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S M Brudzynski

Publications and source records attributed to S M Brudzynski.

36 records · Page 2Linked to original sources

Analysis of 22 kHz ultrasonic vocalization in laboratory rats: long and short calls.

There is a remarkable variation in the length of single ultrasonic calls emitted by adult rats. The duration of calls is likely to convey information for conspecifics. The goal of the present study was to analyze 22 kHz calls emitted by naive laboratory rats in response to contact with the human hand and to measure their acoustic features, with a particular emphasis on call duration. Repeated hand touch applied to the nape of the neck of rats induced ultrasonic calls, 97.4% of which were within the range of 20-29 kHz and 2.6% of which were within 44-67 kHz. Distribution of duration of 6765 calls revealed two subpopulations of 22 kHz calls: 20-300 ms calls with its peak at 150 ms and calls above 310 ms with highest values at approximately 500-600 ms without a clear peak. These two call populations were referred to as short and long calls, respectively. The short and the long vocalizations contained 80% and 100% of calls within the range of the 22 kHz frequency, respectively. The findings indicated that, in the situation studied, the 22 kHz vocalization of adult rats consists of two distinguishable subpopulation of calls: short and long with the boundary between them at 300 ms.

Animal Communication↗

Differential effects of quinpirole in the nucleus accumbens depending on the initial level of locomotor activity.

Effects of dopamine D1 and D2 receptor agonists (SKF 38393 and quinpirole, respectively) on locomotion were studied in two behavioural situations characterized by low and high level of exploratory locomotor activity. Administration of quinpirole bilaterally into the nucleus accumbens increased locomotor activity at the low initial level of activity and decreased locomotor activity at the high activity level, while the administration of SKF 38393 increased locomotor activity in both behavioural situations. It was concluded that quinpirole has differential effects on locomotion, depending on the initial level of activity.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

Emotional-aversive nature of the behavioral response induced by carbachol in cats.

Intrahypothalamic-preoptic application of carbachol induces a characteristic, emotional-aversive response in cats similar to their natural defensive behavior. This study was undertaken to provide quantitative evidence that the magnitude of the carbachol-induced, emotional-aversive response follows the same rules as natural responses to threat. An aversive emotional response can be described in terms of a spatiotemporal relationship between the animal and the relevant threat stimulus (potential danger). The physical distance to the threat stimulus and its movements should be predictive of the magnitude of the emotional response. The goal of the study was to test the relationship for the carbachol-induced response. The presentation of a threat stimulus (a human hand) to cats injected with carbachol caused a significant increase in vocalization. The magnitude of the response was inversely proportional to the physical distance between the cat and the threat stimulus. The hand in motion caused significantly longer vocalization than the immobile hand and cats not familiar with the experimental situation vocalized significantly more than those that had been exposed to the hand before. The spatiotemporal relationship between the animal and the threat stimulus strongly suggests that the carbachol-induced response is emotional and aversive in nature and does not differ from the relevant natural responses.

Animals↗

Ultrasonic vocalization of laboratory rats in response to handling and touch.

The goal of the study was to investigate the ultrasonic vocalization induced in freely behaving, naive rats by gentle touch with a human hand. Thirty-nine rats were tested in an unfamiliar experimental cage with repeatable hand touch. Vocalization appeared with an average latency of 4.6 +/- 5.0 s (SD). The nape of the neck was the most effective area, and after a couple of stimuli applied, 66.7% of rats emitted 21-32 kHz ultrasonic vocalization. It consisted of multiple series of long calls, about 70% of which exceeded 300 ms. The responses quickly habituated from session to session to extinction. Significantly more rats housed in single cages vocalized ultrasonically than animals housed in community cages. The long latencies of the vocalization, their appearance in multiple series to a single touch, and quick habituation to the stimuli indicate that 22 kHz ultrasonic vocalization of rats reflects a distress caused by a potential danger to the animal and it does not necessarily reflect physical discomfort or pain. This vocalization may, therefore, play an adaptive role in increasing chances of survival by conveying information about potential threats to other conspecifics.

