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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.

Animals↗

[Effect of a change in brain monoamine levels on reproduction of an elaborated escape reaction in rats].

An escape reaction was elaborated in Wistar rats in a shuttle box to shocks delivered to the animal's foot in a time stereotype. Single administrations of serotonin precursor--5-Hydroxytryptophane (10 mg/kg) and of catecholamine inhibitor--M-tyrosine (100 mg/kg) had a facilitating effect on this reaction. The animals' behaviour became regulated; this was manifested in a shortening of latencies. Catecholamine precursor d,l-DOPA (35 mg/kg) and serotonin inhibitor p-Chlorophenilalanine (320 mg/kg) worsened the rats' adaptive behaviour in the experimental situation enhancing their fuss movements. The latencies of the escape reactions became longer. The data presented point to a reciprocal--conjugate interaction of serotonin- and noradrenergic brain systems as well as to an antistress serotonin effect on behaviour.

5-Hydroxytryptophan↗

Mathematical modelling of reaction latency. Part II: A model of escape reaction and escape learning.

The results of fitting the linear-dynamic-stochastic model to the latency data from escape conditioning experiment are presented. Two processes can be distinguished: (i) an increase in parameters of the dynamic part of the model (called the static gain and the dynamic gain) which results in a decrease in the reaction latency during learning, (ii) an increase in parameter of the decision part of the model (mean value of the threshold), which results simultaneously in an increase in the reaction latency and a decrease in the inter-trial responses probability. The reaction latency decreases during the learning because the first phenomenon prevails over the second one, but the latter is the only reason of inter-trial responses decrease during learning. Analysis of the results of surgical treatment on the learning process is also presented.

Animals↗

[Substance P in the central mechanisms of the escape reaction].

The role of substance P in the central mechanisms of escape reaction elicited by electrical stimulation of the ventromedial hypothalamus was investigated in chronic experiments on rabbits. Intravenous injection of substance P (30 micrograms/kg) led to a short-term (less than 10 min) increase in the threshold of stimulation of the ventromedial hypothalamus and to more stable (up to 1.5 h) disorders of the hippocampal-hypothalamic relations. After substance P injection the inhibitory effects of the dorsal hippocampus but not the facilitating influences of the midbrain reticular formation on excitability of the hypothalamic motivation center were found to be lacking. Disorders of the central mechanisms of escape reaction after substance P injection correlated with new patterns of the main EEG rhythms in different areas of the brain cortex in response to the ascending excitations of the limbic-midbrain structures. Interpreting the mechanisms of substance P involvement in escape reaction the authors point to the ability of the given peptide to interact with different transmitter systems of the brain and opiate receptors and to alter the brain blood circulation.

Animals↗

[Substance P and effects of ethanol on the central mechanisms of the escape reaction in rabbits].

Substance P (SP) effects on the central mechanisms of escape reaction, elicited by threshold electrical stimulation of the ventromedial hypothalamus were investigated in rabbits pretreated with ethanol (0.5 g/kg). SP (30 micrograms/kg) was demonstrated to normalize in 71.4% of cases the excitability of the ventromedial hypothalamus which was decreased by ethanol and restored in 83.3% of cases the facilitatory effects of the midbrain reticular formation in escape reactions. However, SP was ineffective in the restoration of the inhibitory effects of the dorsal hippocamp on the excitability of the ventromedial hypothalamus that was obvious in intact animals. Partial normalizing effect of SP on escape reaction in rabbits after previous ethanol administration can be accounted for by the fact that both undecapeptide and ethanol are similar in their realization of central effects such as an interaction with the same brain neurotransmitters, interference with neuronal enzyme processes and reactions with opiate receptors.

Animals↗

Presynaptic inhibition is mediated by histamine and GABA in the crustacean escape reaction.

