease leading to motor neuron dysfunction resulting in impairment of neuromuscular transmission. A_2A adenosine receptors have already been considered as a potential therapeutical target for ALS but their neuromodulatory role at the neuromuscular junction in ALS remains to be clarified. In the present work, we evaluated the effects of A_2A receptors on neuromuscular transmission of an animal model of ALS: SOD1(G93A) mice either in the pre-symptomatic (4–6 weeks old) or in the symptomatic (12–14 weeks old) stage. Electrophysiological experiments were performed obtaining intracellular recordings in Mg²⁺ paralyzed phrenic nerve-hemidiaphragm preparations. Endplate potentials (EPPs), quantal content (q. c.) of EPPs, miniature endplate potentials (MEPPs) and giant miniature endplate potential (GMEPPs) were recorded. In the pre-symptomatic phase of the disease (4–6 weeks old mice), the selective A_2A receptor agonist, CGS 21680, significantly enhanced (p<0.05 Unpaired t-test) the mean amplitude and q.c. of EPPs, and the frequency of MEPPs and GMEPPs at SOD1(G93A) neuromuscular junctions, the effect being of higher magnitude (p<0.05, Unpaired t-test) than age-matched control littermates. On the contrary, in symptomatic mice (12–14 weeks old), CGS 21680 was devoid of effect on both the amplitude and q.c. of EPPs and the frequency of MEPPs and GMEPPs (p<0.05 Paired t-test). The results herein reported clearly document that at the neuromuscular junction of SOD1(G93A) mice there is an exacerbation of A_2A receptor-mediated excitatory effects at the pre-symptomatic phase, whereas in the symptomatic phase A_2A receptor activation is absent. The results thus suggest that A_2A receptors function changes with ALS progression.     

Enhanced ER Ca2+ store filling by overexpression of SERCA2b promotes IP3-evoked puffs

Liberation of Ca²⁺ from the endoplasmic reticulum (ER) through inositol trisphosphate receptors (IP₃R) is modulated by the ER Ca²⁺ content, and overexpression of SERCA2b to accelerate Ca²⁺ sequestration into the ER has been shown to potentiate the frequency and amplitude of IP₃-evoked Ca²⁺ waves in Xenopus oocytes. Here, we examined the effects of SERCA overexpression on the elementary IP₃-evoked puffs to elucidate whether ER [Ca²⁺] may modulate IP₃R function via luminal regulatory sites in addition to simply determining the size of the available store and electrochemical driving force for Ca²⁺ release. SERCA2b and Ca²⁺ permeable nicotinic plasmalemmal channels were expressed in oocytes, and hyperpolarizing pulses were delivered to induce Ca²⁺ influx and thereby load ER stores. Puffs evoked by photoreleased IP₃ were significantly potentiated in terms of numbers of responding sites, frequency and amplitude following transient Ca²⁺ influx in SERCA-overexpressing cells, whereas little change was evident with SERCA overexpression alone or following Ca²⁺ influx in control cells not overexpressing SERCA. Intriguingly, we observed the appearance of a new population of puffs that arose after long latencies and had prolonged durations supporting the notion of luminal regulation of IP₃R gating kinetics.     

A model for control of breathing in mammals: coupling neural dynamics to peripheral gas exchange and transport

A new model for aspects of the control of respiration in mammals has been developed. The model integrates a reduced representation of the brainstem respiratory neural controller together with peripheral gas exchange and transport mechanisms. The neural controller consists of two components. One component represents the inspiratory oscillator in the pre-Bötzinger complex (pre-BötC) incorporating biophysical mechanisms for rhythm generation. The other component represents the ventral respiratory group (VRG), which is driven by the pre-BötC for generation of inspiratory (pre)motor output. The neural model was coupled to simplified models of the lungs incorporating oxygen and carbon dioxide transport. The simplified representation of the brainstem neural circuitry has regulation of both frequency and amplitude of respiration and is done in response to partial pressures of oxygen and carbon dioxide in the blood using proportional (P) and proportional plus integral (PI) controllers. We have studied the coupled system under open and closed loop control. We show that two breathing regimes can exist in the model. In one regime an increase in the inspiratory frequency is accompanied by an increase in amplitude. In the second regime an increase in frequency is accompanied by a decrease in amplitude. The dynamic response of the model to changes in the concentration of inspired O₂ or inspired CO₂ was compared qualitatively with experimental data reported in the physiological literature. We show that the dynamic response with a PI-controller fits the experimental data better but suggests that when high levels of CO₂ are inspired the respiratory system cannot reach steady state. Our model also predicts that there could be two possible mechanisms for apnea appearance when 100% O₂ is inspired following a period of 5% inspired O₂. This paper represents a novel attempt to link neural control and gas transport mechanisms, highlights important issues in amplitude and frequency control and sets the stage for more complete neurophysiological control models.     