Animals↗

Involvement of M1 and M2 muscarinic receptors of the basal forebrain in cholinergically mediated changes in the rat locomotion.

1. Wistar rats were implanted with cannulae into the medial preoptic and anterior hypothalamic areas for intracerebral injections. 2. Unilateral intracerebral injections of carbachol (1 microgram) into a limited area of the basal forebrain decreased significantly both the distance travelled by the animals and time spent walking. 3. In addition to the decrease in locomotion, it was demonstrated for the first time that injections of carbachol also slow animal movement by significantly decreasing speed of forward progression. 4. All locomotor effects of carbachol were reversed by local pretreatment with atropine (1 microgram) but not by pirenzepine (2 micrograms) suggesting that these effects were mediated by M2 muscarinic receptors with minimal or no M1 receptor involvement.

Animals↗

Response of neurons of the rat anterior hypothalamic-preoptic area to carbachol.

Behavioural effects of carbachol given into the hypothalamic/preoptic area have been demonstrated but there is a paucity of information about the response of single neurons to carbachol. The aim of the present study was to determine the response of spontaneously firing neurons in the rat hypothalamic/preoptic area to application of carbachol by iontophoresis or by pressure injection in a dose and volume comparable with that used in behavioural studies. Extracellular single unit recordings showed a significant decrease in mean firing rate in 82% of neurons responding to iontophoretic carbachol and in 75.5% of neurons responding to carbachol injected about 600 microns away. An increase in firing rate occurred in only 15 and 17.6% of neurons, respectively. Application of saline did not alter the mean firing rate while application of glutamate into the same areas or ejection into the vicinity of the same neurons caused an increase in mean firing rate in 94% of responding neurons. The results indicate that a decrease in mean firing rate is the predominant neuronal response to carbachol in the anteromedial hypothalamic/preoptic area of the rat and we suggest that this decrease may be associated with behavioural responses to carbachol.

Animals↗

Comparison between cholinergically and naturally induced ultrasonic vocalization in the rat.

Ultrasonic vocalization in rats accompanying stressful situations or induced by direct brain stimulation may be used as a measure of emotionality and as a potential response model for testing anti-anxiety agents. The aim of the present study was to compare physical features of pharmacologically-induced ultrasonic vocalization with naturally triggered vocalization. Ultrasonic calls induced by hand touch, footshock, or by direct intracerebral injection of carbachol in adult rats were compared. Ultrasonic calls obtained in all these situations were described as '22 kHz' vocalization. Average frequencies of vocalization were 24.1 +/- 0.78 kHz, 26.0 +/- 2.64 kHz and 25.0 +/- 1.87 (SD) kHz for handled, footshocked and carbachol injected rats, respectively, and they did not differ significantly from each other. Histograms of single call duration showed similar distribution patterns for all groups with a predominance of long calls, although carbachol-induced calls were shorter than calls induced by touch or footshock. Histograms for inter-call intervals showed one major peak at 100-150 ms for all groups. Sonograms and power spectra showed similar characteristics both for calls induced by intracerebral carbachol and by hand touch or footshock. The results indicate that physical features of ultrasonic vocalization induced by intracerebral carbachol are comparable with those for naturally induced vocalization and fall into the category of '22 kHz' calls.

Animals↗

Ultrasonic vocalization in rats produced by cholinergic stimulation of the brain.

Neurotransmitters involved in production of ultrasounds in rodents have not yet been identified. It is also not known whether brain mechanisms regulating production of ultrasounds and audible sounds are similar or different. The present study provides the first report that intracerebral injection of an acetylcholine agonist, carbachol, in rats induces ultrasonic vocalization. Since the same agent can induce audible vocalization in cats, the finding suggests a possible common neurochemical substrate underlying production of sonic and ultrasonic vocalization in mammals. The data accumulated to date indicate also that these two kinds of vocalization may play a homologous role in animal communication.

Animals↗

Evidence for involvement of endogenous acetylcholine in emotional-aversive response in the cat.