1. Presynaptic inhibition of sensory transmission during the escape reaction in Crustacea has been studied using an in vitro preparation of the crayfish thoracic ganglia. Electrical stimulation of the medial giant fiber mediating the escape reaction induced depolarization in sensory afferent terminals of the coxo-basal chordotonal organ (CBCO). This depolarization was associated with an increase of the membrane conductance and was partially blocked by a gamma-aminobutyric acid (GABA) antagonist, picrotoxin, and by a histamine antagonist, cimetidine. 2. Pressure ejection of histamine on CBCO sensory terminals (CBT) recorded intracellularly, induced a depolarization of the membrane potential accompanied by a large increase of the conductance. Histamine-induced depolarization persisted after blockade of synaptic transmission mediated by Na+ spikes by tetrodotoxin. The amplitude of histamine-induced depolarization increased when negative current was injected into the sensory terminal through the recording electrode. Moreover, injection of chloride into the CBT, which shifts the reversal potential of chloride to a more positive value, resulted in an increase of the amplitude of the histamine-induced depolarization. 3. The existence of separate receptors for GABA and histamine on the CB sensory terminals was demonstrated using two complementary sets of experiments. The first one consisted of using specific blockers of GABA and histamine. Picrotoxin blocked selectively the GABA-induced depolarization of the CB sensory terminals, while it was ineffective in blocking the histamine-induced depolarization. Conversely, cimetidine blocked the histamine-induced depolarization totally, but did not affect the GABA response. The second set of experiments tested for of cross-desensitization between GABA and histamine responses.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗

[Methiothepin-sensitive serotonin receptors are involved in postsynaptic mechanism of sensitization of Helix lucorum escape reaction].

Tetanic electric stimulation of Helix foot evokes sensitization of escape reaction. This behavioral sensitization and posttetanic potentiation (PTP) of acetylcholine-induced inward current (ACh-current) in command Helix neurons of escape behavior were similar. Antagonist of serotonin receptors methiothepin prevents the PTP of the ACh-current and behavioral sensitization. Serotonin disrupts the PTP of the ACh-current. It is suggested that the increase in cholinosensitivity of the command neurons with the involvement of methiothepin-sensitive serotonin receptors may be the cellular postsynaptic mechanism of behavioral sensitization of Helix escape reaction.

Acetylcholine↗

[Role of dorsal regions of the hippocampus and midbrain reticular formation in escape reaction development in rabbits].

Experiments on unrestrained rabbits were carried out to study the role of the dorsal hippocampus (DH) and midbrain reticular formation (MRF) in escape reaction elicited by electrical stimulation of the ventromedial hypothalamus (VMH). DH stimulation made ipsi- or contralaterally to the stimulated hypothalamic center of "affective reactions" increased while MRF stimulation reduced the latency of escape. Coagulation of the structures inhibited escape reaction in rabbits. The inhibition of the latter reaction in hippocampectomized animals was characterized by the increased general motor activities, whereas rabbits with lesions in the MRF were adynamic. That the DH and MRF play a different role in the mechanisms by which excitations spread from the VMH to the neocortical areas was revealed after computer analysis of the power of the main EEG rhythms.

Animals↗

Mucus escape reaction that involves the mandible: a case report and diagnostic imaging considerations.

We present a case of mucus escape reaction in which we encountered difficulty in interpreting the images acquired by plain radiography, computed tomography, and magnetic resonance imaging. The 48-year-old male Japanese patient was referred for evaluation of a gradual swelling subjacent to the inferior border of the left mandible. At the early imaging examinations, magnetic resonance imaging provided information crucial to resolving the issue of whether the lesion consisted of a central malignant disease process or a malignant disease in the submandibular space or both of these two separate disease entities. Magnetic resonance imaging demonstrated no evidence of tumorous lesion, but rather showed a fluid-containing cavity that was also confirmed by the subsequent intrasurgical inspection. On further consideration of these imaging findings, we concluded that the entity was mucus escape reaction with simultaneous occurrence of an intraconnective tissue hemorrhage adjacent to the left submandibular gland, concomitant extensive bony defect of the left mandible and lingual cortical defect, and chronic sialoadenitis of the left submandibular gland.

Diagnosis, Differential↗

Effect of NaCl addition on nanosecond O2 escaping reaction of myoglobin: evidences for the transition of myoglobin dynamic structure at 20 degrees C.

We studied the nanosecond (ns) geminate O2 escape reaction from the protein interior of myoglobin (Mb) to the solvent phase in the temperature range of 5-40 degrees C containing 0-0.1 M NaCl. In the flash photolysis experiments, we found that both the rate constant, kout, and its Arrhenius plot changed upon the variation of the NaCl concentration. In particular, it was noteworthy that the Arrhenius plot of kout dramatically changed in its slope, keeping the break at 20 degrees C, upon the addition of NaCl, indicating that the thermodynamic parameters such as an enthalpy of activation (delta H not equal to) and an entropy of activation (delta S not equal to) are different between above and below 20 degrees C, and that they are further altered upon the NaCl addition to the sample solution. From these results, we suggested that the Mb dynamic structure in the ns geminate O2 escape reaction is sensitively regulated by the interaction of the protein surface and the salt. The present study also showed that an inconsistency of the Arrhenius plot of kout between Chatfield et al. ((1990) J. Am. Chem. Soc. 112, 4680-4687) and us ((1990) J. Biol. Chem. 265, 18823-18828) is probably due to the difference in the solution condition.

