Whole body vibration and post-activation potentiation: a study with repeated measures.

The objective of this study was to assess the acute effect of different intensities of whole body vibration (WBV) on muscle performance. 8 recreationally trained males were randomly subjected to one of 3 experimental conditions: (A) WBV 2 mm [45 Hz and 2 mm], (B) WBV 4 mm [45 Hz and 4 mm], and (C) no WBV. To assess PAP, the peak concentric torque of knee flexors and extensors was measured during a set of 3 unilateral knee flexor-extensions at 60°/s(-1) in an isokinetic dynamometer. The power output and height during vertical jumps were also evaluated. These measurements were performed both before and after the experimental conditions and then compared. Comparing the knee flexion data from the conditions with and without WBV indicate that WBV potentiated the peak torque during unilateral knee flexion in the isokinetic test (p < 0.05). In addition, the power output (p = 0.01) and vertical height of jump (p = 0.03) were also potentiated by WBV. However, increasing the vibratory stimulus did not further potentiate the results. Thus, it is suggested that WBV be used before explosive events competition because WBV promotes post-activation potentiation.

Cardiovascular and behavioural responses to conditioned fear and restraint are not affected by retrograde lesions of A5 and C1 bulbospinal neurons.

The aim of this study was to test a possible role of A5 neurons in the expression of the pressor and tachycardic responses to conditioned fear and restraint, two forms of psychological stress. Previous Fos studies have shown that the C1 adrenergic neurons and spinally projecting neurons in the vasopressor region of the rostral ventrolateral medulla are not activated by these two stressors, suggesting that these cardiovascular changes may be mediated by other premotor sympathetic (presympathetic) cell groups. The same studies also revealed that the A5 noradrenergic group was one of the main presympathetic cell groups to be activated in response to these two stressors. Thus, we hypothesized that the A5 group could mediate these cardiovascular responses. Conditioned fear and restraint were tested in rats implanted with radiotelemetric probes before and after retrograde lesion with the selective toxin anti-dopamine-beta-hydroxylase-saporin bilaterally injected in the spinal cord at T2-T3. Six animals were selected that had the most extensive loss of spinally projecting catecholaminergic neurons: A5 (81%-95%) and rostral C1 (59%-86%, which would include most C1 bulbospinal neurons). However, despite this major loss of noradrenergic and adrenergic presympathetic neurons, the magnitude of the cardiovascular response to conditioned fear and restraint was the same before and after the lesion. Associated behavioural changes were not affected either. The results indicate that A5 presympathetic neurons are not essential for the expression of the tachycardic and pressor responses to conditioned fear and restraint. They also confirm that C1 bulbospinal neurons are not involved in these responses. The presympathetic neurons driving the tachycardic and pressor responses to conditioned fear and restraint must be elsewhere.

Cardiovascular and behavioral responses to conditioned fear after medullary raphe neuronal blockade.

Conditioned fear to context in the rat leads to a host of sympathetically mediated physiological changes, including a marked rise in mean arterial pressure, a delayed rise in heart rate and a marked cutaneous vasoconstriction, along with the behavioral responses of freezing and ultrasonic vocalization. In this study we examine the role of the rostral ventromedial medulla (RVM), which includes raphe nuclei pallidus and magnus, in the expression of these changes. RVM is a major premotor sympathetic and somatic center and an important integrating center in the descending emotional motor system. To evaluate its role, conditioned fear was tested after temporary blockade with microinjections (0.4 microl) of the GABA-A receptor agonist muscimol (0.2 mM) or the glutamate receptor antagonist kynurenic acid (0.1 M). Changes in mean arterial pressure, heart rate and activity were recorded by radio-telemetry. Cutaneous vasoconstriction in the tail was recorded indirectly by infrared thermography. Muscimol and kynurenic acid had different, almost complementary effects. Muscimol abolished the skin vasoconstrictor response and significantly reduced the tachycardic response, but did not reduce the pressor response significantly and had little effect on the somatic motor components, freezing and ultrasonic vocalization. In contrast, kynurenic acid abolished ultrasonic vocalization and significantly reduced freezing but had no effect on the cardiovascular components. The results show that neurons in the rostral ventromedial medulla are implicated in the expression of some of the cardiac, vascular and somatic motor components of conditioned fear. Most importantly, these cardiovascular components are not under local glutamatergic control whereas the somatic motor components are.

Anatomical connections of the periaqueductal gray: specific neural substrates for different kinds of fear

The periaqueductal gray (PAG) has been traditionally considered to be an exit relay for defensive responses. Functional mapping of its subdivisions has advanced our knowledge of this structure, but synthesis remains difficult mainly because results from lesion and stimulation studies have not correlated perfectly. After using a strategy that combined both techniques and a reevaluation of the available literature on PAG function and connections, we propose here that freezing could be mediated by different PAG subdivisions depending on the presence of immediate danger or exposure to related signaling cues. These subdivisions are separate functional entities with distinct descending and ascending connections that are likely to play a role in different defensive responses. The existence of ascending connections also suggests that the PAG is not simply a final common path for defensive responses. For example, the possibility that indirect ascending connections to the cingulate cortex could play a role in the expression of freezing evoked by activation of the neural substrate of fear in the dorsal PAG has been considered

Anatomical connections of the periaqueductal gray: specific neural substrates for different kinds of fear.