1. The purpose of the present study was to provide evidence for involvement of endogenous acetylcholine in naturally as well as pharmacologically induced emotional behaviour in the cat. 2. Emotional-aversive responses of 10 cats were naturally evoked by presentation of a dog or the responses were pharmacologically induced by intracerebral injections of cholinomimetics. 3. Naturally evoked emotional behaviour was abolished by i.p. pretreatment with atropine sulfate (1 mg/kg), but not by atropine methyl nitrate, or it was significantly decreased by bilateral intracerebral injection of atropine sulfate (5 micrograms/microliter). 4. On the other hand, intracerebral injections of physostigmine (100 micrograms/microliter), an acetylcholinesterase inhibitor which elevates the level of endogenous acetylcholine, induced the fully developed emotional-aversive response comparable with natural behaviour and with responses induced by carbachol (10 micrograms/microliter). 5. The results demonstrate that the endogenous acetylcholine in the basal forebrain and diencephalic areas play a role in naturally occurring emotional aversive behaviour in cats.

Acetylcholine↗

Cholinergically mediated reduction of locomotor activity from the basal forebrain of the rat.

Carbachol when injected into the basal forebrain alters spontaneous motor behavior and usually decreases locomotion. However, the extent of the brain area producing this effect has not yet been determined. The goal of the present study was to use quantitative mapping of injection sites to further localize the effect of carbachol on spontaneous locomotion of rats. The distance travelled by an animal and the time spent moving were simultaneously measured before and after injection of carbachol or saline into 96 sites in the basal forebrain. Each site was injected with 1.0 microgram (5.47 nmol) of carbachol, a dose close to ED50, in a volume of 0.2 microliter. A decrease in spontaneous locomotion was obtained as a result of injections of carbachol into the preoptic and anterior hypothalamic areas, particularly into the medial preoptic nucleus and the latero-anterior hypothalamic nucleus. The area from which a consistent decrease in spontaneous locomotion was obtained was surrounded by an area producing an increase in locomotion with a narrow zone of overlap. This decrease in locomotion was dose dependent and reversed by atropine. The results indicate that both the decreasing and increasing effects of carbachol on locomotion are anatomically specific and that the decreasing effects can be elicited from a limited forebrain area. It is suggested that muscarinic cholinergic mechanisms in the basal forebrain may be involved in the pathogenesis of neural dysfunction associated with locomotor activity in man.

Animals↗

Modulation of locomotor activity induced by injections of carbachol into the tegmental pedunculopontine nucleus and adjacent areas in the rat.

The pedunculopontine nucleus (PPN) is a major component of the mesencephalic locomotor region. There is little known, however, about neurotransmitters in the PPN associated with locomotor activity. The purpose of the present study was to investigate a possible modulatory effect of the cholinergic system on locomotion. The effects of application of carbachol (CCh) into the PPN on locomotor activity of freely moving rats were studied. Unilateral injections of CCh into the PPN decreased spontaneous locomotor activity of rats. On the other hand, an increase in locomotor activity resulted from CCh injections into sites surrounding the PPN. These CCh-induced changes in locomotion were no longer observed after pretreatment of the PPN with atropine. Locomotor activity induced by injections of amphetamine into the nucleus accumbens was also reduced to control levels by ipsilateral injections of CCh into the PPn, whereas contralateral injections of CCh were ineffective. The results suggest that the muscarinic cholinergic system has a modulatory influence on locomotor activity presumably by affecting PPN cells involved in relaying locomotion-associated signals. The PPN receives signals from higher structures involved in initiation of locomotion while the muscarinic system seems to play a role in attenuation or inhibition of locomotor behaviour.

Amphetamine↗

Vocalization accompanying emotional-aversive response induced by carbachol in the cat. Reproducibility and dose-response study.