Changes in miniature endplate potential frequency during repetitive nerve stimulation in the presence of Ca2+, Ba2+, and Sr2+ at the frog neuromuscular junction

Miniature endplate potentials (MEPPs) were recorded from frog sartorious neuromuscular junctions under conditions of reduced quantal contents to study the effect of repetitive nerve stimulation on asynchronous (tonic) quantal transmitter release. MEPP frequency increased during repetitive stimulation and then decayed back to the control level after the conditioning trains. The decay of the increased MEPP frequency after 100-to 200-impulse conditioning trains can be described by four components that decayed exponentially with time constants of about 50 ms, 500 ms, 7 s, and 80 s. These time constants are similar to those for the decay of stimulation-induced changes in synchronous (phasic) transmitter release, as measured by endplate potential (EPP) amplitudes, corresponding, respectively, to the first and second components of facilitation, augmentation, and potentiation. The addition of small amounts of Ca2+ or Ba2+ to the Ca2+-containing bathing solution, or the replacement of Ca2+ with Sr2+, led to a greater increase in the stimulation-induced increases in MEPP frequency. The Sr-induced increase in MEPP frequency was associated with an increase in the second component of facilitation of MEPP frequency; the Ba-induced increase with an increase in augmentation. These effects of Sr2+ and Ba2+ on stimulation-induced changes in MEPP frequency are similar to the effects of these ions on stimulation- induced changes in EPP amplitude. These ionic similarities and the similar kinetics of decay suggest that stimulation induced changes in MEPP frequency and EPP amplitude have some similar underlying mechanisms. Calculations are presented which show that a fourth power residual calcium model for stimulation-induced changes in transmitter release cannot readily account for the observation that stimulation- induced changes in MEPP frequency and EPP amplitude have similar time- courses.     

EMG amplitude and frequency parameters of muscular activity: Effect of resistance training based on electromyographic fatigue threshold

The present study aimed to evaluate the effect of a resistance training program based on the electromyographic fatigue threshold (EMG_FT, defined as the highest exercise intensity performed without EMG alterations), on the EMG amplitude (root mean square, RMS) and frequency (median frequency, MF) values for biceps brachii (BB), brachioradialis (BR), triceps brachii (TB) and multifidus (MT). Twenty healthy male subjects, (training group [TG], n = 10; control group [CG], n = 10), firstly performed isometric contractions, and after this, dynamic biceps curl at four different loads to determine the EMG_FT. The TG training program used the BB EMG_FT value (8 weeks, 2 sessions/week, 3 exhaustive bouts/session, 2 min rest between bouts). No significant differences were found for the isometric force after the training. The linear regression slopes of the RMS with time during the biceps curl presented significant decrease after training for the BB, BR and TB muscles. For the MT muscle, the slope and MF intercept values changed with training. The training program based on the EMG_FT influenced EMG the amplitude more than EMG frequency, possibly related to the recruitment patterns of the muscles, although the trunk extensor muscles presented changes in the frequency parameter, showing adaptation to the training program.     

BDNF-induced presynaptic facilitation of GABAergic transmission in the hippocampus of young adults is dependent of TrkB and adenosine A<Subscript>2A</Subscript> receptors

