Immobility Response In Rats Research Articles

Pain chronification and chronic pain impair a defensive behavior, but not the ability of acute pain to facilitate it, through the activation of an endogenous analgesia circuit.

The endogenous ability to decrease pain perception during life-threatening situations is crucial to the prevention of recuperative behaviors and to leave the subject free to engage in appropriated defensive responses. We have previously shown that acute pain activates the ascending nociceptive control-an endogenous analgesia circuit dependent on opioid mechanisms within nucleus accumbens-to facilitate the tonic immobility response, an innate defensive behavior. Now we asked whether chronic pain and pain chronification impairs either the tonic immobility response or the ability of acute pain to facilitate it by activating the ascending nociceptive control. We found a significant decrease in the duration of the tonic immobility response in rats during the induction and maintenance phases of the persistent mechanical hyperalgesia. This finding suggests that chronic pain and its development impair defensive responses. However, during the induction and maintenance phases of persistent hyperalgesia, the ascending nociceptive control activation, by a forepaw capsaicin injection, increased the tonic immobility response, an effect prevented by the blockade of μ-opioid receptors within nucleus accumbens. This finding suggests that pain chronification and chronic pain do not prevent the ability of acute pain to facilitate the defensive behavior of tonic immobility by activating the ascending nociceptive control. Therefore, although chronic pain states decrease the ability to engage in a defensive behavior, they may not prevent the expression of defensive behaviors during life-threatening situations accompanied by acute pain. The biological purpose of such a mechanism may be to increase the chances of survival of a wounded subject exposed to acute pain in a novel life-threatening situation. (PsycINFO Database Record (c) 2018 APA, all rights reserved).

The functional role of ascending nociceptive control in defensive behavior

Ascending nociceptive control is a novel spino-striato-rostral ventral medulla pain modulation pathway that mediates heterosegmental pain-induced analgesia, i.e., noxious stimulus-induced antinociception. In this study, we used the dorsal immobility response in rats as a model of the defensive responses. We demonstrated that the activation of ascending nociceptive control by peripheral noxious stimulation and spinal AMPA and mGluR1 receptor blockade significantly potentiated the duration of the dorsal immobility response in rats via an opioid-dependent mechanism in the nucleus accumbens. These results demonstrated the functional role of ascending nociceptive control in the modulation of defensive responses and spinal glutamatergic receptors in the dorsal immobility response. The immobility response is an antipredator behavior that reflects the underlying state of fear, and ascending nociceptive control may modulate fear.

The effects of acute stress and acute corticosterone administration on the immobility response in rats

The immobility response is an innate antipredatory behavior in a broad variety of species. The immobility response varies in its postural components but in general is characterized by an absence of movement and a relative unresponsiveness to stimuli. Experimentally in rats, clamping the neck followed by body inversion and manual restrain elicits a response called “immobility by clamping the neck”. Stress reactions protect animals against predators and are characterized by activation of the sympathetic and hypothalamic–pituitary–adrenal systems. However, in mammals, the role of acute stress as a modulator of immobility response has been less studied. The aim of our study was to assess the effects of acute stress and the injection of corticosterone (5 mg/kg, ip) on immobility by clamping the neck in rats. We observed that either previous acute stress caused by forced exposure to elevated open platform or application of a heat-pain stimulus to the rat's tail during the immobility increased the duration of the immobility response caused by clamping the neck. Also, the corticosterone produced a rapid increase (15 min after injection) in the duration of this immobility response. Our results show that the acute stress, in rats, is a facilitator of the immobility response and suggest a possible nongenomic rapid action of corticosterone over brain structures that control this behavior.

Effect of excitotoxic lesions of the neonatal ventral hippocampus on the immobility response in rats

Rats with neonatal ventral hippocampal (nVH) lesions show postpubertal hypersensitivity to dopamine agonists, which may be reversed by neuroleptic treatment. In addition, the immobility response (IR) may be regulated by dopaminergic activity. We investigated the influence of the IR caused by clamping the neck of rats that had received bilateral ibotenic acid lesions of the ventral hippocampus at postnatal day 7 (PD7). At both ages, prepubertal (PD35) and postpubertal (PD56), the duration of the IR was significantly increased in animals with lesions when compared to controls. These findings indicate that nVH damage results in behavioral changes, such as enhancement of the IR, related to mesolimbic dopaminergic transmission.