Myoglobin↗

Cooperativity-dependent long-lasting potentiation in the crayfish lateral giant escape reaction circuit.

The ability of sensory neuron firing to cause the lateral giant escape reaction increases following repeated sensory volleys at 4 Hz for 10 sec. The increase occurs only when relatively large numbers of afferents are repetitively stimulated, decays with a mean time constant of 21 hr, is confined to the ganglia at which the repeated sensory volleys enter the nerve cord, and is at least partially specific to those roots of a ganglion that were tetanized. Transmission at the chemical synapses between afferents and the largest of the first-order sensory neurons that link afferents to the lateral giants displays a similar potentiation. This phenomenon shares many properties with hippocampal long-term potentiation.

Animals↗

Direct chemically mediated synaptic transmission from mechanosensory afferents contributes to habituation of crayfish lateral giant escape reaction.

The neural mechanism of habituation of the crayfish lateral giant-mediated escape reaction was analyzed electrophysiologically and pharmacologically. Upon repeated stimulation of tailfan afferents (at 0.2-1 Hz) lateral giant showed rapid habituation and failed to spike. Upon low-intensity sensory stimulation, the lateral giant responded with two subthreshold excitatory post-synaptic potentials, the alpha and beta components. A third component, the alpha' component, was discriminated at the boundary of excitatory post-synaptic potentials between the late alpha and early beta components with stimulation just subthreshold or suprathreshold to evoke lateral giant spikes. This alpha' component increased in amplitude with hyperpolarizing current injected into the lateral giants, although the amplitude of both the alpha and beta components remained constant. Furthermore, bath application of the nicotinic antagonist, d-tubocurarine caused a rapid reduction in the amplitude of the alpha' component while the amplitude of the beta component was reduced gradually and that of the alpha component remained unchanged. Single-hair stimulation indicated that some sensory afferents made direct connections with the lateral giants mediated by chemical synapses and form the potential of alpha' component of the lateral giants. Since lateral giant inactivation was associated with a reduction of excitatory post-synaptic potential amplitude of the alpha' component, connection from these afferents could contribute, at least in part, to lateral giant habituation.

Animals↗

Sensitization of the crayfish lateral giant escape reaction.

Most behavioral reactions that habituate can also be dishabituated by strong stimuli. In the best studied cases, dishabituation seems to be the result of an independent "sensitization" of the behavioral reaction that compensates for habituation without necessarily abolishing it. Crayfish lateral giant (LG) neuron-mediated escape reactions are one of the most fully analyzed behavioral reactions that are prone to habituation; however, sensitization/dishabituation of LG escape has not previously been reported. Here, the effect of strong AC shocks to head or abdomen on the ability of 0.1 msec "test" shocks to sensory roots innervating the tailfan to elicit an LG escape response was examined. Following single AC shocks, test shock threshold for eliciting LG escape reliably fell 5-80% and recovered over 15 min to 1 hr. When AC shocks and test shocks alternated at 90 sec intervals, test shock threshold rapidly dropped to an asymptote that was maintained as long as AC shocks were given (up to 2 hr); following such repeated AC shocks, recovery often required a number of hours but was complete within 24. Comparable sensitization is seen in the response of interneuron A, the largest of a set of sensory interneurons that links afferents to LGs. AC shocks (to either head or tail) no longer sensitize abdominal LG reflex circuitry if the nerve cord is severed between thorax and abdomen. Thus, sensitization appears to depend on a neurally conducted influence that arises in the rostral half of the animal. Pharmacological evidence suggests that octopamine may mediate the sensitization.

Animals↗

Serotonin and octopamine have opposite modulatory effects on the crayfish's lateral giant escape reaction.