Brain-derived neurotrophic factor (BDNF) and adenosine are widely recognized as neuromodulators of glutamatergic transmission in the adult brain. Most BDNF actions upon excitatory plasticity phenomena are under control of adenosine A_2A receptors (A_2ARs). Concerning gamma-aminobutyric acid (GABA)-mediated transmission, the available information refers to the control of GABA transporters. We now focused on the influence of BDNF and the interplay with adenosine on phasic GABAergic transmission. To assess this, we evaluated evoked and spontaneous synaptic currents recorded from CA1 pyramidal cells in acute hippocampal slices from adult rat brains (6 to 10 weeks old). BDNF (10–100 ng/mL) increased miniature inhibitory postsynaptic current (mIPSC) frequency, but not amplitude, as well as increased the amplitude of inhibitory postsynaptic currents (IPSCs) evoked by afferent stimulation. The facilitatory action of BDNF upon GABAergic transmission was lost in the presence of a Trk inhibitor (K252a, 200 nM), but not upon p75^NTR blockade (anti-p75^NTR IgG, 50 μg/mL). Moreover, the facilitatory action of BDNF onto GABAergic transmission was also prevented upon A_2AR antagonism (SCH 58261, 50 nM). We conclude that BDNF facilitates GABAergic signaling at the adult hippocampus via a presynaptic mechanism that depends on TrkB and adenosine A_2AR activation.     

Weak coherent radiation of OH and ortho-H2O space masers as a carrier in biocommunication: ortho/para conversion of H2O spin isomers?

Formulated and substantiated is a hypothesis of biocommunication based on the radiophysical principle of amplitude modulation of the carrier frequency provided the presence of resonant circuits in the transmitter-receiver devices. Coherent radiation of space OH masers (1.6–1.72 GHz) and ortho-H₂O masers (22.3 GHz) incessantly irradiating the Earth is proposed in the capacity of a source of the carrier frequency during transmission of the emotional state “good-bad” or stress. The narrow lines discovered by us on rotational transitions of H₂O and OH molecules in water and water solutions of biomolecules are considered as resonances of circuits for ensuring the selectivity of communication. Discussed is the possibility of ortho/para conversion of H₂O spin isomers induced by weak electromagnetic fields.     

Changes in synaptic transmission produced by hydrogen peroxide

The effect of hydrogen peroxide (H₂O₂) on excitatory and inhibitory synaptic transmission was studied at the lobster neuromuscular junction. H₂O₂ produced a dose dependent decrease in the amplitude of the junction potential (V_ejp). This decrease was due to changes in both presynaptic transmitter release and the postsynaptic response to the neurotransmitter. Observed presynaptic changes due to exposure to H₂O₂ were a decrease in the amount of transmitter released, that is, quantal content, as well as a decrease in the fast facilitation, that is, the amplitude increase of successive excitatory junction potentials at a rate of 3 Hz. To discern postsynaptic changes, glutamate, the putative excitatory neurotransmitter for this preparation was applied directly to the bathing medium in order to bypass the presynaptic release process. H₂O₂ produced a decreased response of the glutamate receptor/ ionophore. The action of H₂O₂ was not selective to excitatory (glutamate-mediated) transmission because inhibitory (GABA-mediated) transmission was also depressed by H₂O₂. This effect was primarily presynaptic since H₂O₂ produced no change in the postsynaptic response to applied GABA.     

PKCδ Knockout Mice Are Protected from Dextromethorphan-Induced Serotonergic Behaviors in Mice: Involvements of Downregulation of 5-HT<Subscript>1A</Subscript> Receptor and Upregulation of Nrf2-Dependent GSH Synthesis

We investigated whether a specific serotonin (5-HT) receptor-mediated mechanism was involved in dextromethorphan (DM)-induced serotonergic behaviors. We firstly observed that the activation of 5-HT_1A receptor, but not 5-HT_2A receptor, contributed to DM-induced serotonergic behaviors in mice. We aimed to determine whether the upregulation of 5-HT_1A receptor induced by DM facilitates the specific induction of certain PKC isoform, because previous reports suggested that 5-HT_1A receptor activates protein kinase C (PKC). A high dose of DM (80 mg/kg, i.p.) induced a selective induction of PKCδ out of PKCα, PKCβI, PKCβII, PKCξ, and PKCδ in the hypothalamus of wild-type (WT) mice. More importantly, 5-HT_1A receptor co-immunoprecipitated PKCδ in the presence of DM. Consistently, rottlerin, a pharmacological inhibitor of PKCδ, or PKCδ knockout significantly protected against increases in 5-HT_1A receptor gene expression, 5-HT turnover rate, and serotonergic behaviors induced by DM. Treatment with DM resulted in an initial increase in nuclear factor erythroid-2-related factor 2 (Nrf2) nuclear translocation and DNA-binding activity, γ-glutamylcysteine (GCL) mRNA expression, and glutathione (GSH) level. This compensative induction was further potentiated by rottlerin or PKCδ knockout. However, GCL mRNA and GSH/GSSG levels were decreased 6 and 12 h post-DM. These decreases were attenuated by PKCδ inhibition. Our results suggest that interaction between 5-HT_1A receptor and PKCδ is critical for inducing DM-induced serotonergic behaviors and that inhibition of PKCδ attenuates the serotonergic behaviors via downregulation of 5-HT_1A receptor and upregulation of Nrf2-dependent GSH synthesis.     

