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Results for “Escape Reaction”

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At least 19 recordsLinked to original sources
PubMedDate not supplied

[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↗
PubMed1985

[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↗
PubMed1988

[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↗
PubMed1992

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↗
PubMed1987

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↗
PubMed1986

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↗
PubMed1991

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↗
PubMedDate not supplied

[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↗
PubMed1991

[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↗
PubMed1986

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↗
PubMed1992

Cholinergic transmission at the first synapse of the circuit mediating the crayfish lateral giant escape reaction.

1. The chemical synapses between mechanoreceptor neurons and first-order interneurons in the lateral giant (LG) neuron escape circuit of the crayfish have plastic properties, some of which are believed to be the basis for behavioral habituation and sensitization. In this investigation pharmacological experiments were conducted to assess the role of cholinergic synaptic transmission in this pathway. 2. Arterial perfusion of the cholinergic agonist carbachol produced increased activity of many abdominal nerve cord units, including an identified first-order interneuron (interneuron A) in the LG circuit. A general increase in activity of interneurons in this circuit in the presence of certain cholinergic agonists was inferred from an increase in the frequency of occurrence of spontaneous excitatory postsynaptic potentials (EPSPs) recorded in the LG. 3. Cholinergic antagonists reduced the amplitude of spontaneous and evoked sensory neuron-to-interneuron A EPSPs and decreased the disynaptic (via 1st-order interneurons) component of evoked EPSPs in the LG. These effects indicate that postsynaptic cholinergic receptors are utilized in mechanosensory synaptic transmission to the first-order interneurons of this circuit. The relative potencies of the blockers tested (mecamylamine > picrotoxin >>> curare > atropine) suggest that the receptors on the interneurons belong to a previously characterized class of crustacean cholinergic receptors that resemble the ganglionic nicotinic subtype of vertebrates. 4. Nicotinic agonists (carbachol, tetramethylammonium hydroxide, 1,1-dimethyl-4-phenyl-piperazium iodide) produced depolarizing (decreased input resistance) responses on the LG neuron itself. These responses persisted during blockade of chemical transmission by cobalt. The presence of cholinergic receptors on the LG, a cell in which all known inputs mediating sensory excitation are electrical, is discussed. 5. Application of muscarinic agonists (pilocarpine, oxotremorine) resulted in a long-lasting reduction of the evoked sensory neuron-to-interneuron A EPSP and the disynaptic component of the evoked EPSP in the LG. No effects on the membrane potential or input resistance of the interneurons were detected. It is proposed that presynaptic receptors with a muscarinic profile are present on mechanosensory neurons and that these receptors mediate a reduction of transmitter release.

Acetylcholine↗