Communication calls produced by electrical stimulation of four structures in the guinea pig brain.
Female; Male; Animals; Acoustic Stimulation/methods; Auditory Perception/physiology; Brain/*physiology; Electric Stimulation/methods; Guinea Pigs; Neurons/physiology; Animal/physiology; Vocalization
One of the main central processes affecting the cortical representation of conspecific vocalizations is the collateral output from the extended motor system for call generation. Before starting to study this interaction we sought to compare the characteristics of calls produced by stimulating four different parts of the brain in guinea pigs (Cavia porcellus). By using anaesthetised animals we were able to reposition electrodes without distressing the animals. Trains of 100 electrical pulses were used to stimulate the midbrain periaqueductal grey (PAG), hypothalamus, amygdala, and anterior cingulate cortex (ACC). Each structure produced a similar range of calls, but in significantly different proportions. Two of the spontaneous calls (chirrup and purr) were never produced by electrical stimulation and although we identified versions of chutter, durr and tooth chatter, they differed significantly from our natural call templates. However, we were routinely able to elicit seven other identifiable calls. All seven calls were produced both during the 1.6 s period of stimulation and subsequently in a period which could last for more than a minute. A single stimulation site could produce four or five different calls, but the amygdala was much less likely to produce a scream, whistle or rising whistle than any of the other structures. These three high-frequency calls were more likely to be produced by females than males. There were also differences in the timing of the call production with the amygdala primarily producing calls during the electrical stimulation and the hypothalamus mainly producing calls after the electrical stimulation. For all four structures a significantly higher stimulation current was required in males than females. We conclude that all four structures can be stimulated to produce fictive vocalizations that should be useful in studying the relationship between the vocal motor system and cortical sensory representation.
Green David B; Shackleton Trevor M; Grimsley Jasmine M S; Zobay Oliver; Palmer Alan R; Wallace Mark N
PloS one
2018
1905-07
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1371/journal.pone.0194091" target="_blank" rel="noreferrer noopener">10.1371/journal.pone.0194091</a>
Daily spontaneous running attenuated the central gain of the arterial baroreflex.
Animal; Animals; Arteries/*physiology; Baroreflex/*physiology; Brain/*physiology; Female; Male; Motor Activity/*physiology; Physical Conditioning; Rats; Sprague-Dawley
Exercise training attenuates arterial baroreflex function. Mechanisms responsible may include an attenuated aortic baroreceptor reactivity (afferent mechanisms) and/or an attenuated central baroreflex gain. We tested the hypothesis that the aortic baroreceptor reactivity and/or central gain is attenuated by daily spontaneous running (DSR). Eighteen anesthetized Sprague-Dawley rats (11 control and 7 DSR) were tracheotomized and instrumented with femoral venous and right carotid arterial catheters. Electrodes were placed around the left aortic depressor nerve and the lumbar sympathetic trunk. Eight to thirteen weeks of DSR were associated with a 20% increase in heart weight-to-body weight ratio (2.83 +/- 0.04 vs. 3.39 +/- 0.10 g/kg; P \textless 0.001) and resting bradycardia (413 +/- 6 vs. 384 +/- 10 beats/min; P = 0.01). DSR reduced the central gain of the baroreflex regulation of heart rate (0.210 +/- 0.046 vs. 0.005 +/- 0.021 beats.min-1.%-1; P = 0.004) during decreases in arterial pressure. However, the reactivity of aortic baroreceptor afferents and the central gain of the baroreflex control of lumbar sympathetic nerve activity were not different in control and DSR rats. Thus DSR reduced the central gain of the arterial baroreflex regulation of heart rate without changing the reactivity of aortic baroreceptor afferents. We conclude that afferent mechanisms are not responsible for the training-induced reduction in arterial baroreflex function.
Chen C Y; DiCarlo S E; Scislo T J
The American journal of physiology
1995
1995-02
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1152/ajpheart.1995.268.2.H662" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.1995.268.2.H662</a>
Lack of an inhibitory effect of hyperprolactinemia on androgen-dependent marking.
Animal/*physiology; Animals; Arousal/physiology; Brain/*physiology; Defecation/physiology; Inbred F344; Male; Mesencephalon/physiology; Neural Inhibition/*physiology; Neural Pathways/physiology; Preoptic Area/physiology; Prolactin/*physiology; Rats; Sex Attractants/*urine; Sexual Behavior; Testosterone/*physiology; Urination/*physiology
An experiment was performed to determine if hyperprolactinemia (chronically elevated serum prolactin levels), which inhibits testosterone-activated male sexual activity, also affects other androgen-dependent behaviors. Thus defecation and urine marking in response to a novel environment were examined in sham-operated and pituitary-grafted (hyperprolactinemic) male rats that had been castrated or castrated and given subcutaneous testosterone implants. Both castration and pituitary grafting significantly inhibited defecation, with the inhibitory effects of hyperprolactinemia being most pronounced in the castrated non-testosterone-treated animals. In contrast, castration significantly reduced the amount of urine marking observed, but pituitary grafting was without effect on this behavior. Thus, although hyperprolactinemia may inhibit sexual activity through an antagonism of the activational effects of testosterone, these results suggest that this effect is specific to sexual behavior and does not involve a more generalized inhibition of the effects of testosterone on androgen-dependent behaviors.
Doherty P C
Physiology & behavior
1991
1991-11
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/0031-9384(91)90435-q" target="_blank" rel="noreferrer noopener">10.1016/0031-9384(91)90435-q</a>
Use of brain slices to study long-term potentiation and depression as examples of synaptic plasticity.
*Long-Term Potentiation; *Neuronal Plasticity; Animals; Brain/*physiology; Electrophysiology/methods; Glutamic Acid/physiology; In Vitro Techniques; Memory/*physiology; Models; Neurological; Synapses/*physiology; Synaptic Transmission
Brain slices have been responsible for the majority of advances in our understanding of the cellular aspects of altered synaptic strength underlying memory, long-term potentiation (LTP) and long-term depression (LTD), and increases and decreases, respectively, in synaptic strength at glutamatergic synapses. Our current understanding of LTP and LTD has come largely from studies in hippocampal slices. We consider the strengths and limitations of brain slice technology applied to this subject and conclude that they will continue to have an important role in future studies into the cellular machinery underlying changes in synaptic strength.
Teyler T J
Methods (San Diego, Calif.)
1999
1999-06
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1006/meth.1999.0764" target="_blank" rel="noreferrer noopener">10.1006/meth.1999.0764</a>