Impaired Chemosensitivity of Mouse Dorsal Raphe Serotonergic Neurons Overexpressing Serotonin 1A (Htr1a) Receptors

Background

Serotonergic system participates in a wide range of physiological processes and behaviors, but its role is generally considered as modulatory and noncrucial, especially concerning life-sustaining functions. We recently created a transgenic mouse line in which a functional deficit in serotonin homeostasis due to excessive serotonin autoinhibition was produced by inducing serotonin 1A receptor (Htr1a) overexpression selectively in serotonergic neurons (Htr1a raphe-overexpressing or Htr1a^RO mice). Htr1a^RO mice exhibit episodes of autonomic dysregulation, cardiovascular crises and death, resembling those of sudden infant death syndrome (SIDS) and revealing a life-supporting role of serotonergic system in autonomic control. Since midbrain serotonergic neurons are chemosensitive and are implicated in arousal we hypothesized that their chemosensitivity might be impaired in Htr1a^RO mice.

Principal findings

Loose-seal cell-attached recordings in brainstem slices revealed that serotonergic neurons in dorsal raphe nucleus of Htr1a^RO mice have dramatically reduced responses to hypercapnic challenge as compared with control littermates. In control mice, application of 9% CO₂ produced an increase in firing rate of serotonergic neurons (0.260±0.041 Hz, n = 20, p = 0.0001) and application of 3% CO₂ decreased their firing rate (−0.142±0.025 Hz, n = 17, p = 0.0008). In contrast, in Htr1a^RO mice, firing rate of serotonergic neurons was not significantly changed by 9% CO₂ (0.021±0.034 Hz, n = 16, p = 0.49) and by 3% CO₂ (0.012±0.046 Hz, n = 12, p = 0.97).

Conclusions

Our findings support the hypothesis that chemosensitivity of midbrain serotonergic neurons provides a physiological mechanism for arousal responses to life-threatening episodes of hypercapnia and that functional impairment, such as excessive autoinhibition, of midbrain serotonergic neuron responses to hypercapnia may contribute to sudden death.     

Influence of electrochemical proton gradient on electron flow in photosystem I of pea leaves

Photoinduced changes in the redox state of photosystem I (PSI) primary donor, chlorophyll P700 were studied by measuring differential absorbance changes of pea leaves at 810 nm minus 870 nm (ΔA ₈₁₀). The kinetics of ΔA ₈₁₀ induced by 5-s pulses of white light were strongly affected by preillumination. In dark-adapted leaves, the light pulse caused a transient oxidation of P700 and its subsequent reduction. An identical pulse, applied after 30-s preillumination with white light, induced sequential appearance of two peaks of P700 oxidation. These kinetic differences of ΔA ₈₁₀ reflect regulatory changes of electron flow on the donor and acceptor sides of PSI induced by illumination of leaf for 20–40 s. The amplitude of ΔA ₈₁₀ second peak depended nonmonotonically on the dark interval preceding illumination: it increased with the length of dark period in the range 3–10 s and decreased upon longer dark intervals. The second wave of ΔA ₈₁₀ disappeared after the treatment with combination of ionophores preventing ΔpH and electric potential formation at the thylakoid membrane. In leaves treated with monensin eliminating ΔpH only, the ΔA ₈₁₀ signals become incompletely reversible and were characterized by slow relaxation in darkness. The results indicate an important role of electrochemical proton gradient in generation of the second wave of light-induced P700 oxidation.     