Vocalization induced by injections of carbachol into the anterior hypothalamic/preoptic area is regarded as an index of emotional behavior and offers a useful measure of emotional expression. Reproducibility and dose-dependence of the carbachol-induced vocalization, however, have not previously been systematically studied. The present study showed that the magnitude of vocalization was dose-dependent within the range of eight doses and increased in a 20-fold range from 0.5 to 10.0 micrograms, reaching its maximal plateau between 10.0 and 20.0 micrograms. Higher doses (20.0 to 80.0 micrograms) caused a decline of the vocalization. In contrast, the magnitude of vocalization was reproducible for eight injections of the same dose (10.0 micrograms). The carbachol-induced responses were decreased by repeated injections of high dosage or large volume of carbachol solution, and were reversed by atropine. The present results support the suggestion that carbachol-induced vocalization may serve as a measurable model for studying emotional behavior.

Animals↗

Decrease of locomotor activity by injections of carbachol into the anterior hypothalamic/preoptic area of the rat.

Cholinergic elements in forebrain structures are implicated in locomotion but their role is still unclear. In the present study, the effects of intracerebrally injected carbachol or atropine on spontaneous locomotion and rearing activity were investigated. Effective injection sites were found in the area between frontal planes 5.3 and 6.3 mm from interaural plane and between the ventricle wall and lateral plane 1.1 mm from the midline which corresponds to the medial anterior hypothalamic/preoptic area. Injections of 1.0 micrograms of carbachol into this area decreased locomotor activity and rearing to one-third of the control level during the first 5 min of recording. These reductions of locomotion and rearing were dose-dependent and reversed by 1.5 microgram of atropine. Atropine alone, at this dose, had no effect on locomotion but higher doses (20.0-60.0 micrograms) of atropine produced a dose-dependent increase of locomotion. A comparison of the injection sites with recent maps of the cholinergic system indicates that muscarinic cholinoceptive, presumably non-cholinergic, cells throughout the medial AH/POA might be associated with a decrease of locomotor activity caused by intracerebral injections of carbachol.

Animals↗

Inhibition of amphetamine-induced locomotor activity by injection of carbachol into the anterior hypothalamic/preoptic area: pharmacological and electrophysiological studies in the rat.

The effects of carbachol injected into the anterior hypothalamic/preoptic area on locomotion initiated by intra-accumbens injections of amphetamine were investigated. Changes of locomotion following intracerebral injections were measured in an automated activity box and the mean firing rate (m.f.r.) from neurons in the mesencephalic locomotor region (MLR) recorded in parallel acute electrophysiological experiments. Amphetamine (20.0 micrograms) injected to the nucleus accumbens caused a 2.5-fold increase in locomotion of rats. Subsequently, injections of carbachol (0.5 or 1.0 microgram) into the hypothalamic/preoptic area reduced the amphetamine-induced locomotion. These effects were stronger with ipsilateral than with contralateral injections and were reversed by pretreating the hypothalamic/preoptic area with 1.5 micrograms of atropine before carbachol injection. In electrophysiological experiments, injecting carbachol into the hypothalamic/preoptic area reduced the m.f.r. of MLR neurons from 8.3 +/- 0.7 to 4.1 +/- 0.5 per s and reduced the m.f.r. of 13 of 17 MLR neurons recorded continuously before and after injection. In contrast, injecting amphetamine into the nucleus accumbens increased the m.f.r. of units from 8.3 +/- 0.7 to 12.8 +/- 1.0 per s and increased the m.f.r. of 11 of 12 MLR neurons recorded continuously before and after injection. These results suggest that the hypothalamic/preoptic area contains muscarinic cholinoceptive areas which reduce locomotor activity by direct or indirect effects on the MLR.

Amphetamine↗

Involvement of neuronal cell bodies of the mesencephalic locomotor region in the initiation of locomotor activity of freely behaving rats.

The locomotor activity of freely-moving rats was increased substantially by injections of L-sodium glutamate or of picrotoxin, a GABA antagonist, into the region of the tegmental pedunculopontine nucleus. The onset of hyper-motility was more rapid with L-glutamate than with picrotoxin and the duration shorter. Locomotor activity from injecting amphetamine unilaterally into the nucleus accumbens was reduced by injections of GABA into the ipsilateral pedunculopontine nucleus. These observations provide additional evidence implicating neurons of the MLR and possibly GABA synaptic inputs to these neurons in locomotor activity and suggest that they may mediate indirect inputs from the nucleus accumbens.

