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Biomedical subjects

S K Manchanda

Publications and source records attributed to S K Manchanda.

At least 19 recordsLinked to original sources
PubMed1997

Role of midbrain ventro-lateral tegmental area (VTA) enkephalinergic mechanisms in the facilitation of hypothalamically-induced predatory attack behaviour.

Bipolar concentric electrodes were implanted in five cats in extreme lateral regions of hypothalamus. These sites were electrically stimulated using biphasic square wave pulses at a current strength ranging from 300-800 microA to evoke predatory attack on an anaesthetized but live rat. At lower current strength (300 microA) only alertness with pupillary dilatation was produced. Gradual increase in the current strength led to the recruitment of somatic and affective components and a predatory attack was exhibited at a mean current strength of 700 microA. A scoring system allowed the construction of stimulus response curves, which remained fairly constant when repeated over a period of 3-4 weeks. Bilateral microinjections of delta-alanine methoinine enkephaline (DAME) (500 ng in 0.5 microliter saline) in ventrolateral tegmental area (VTA) elevated the mean threshold current strength for affective components while somatomotor components were totally inhibited. The blocking effect of DAME persisted for 1 hour. Microinjections of naloxone (1 microgram) in similar volumes facilitated the response as indicated by a reduction in threshold current strength for somatomotor and affective components. Microinjections of naloxone (1 microgram) in similar volumes facilitated the response as indicated by a reduction in threshold current strength for somatomotor and affective components. Microinjections of naloxone (1 microgram) also reversed the blocking effect of DAME and the thresholds returned to the control level within 10 min while microinjection of normal saline as control had no effect. The excitatory effects of naloxone and inhibitory effects of DAME were statistically significant at P < 0.01 and P < 0.05 respectively with Wilcoxon's signed rank test. The present study indicates that enkephalinergic as well as opioidergic mechanisms operating at the midbrain (VTA) level are involved in the inhibition of predatory attack as elicited from lateral hypothalamus.

Animals↗
PubMed1997

Role of midbrain ventro-lateral tegmental area (VTA) adrenergic mechanisms in facilitation of hypothalamically-induced predatory attack behaviour.

Bipolar concentric electrodes were implanted in extreme lateral regions of hypothalamus having coordinates (A12.5 mm, L 3.5-3.7 mm, V 3.0-3.7 mm). These sites were electrically stimulated using biphasic square wave pulses (1 ms, 60 Hz) at a current strength ranging from 300-800 microA to evoke predatory attack on an anaesthetized rat. At lower current strengths of 300 microA only altertness with pupillary dilatation was produced. Gradual increase in the current strength led to recruitment of somatic and affective components and a full blown predatory attack on a rat was produced at a mean current strength of 700 microA. A scoring system allowed the construction of stimulus response curve, which remained fairly constant when repeated over a period of 3-4 weeks. In ventrolateral tegmental area (VTA), bilateral microinjections of norepinephrine (NE 10 micrograms in 0.5 microliter saline, pH 7.4) lowered the mean threshold current strength to 100 microA while predatory attack was produced at 500 microA. Clonidine (5 micrograms in 0.5 microliter propylene glycol, pH 7.4) an alpha-2 agonist similarly lowered the mean threshold to 100 microA and predatory attack threshold to 400 microA. The effects of clonidine appeared within 20 min of microinjection and persisted up to 6 hr. Yohimbine, an alpha-2 antagonist (4 micrograms in 0.5 microliter propylene glycol. pH 7.4) when microinjected into the same locus (VTA), completely blocked predatory attack behaviour for 3 days, the peak period of the blocking effects were between 3-8 hr, after microinjection. Isoproterenol (beta agonist), propranolol (beta blocker), prazosin (alpha-1 antagonist) and phenoxybenzamine (alpha antagonist) failed to produce any effect. Normal saline and propylene glycol in similar volumes served as controls. The excitatory effects of NE and clonidine and inhibitory effects of Yohimbine were significant at P < 0.01 and P < 0.05 respectively with Wilcoxon's signed rank test. The present study indicates the involvement of alpha-2 adrenoceptive mechanisms operating at the midbrain (VTA) level in the elicitation of predatory attack from lateral hypothalamus.

Adrenergic alpha-Agonists↗
PubMed1997

Enkephalinergic mechanisms in midbrain (dPAG) in modulation of hypothalamically-induced predatory attack behaviour.