Downregulation of Serotonergic Gene Expression in the Raphe Nuclei of the Midbrain Under Chronic Social Defeat Stress in Male Mice

There is ample experimental evidence supporting the hypothesis that the brain serotonergic system is involved in the control of chronic social defeat stress (CSDS), depression, and anxiety. The study aimed to analyze mRNA levels of the serotonergic genes in the raphe nuclei of midbrain that may be associated with chronic social defeats consistently shown by male mice in special experimental settings. The serotonergic genes were the Tph2, Sert, Maoa, and Htr1a. The Bdnf and Creb genes were also studied. The experimental groups were composed of male mice with experience of defeats in 21 daily encounters and male mice with the same track record of defeats followed by a no-defeat period without agonistic interactions (relative rest for 14 days). It has been shown that mRNA levels of the Tph2, Maoa, Sert, Htr1a, Bdnf, and Creb genes in the raphe nuclei of defeated mice are decreased as compared with the controls. The expression of the serotonergic genes as well as the Creb gene is not restored to the control level after the 2 weeks of relative rest. mRNA levels of Bdnf gene are not recovered to the control levels, although some upregulation was observed in rested losers. CSDS experience inducing the development of mixed anxiety/depression-like state in male mice downregulates the expression of serotonergic genes associated with the synthesis, inactivation, and reception of serotonin. The Bdnf and Creb genes in the midbrain raphe nuclei are also downregulated under CSDS. Period of relative rest is not enough for most serotonergic genes to recover expression to the control levels.     

Temporal changes in circulating steroids during prostaglandin F2α induced abortion in the rat and rabbit

The serum levels of progesterone (Δ⁴P), 20α-dihydroxyprogesterone (20α-DHP), pregnenolone (Δ⁵P) and estrogens at different time intervals during Silastic-PVP-PGF_2α tube induced midterm abortion were measured by radioimmunoassay in the rat and rabbit. The concentrations of ⁴P and Δ⁵P were significantly reduced but that of 20α-DHP was increased significantly as early as 20 hours after PGF_2α treatment. Estrogen levels showed slight reduction in the rat but remained unchanged in the rabbit. The ratio of Δ⁴P/20α-DHP recorded were 2.15 and 16.86 (pretreatment) and dropped to 0.08 and 0.37 (60 hours after insertion of Silastic-PVP-PGF_2α tube) in the rat and rabbit, respectively. These findings suggest that the suppression of circulating Δ⁴P by PGF_2α might be the result of a reduced precursor (Δ⁵P) pool size as well as changes in the enzymic systems responsible for the formation and conversion of Δ⁴P. It is still to be determined if changes in estrogen levels in the rat have any bearing on abortion induced by PGF_2α.     

Involvement of plasma membrane Ca2+ channels,IP3 receptors,and ryanodine receptors in the generation of spontaneous rhythmic contractions of the cricket lateral oviduct

In the present study, the isolated cricket (Gryllus bimaculatus) lateral oviduct exhibited spontaneous rhythmic contractions (SRCs) with a frequency of 0.29 ± 0.009 Hz (n = 43) and an amplitude of 14.6 ± 1.25 mg (n = 29). SRCs completely disappeared following removal of extracellular Ca²⁺ using a solution containing 5 mM EGTA. Application of the non-specific Ca²⁺ channel blockers Co²⁺, Ni²⁺, and Cd²⁺ also decreased both the frequency and amplitude of SRCs in dose-dependent manners, suggesting that Ca²⁺ entry through plasma membrane Ca²⁺ channels is essential for the generation of SRCs. Application of ryanodine (30 μM), which depletes intracellular Ca²⁺ by locking ryanodine receptor (RyR)-Ca²⁺ channels in an open state, gradually reduced the frequency and amplitude of SRCs. A RyR antagonist, tetracaine, reduced both the frequency and amplitude of SRCs, whereas a RyR activator, caffeine, increased the frequency of SRCs with a subsequent increase in basal tonus, indicating that RyRs are essential for generating SRCs. To further investigate the involvement of phospholipase C (PLC) and inositol 1,4,5-trisphosphate receptors (IP₃Rs) in SRCs, we examined the effect of a PLC inhibitor, U73122, and an IP₃R antagonist, 2-aminoethoxydiphenyl borate (2-APB), on SRCs. Separately, U73122 (10 μM) and 2-APB (30–50 μM) both significantly reduced the amplitude of SRCs with little effect on their frequency, further indicating that the PLC/IP₃R signaling pathway is fundamental to the modulation of the amplitude of SRCs. A hypotonic-induced increase in the frequency and amplitude of SRCs and a hypertonic-induced decrease in the frequency and amplitude of SRCs indicated that mechanical stretch of the lateral oviduct is involved in the generation of SRCs. The sarcoplasmic reticulum Ca²⁺-pump ATPase inhibitors thapsigargin and cyclopiazonic acid impaired or suppressed the relaxation phase of SRCs. Taken together, the present results indicate that Ca²⁺ influx through plasma membrane Ca²⁺ channels and Ca²⁺ release from RyRs play an essential role in pacing SRCs and that Ca²⁺ release from IP₃Rs may play a role in modulating the amplitude of SRCs, probably via activation of PLC.     