Serotonin and octopamine have opposite effects on a simple behavioral response, the crayfish's lateral giant escape reaction. Specifically, serotonin depresses the lateral giants' responsiveness, whereas octopamine enhances it. Both effects are largely confined to the disynaptic pathway from the sensory afferents to the lateral giants, although, occasionally, small effects are also seen in the monosynaptic pathway to the lateral giants. One specific locus of the octopaminergic effect is the synapse between the afferents and the largest of the sensory interneurons in the disynaptic pathway, interneuron A. Serotonin, however, does not have a consistent effect at this synapse. Although serotonin and octopamine modulate the excitability of the escape response, neither monoamine appears to significantly alter the rate at which this response habituates.

Animals↗

Impaired escape reaction from noxious and nonnoxious heat in rats treated with the selective noradrenergic neurotoxin DSP-4.

The escape reaction, as an indicator of behavioral thermoregulation, was studied in rats pretreated with the selective noradrenergic neurotoxin DSP-4. The animals were kept for 30 min in a heated floor (42, 44, 46, 48 and 50 degrees C) cage containing a wooden platform placed at a height of 12 cm, which enabled the rats to escape from the warm floor. The latency of escape and the time spent on the platform were recorded. The performance of DSP-4-treated rats was significantly inferior to that of the control rats at all tested temperatures. These findings indicate a general function of the central noradrenergic neurons in defense alarm reactions, including a significant role in heat defense behavior.

Animals↗

[Role of the motor area of the cortex in the performance of the postural escape reaction].

It has been shown on three dogs that unilateral ablation of the cortical motor area temporally disturbs previously acquired and opposite to the innate postural escape reaction to electric stimulation of the contralateral forepaw by increasing its pressure on the support. After 3-4 months of repeated training, compensation is possible. Bilateral ablation of the motor cortex elicits stable and unreversible disturbance of the acquired reaction. In reorganization of postural coordinations, motor cortex functions are connected with the inhibition of innate coordinations preventing performance of the reaction.

Animals↗

[Enhancement of the resistance of the escape reaction to ethanol after substance P].

An ability of substance P (30 micrograms/kg intravenously) to prevent deleterious effects of ethanol (E) (0.5 g/kg intravenously) on central mechanisms of escape reaction elicited by threshold electrical stimulation of the ventromedial hypothalamus was investigated in chronic experiments upon rabbits. Substance P was found to prevent E effects on excitability of the ventromedial hypothalamus (VMH) and on facilitatory influences of the midbrain reticular formation on this emotional centre which were observed in intact animals. Inhibitory effects of the dorsal hippocampus on the VMH could not be evaluated due to its alterations in response to previous substance P administration. The authors suggest that substance P can be considered to be a possible endogenous factor to increase a tolerance of emotional behavioural reactions of an organism to alcohol.

Animals↗

5,7-Dihydroxytryptamine lesions of crayfish serotonin-containing neurons: effect on the lateral giant escape reaction.

The crayfish's lateral giant escape response, a relatively simple behavioral reaction, is readily modulated in certain situations. For example, when a crayfish is restrained, its lateral giant (LG) fibers--command neurons that mediate the escape response--are strongly inhibited (Krasne and Wine, 1975). Previous work (Glanzman and Krasne, 1983) had suggested that serotonin (5-HT) might mediate this restraint-induced inhibition of the escape response. To test this possibility, we attempted to lesion serotonergic neurons in crayfish with the 5-HT neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT). We compared the levels of 5-HT-immunoreactive staining in nerve cords from 5,7-DHT-treated and from normal crayfish to assess 5,7-DHT's effectiveness. Levels of immunoreactive staining, as judged by ratings of the visibility of immunofluorescence, were significantly lower in nerve cords from crayfish that had received injections of 5,7-DHT (1.0-4.0 mg) than in nerve cords from normal crayfish. In addition, some serotonergic neurons in the neurotoxin-treated crayfish developed an abnormal brown pigmentation. To assess the behavioral consequence of central serotonergic lesions, we compared the responsiveness of escape in crayfish treated with 5,7-DHT (2.0-2.75 mg) and in normal crayfish. The threshold for firing the LGs was significantly lower in restrained neurotoxin-treated animals than in restrained normal animals. Furthermore, the responsiveness of the LGs in neurotoxin-treated crayfish approximated that in crayfish whose nerve cords had been severed between the thorax and abdomen, a procedure known to abolish restraint-induced inhibition (Krasne and Wine, 1975).(ABSTRACT TRUNCATED AT 250 WORDS)

5,7-Dihydroxytryptamine↗