Neuronal reactions in the dorsolateral pontine area during the immobility response in rats

Reactions of 277 neurones located in the brain pons dorsolateral portion were analised in staying awake and narcotized rats during immobility reflex, induced by the skin constriction on the neck dorsal surface. Got excited: fast adaptive tactile neurons (n = 32), interneurons (n = 42), and cells forming monosynaptic inputs to the parts of medulla oblongata, which inhibit the movements (n = 10). Were inhibited: somatosensory (n = 42), nociceptive (n = 24) and nonidentificated (n = 14) neurons. In some neurons charge characteristics were stable or slightly modified, namely: respiratory neurons (n = 16), cell group, having stable background firing (n = 72) and stimulating antidromically spontaneously silent ponto-medullar neurons (n = 22).

The effects of methionine-enkephalin and its related metabolites upon the duration of the dorsal immobility response in rats

The effects of SC injections of methionine-enkephalin (Met 1−5-Enk) and its N-terminal and C-terminal fragments upon the duration of the dursal immobility response (DIR) over a 60-min time course were investigated. Experiment 1 analyzed the effects of various dosages (0.00–100.0 μg/kg) on DIR resulting in a potentiation of the duration in a dose-time course function. The effects of various fragments of Met 1−5-Enk (10.0 μg/kg) from the N-terminal in Experiment 2 and from the C-terminal in Experiment 3 on the DIR resulted in the potentiation of the duration with the Met 2−5-Enk and Met 1−3-Enk fragments. All other fragments were not significant. The results were discussed in reference to the processing and metabolism of Met 1−5-Enk.

Intrastriatal injections of dynorphin a fragments potentiate the dorsal immobility response in rats

The effects of bilateral intrastriatal injections (2.0 μg/side) of Dynorphin A 1–17 (Dyn A 1–17) and Dynorphin A 1–8 (Dyn A 1–8) and their related nonopioid fragments upon the dorsal immobility response (DIR) over a 1-h time course were investigated. Dyn A 1–17 and Dyn A 2–17 potentiated the duration of the DIR 5 min postinjection, whereas Dyn A 1–8 and Dyn A 2–8 potentiated the DIR duration at each time point over the hour with their greatest effect at 15 min. An SC injection of 4 mg/kg naloxone 15 min prior to central injections blocked the potentiation of the DIR effects of Dyn A.

Differential effects of dopamine D 2 agonist quinpirole upon the dorsal immobility response in rats

The effects of various dose levels of systemically injected quinpirole upon the dorsal immobility response (DIR) over a time course was investigated in male rats. A low dose of quinpirole (0.01 mg/kg) significantly attenuated the duration of the DIR following the 10-min interval, whereas the highest dose (1.0 mg/kg) had a biphasic effect so that at the 10-min interval the duration of the DIR was significantly potentiated and at the 60-min interval the duration of the DIR was significantly attenuated. The intermediate dose (0.1 mg/kg) had intermediate behavioral effects. The data support the growing evidence that quinpirole has differential effects upon behavior over time as a function of the dose levels. The present data were discussed in reference to presynaptic and postsynaptic dopamine D 2 receptor theory.

Dopamine D 1 antagonists potentiate the durations of bar and cling catalepsy and the dorsal immobility response in rats

The effects of dopamine D 1 antagonists SCH 23390 or SK&F 83566 (at SC doses of 0.00, 0.01, 0.05, and 0.1 mg/ kg) were tested for 2 h on bar and cling catalepsy and the dorsal immobility response. Each of the drugs potentiated the duration of each of the three measures of immobility in a dose- and time-dependent manner. Each of the drugs had rapid but brief effects on all three response measures; the peak effect of SK&F 83566 took place at 20 min and that for SCH 23390 at 40 min for each behavior. At each effective drug dose, SCH 23390 had a greater effect than SK&F 83566 on each behavior. Dopamine D 1 antagonists potentiated three different immobility responses, as do dopamine D 2 antagonists.