Comparative proteomic analysis of amaranth mesophyll and bundle sheath chloroplasts and their adaptation to salt stress

The effect of salt stress was analyzed in chloroplasts of Amaranthus cruentus var. Amaranteca, a plant NAD-malic enzyme (NAD-ME) type. Morphology of chloroplasts from bundle sheath (BSC) and mesophyll (MC) was observed by transmission electron microscopy (TEM). BSC and MC from control plants showed similar morphology, however under stress, changes in BSC were observed. The presence of ribulose bisphosphate carboxylase/oxygenase (RuBisCO) was confirmed by immunohistochemical staining in both types of chloroplasts. Proteomic profiles of thylakoid protein complexes from BSC and MC, and their changes induced by salt stress were analyzed by blue-native polyacrylamide gel electrophoresis followed by SDS-PAGE (2-D BN/SDS-PAGE). Differentially accumulated protein spots were analyzed by LC–MS/MS. Although A. cruentus photosynthetic tissue showed the Kranz anatomy, the thylakoid proteins showed some differences at photosystem structure level. Our results suggest that A. cruentus var. Amaranteca could be better classified as a C₃–C₄ photosynthetic plant.     

A gastrointestinal function bioassay evaluation of the mycotoxin,T-2 trichothecene

The Fusarium-produced mycotoxin T-2 trichothecene toxin was administered to two groups of young CD-1 mice to test the effects on three parameters of intestinal motility. The criteria selected included composite motility (cm²/min), peak amplitude (mm) and contraction frequency (recorded peaks/min). T-2 treated mice showed an increase in composite motility in response to low dosage (0·085 mg/kg), and at the higher dosage (0·250 mg/kg) a decreased motility. In the lowest treatment group there was a mean decrease of 39·54% in contraction amplitude while contraction frequency increased by 24·84%. The motility measurements were obtained by perfusing 2 cm sections of small intestine, including the entire duodenum excised from mice pre-treated with mycotoxin. Contractions were recorded with a physiograph and the composite motility measurements were taken using a computer program to determine the area of the data curves. T-2 toxin caused an alteration in the amplitude and frequency of motility measurements, but no overall concentration-related changes were noted. T-2 toxin causes measurable responses in the duodenum which may be one of the sites-of-action for this mycotoxin.     

The visual response from the compound eye of Oncopeltus fasciatus: Effects of temperature and sensory adaptation

The effects of temperature (10–30°C) on response latency and amplitude were determined in the dark- and light-adapted compound eye of the milkweed bug, Oncopeltus fasciatus. Response amplitude was an inverse function of temperature under dark-adapted conditions, but was nearly independent of temperature when superimposed on a background field. Response amplitude to a test stimulus (S₂) was maximum at 15–20°C when presented 10 sec after an adapting stimulus (S₁). The optimum temperature (10°C or less) for maximum response amplitude from dark-adapted eyes was far below the temperature at which the animals were grown (19–25°C) and lower than previously reported for insect compound eyes. These results are discussed in terms of the adaptive implications for diurnal, terrestrial ectotherms.Response latency from dark-adapted eyes was an inverse exponential function of temperature with an apparent activation energy of 13·6 kcal mole⁻¹. No change in activation energy could be attributed to light adaptation.Reductions of S₂ response latency and amplitude, during the adaptation régimes employed in this study, were different functions of temperature. Adapting stimuli, which were equally effective at reducing S₂ latency, had different effects on S₂ response amplitude. Recovery of S₂ response latency and amplitude were not related at either 20 or 10°C. Therefore, changes in S₂ response latency as a function of adaptation appeared independent of changes in S₂ response amplitude.