The periaqueductal gray (PAG) has been traditionally considered to be an exit relay for defensive responses. Functional mapping of its subdivisions has advanced our knowledge of this structure, but synthesis remains difficult mainly because results from lesion and stimulation studies have not correlated perfectly. After using a strategy that combined both techniques and a reevaluation of the available literature on PAG function and connections, we propose here that freezing could be mediated by different PAG subdivisions depending on the presence of immediate danger or exposure to related signaling cues. These subdivisions are separate functional entities with distinct descending and ascending connections that are likely to play a role in different defensive responses. The existence of ascending connections also suggests that the PAG is not simply a final common path for defensive responses. For example, the possibility that indirect ascending connections to the cingulate cortex could play a role in the expression of freezing evoked by activation of the neural substrate of fear in the dorsal PAG has been considered.

Defensive freezing evoked by electrical stimulation of the periaqueductal gray: comparison between dorsolateral and ventrolateral regions.

Previous reports indicated that ventrolateral periaqueductal gray (vlPAG) plays a role in the expression of freezing behavior whereas dorsolateral periaqueductal gray (dlPAG) is involved on both freezing and active forms of defensive behaviors. In order to evaluate the role of each of these areas in the occurrence of defensive reactions, rats were electrically stimulated either in the dlPAG or vlPAG with different stimulus frequencies. Stepwise increases in the electrical stimulation of both dlPAG or vlPAG induced initially freezing and then a jumping response. Freezing induced by vlPAG stimulation had a tendency to disappear when the stimulation was turned off whereas freezing induced by dlPAG stimulation remained high in the absence of the stimulation. These results suggest that dlPAG and vlPAG are involved on defensive freezing probably through different neural circuitries.

Lesion of the ventral periaqueductal gray reduces conditioned fear but does not change freezing induced by stimulation of the dorsal periaqueductal gray.

Previously-reported evidence showed that freezing to a context previously associated with footshock is impaired by lesion of the ventral periaqueductal gray (vPAG). It has also been shown that stepwise increase in the intensity of the electrical stimulation of the dorsal periaqueductal gray (dPAG) produces alertness, then freezing, and finally escape. These aversive responses are mimicked by microinjections of GABA receptor antagonists, such as bicuculline, or blockers of the glutamic acid decarboxylase (GAD), such as semicarbazide, into the dPAG. In this work, we examined whether the expression of these defensive responses could be the result of activation of ventral portion of the periaqueductal gray. Sham- or vPAG electrolytic-lesioned rats were implanted with an electrode in the dPAG for the determination of the thresholds of freezing and escape responses. The vPAG electrolytic lesions were behaviorally verified through a context-conditioned fear paradigm. Results indicated that lesion of the vPAG disrupted conditioned freezing response to contextual cues associated with footshocks but did not change the dPAG electrical stimulation for freezing and escape responses. In a second experiment, lesion of the vPAG also did not change the amount of freezing and escape behavior produced by microinjections of semicarbazide into the dPAG. These findings indicate that freezing and escape defensive responses induced by dPAG stimulation do not depend on the integrity of the vPAG. A discussion on different neural circuitries that might underlie different inhibitory and active defensive behavioral patterns that animals display during threatening situations is presented.

Dorsolateral and ventral regions of the periaqueductal gray matter are involved in distinct types of fear.

Stepwise increases in the electrical stimulation of the dorsolateral periaqueductal gray (dlPAG) produces alertness, then freezing and finally escape. This paper examines whether this freezing is (i) caused by Pavlovian fear conditioning to the contextual cues present during stimulation and (ii) the result of the stimulation of neurons located inside the dlPAG or elsewhere. To this end, freezing behavior was assessed in rats exposed either to the same or a different environment (context shift test) following the application of either footshocks or stimulation of the dlPAG at the freezing threshold. Rats submitted to footshocks presented freezing to the context 24h later whereas rats submitted to the dlPAG stimulation showed freezing only immediately after the stimulation, regardless of the context. In the second experiment, aversive states generated by activation of the dlPAG were assessed either by measuring the thresholds for freezing and escape responses or the duration of these responses following microinjections of semicarbazide inside the dlPAG. The duration of freezing behavior was also measured in rats submitted to a contextual fear-conditioning paradigm using footshocks as unconditioned stimulus. Lesions of the ventral periaqueductal gray (vPAG) disrupted conditioned freezing to contextual cues associated to footshocks but vPAG lesions did not change the threshold of either freezing or escape responses elicited by electrical stimulation of the dlPAG. Lesions of the vPAG did not change the amount of freezing or escape responses produced by microinjections of semicarbazide into the dlPAG. These results indicate that stimulation of dlPAG neurons produce freezing behavior independent of any contextual fear conditioning and add to previously reported evidence showing that the vPAG is a critical structure for the expression of conditioned fear. In contrast, the neural substrate of unconditioned dlPAG stimulation-induced freezing is likely to elaborate unconditioned fear responses to impending danger, which have been implicated in panic disorder.