Amphetamine↗

The related roles of dopamine and glutamate in the initiation of 50-kHz ultrasonic calls in adult rats.

Effects of amphetamine on the production of 50-kHz ultrasonic calls were studied. Calls were emitted spontaneously or were induced by an intrahypothalamic-preoptic injection of glutamate. Sonographic analysis of recorded calls revealed that they were within the 35-70-kHz sound frequency range reported for the 50-kHz call type. Systemic amphetamine (AMPH, 2 mg/kg) significantly increased the number of spontaneously emitted 50-kHz calls and the effect of AMPH was dose-dependent. Low dose of intracerebral glutamate (17 microg) had no additive effect on the number of AMPH-induced calls. Higher dose of intracerebral glutamate alone (34 microg) significantly increased the number of 50-kHz calls, which was completely reversed by systemic application of haloperidol (2 mg/kg), a dopamine antagonist. The results suggest that glutamate-induced or spontaneously occurring 50-kHz calls in adult rats are dependent upon dopaminergic transmission. It is postulated that this type of calls may be indicative of dopamine mediated affective state in adult rats.

Aging↗

Decreases in rat locomotor activity as a result of changes in synaptic transmission to neurons within the mesencephalic locomotor region.

The mesencephalic locomotor region is defined as a functional region sending signals to the spinal cord generators of rhythmical limb movements for locomotion. It has been shown that the mesencephalic locomotor region plays a critical role in locomotion initiated from the nucleus accumbens or from the subpallidal region. However, there are conflicting data on whether synaptic input from the nucleus accumbens--subpallidal region to the mesencephalic locomotor region mediates locomotion. The purpose of the study was to determine the role of synaptic input to different subregions of the mesencephalic locomotor region in locomotion induced by injecting dopamine into the nucleus accumbens or by injecting picrotoxin into the subpallidal region in freely behaving rats. Synaptic transmission in the mesencephalic locomotor region was eliminated by excitotoxic lesions or was reversibly interrupted by injecting cobalt chloride, which can block synaptic transmission. Excitotoxic lesions or injections of cobalt into subregions of the mesencephalic locomotor region significantly decreased, although did not completely block, locomotion. The most effective sites for cobalt- and lesion-induced reduction in locomotion were consistent with localization of the mesencephalic locomotor region. Effective sites for cobalt and lesions markedly overlapped but were not identical. The results indicate that synaptic transmission within the mesencephalic locomotor region contributes to dopamine- or picrotoxin-induced locomotion.

Animals↗

Functional interaction of dopamine and glutamate in the nucleus accumbens in the regulation of locomotion.

The interaction of dopamine and glutamate in the nucleus accumbens in the regulation of locomotion was investigated. Microinjection of N-methyl-D-aspartic acid (NMDA, a glutamatergic NMDA receptor agonist) or alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA, a quisqualic receptor agonist which is a glutamatergic non-NMDA receptor agonist) into the nucleus accumbens caused a substantial increase in locomotor activity. This increase in locomotor activity was significantly reduced by prior administration of the dopamine D2 agonist quinpirole, but not the D1 agonist, SKF 38393, into the same brain sites. The reduction in locomotion produced by quinpirole was dose dependent. Eight days after the ventral tegmental area was lesioned with 6-hydroxydopamine to destroy the dopamine projection and the axon terminals of the mesolimbic dopamine neurons in nucleus accumbens, the hyperkinetic effects produced by injections of NMDA and AMPA into the nucleus accumbens were substantially reduced. These results suggested that the glutamate agonist induced locomotion is mediated by dopamine. Thus, it appears that NMDA- or AMPA-induced locomotion is due to the activation of glutamate receptors on the mesolimbic dopamine terminals in the nucleus accumbens which release dopamine and subsequently increase locomotion.

Animals↗