Present study was carried out in nine cats which did not attack the rats spontaneously. Predatory attack on an anaesthetized rat was elicited by electrical stimulation of lateral hypothalamus at a mean current strength of 690 microA. The attack was accompanied by minimal affective display and culminated in neck biting. Microinjections of delta-alanine methionine enkephaline (DAME) in 250 ng dose in dorsal periaqueductal gray completely suppressed the predatory attack. There was a significant increase in the threshold current strength for affective display components while the somatic components were completely inhibited even when the current strength was increased to 1000 microA. Microinjections of naloxone, an opioid antagonist in 1 microgram dose reversed the DAME blocking effect and the thresholds returned to control levels within 10 min of microinjections. Microinjections of naloxone alone in similar dose facilitated the response as indicated by a decrease in threshold current strengths for both affective display and somatomotor components. Control injections of saline in similar volumes (0.5 microliter) failed to produce any change. These findings indicate that hypothalamically induced predatory attack is inhibited by enkephalinergic mechanisms operating at the dPAG level in the midbrain.

Animals↗
PubMed1996

beta-adrenergic modulation of male sexual behavior elicited from the medial preoptic area in rats.

This study was aimed at investigating the role of the adrenergic mechanism in the medial preoptic area (mPOA) in sexual arousal and copulatory performance. Saline, norepinephrine (NE), phenoxybenzamine (PBZ) and propranolol (PROP) were injected into the mPOA in different groups of rats. NE application (3 micrograms) facilitated the male sexual behavior by increasing sexual arousal and copulatory performance. On the other hand, application of PROP and PBZ produced inhibition of male sexual behavior. Effects produced by low doses of PROP were more significant than PBZ. The results, viewed in the light of other available reports, suggest that the mPOA beta-adrenergic mechanism is important in the elaboration of male sexual behavior.

Adrenergic alpha-Agonists↗
PubMed1996

2-buten 4 olide affects feeding behavior of rhesus monkey.

1. Endogenous satiety substance 2-Buten 4 Olide (2-B40- a short chain sugar derivative) effect on feeding behaviour of rhesus monkey was studied. 2. The cannula was implanted in the third ventricle of three, adult, male, rhesus monkeys. 3. Monkeys were conditioned to ingest their daily requirement of food during one hour. 4. Their daily food intake was recorded. 5. Various doses of 2-B40 (1.6, 2.1, 2.7, 4.3, 10.6, 20 and 25 mg)were administered intracerebroventricularly on different days five minutes prior to presentation of food. 6. The effective dose for inducing significant satiety effect was 20.0 mg, while 10.6 mg induced a mild and 25.0 mg a severe effect. 7.However, when administered intraperitoneally 43 mg/kg bw 2-B40 induced satiety effect, but was ineffective in doses of 1.5 to 21.5 mg bw. 8. This study is suggestive of the presence of 2-B40 satiety mechanism in monkeys almost in doses similar to those previously reported for rats.

4-Butyrolactone↗
PubMed1996

Vasopressor responses in autosomal dominant cerebellar ataxia.

Thirteen patients with autosomal dominant cerebellar ataxia were investigated for autonomic functions using standard tests. Patients showed no significant reduction in parasympathetic responses as measured by heart rate response to slow breathing and Valsalva manoeuvre. Measurement of blood pressure response to isometric exercise, cold exposure and 70 degrees head-up tilt showed a significant decrease in sympathetic pressor response.

Adult↗
PubMed1995

Electrical and chemical stimulation of the same hypothalamic loci in relation to agressive behaviour in cats: a comparison study.

Chemitrodes which permit electrical and chemical stimulation of the same hypothalamic loci were implanted in anterior hypothalamic and preoptic regions. These sites were stimulated electrically using biphasic square wave pulse (1 ms, 60 Hz) at a current strength ranging from 150-800 microA to evoke an aggressive response. At lower current strength of 150-200 micro A, defence response, a sort of non-specific response can be elicited from these regions. Increasing the current strength to 400 microA led to the recruitment of affective and somatic components and changed the response pattern either to affective attack or flight. The loci producing affective attack response were localized more laterally and ventrally while the loci producing flight response were located in the dorsomedial regions of the hypothalamus. In this response the animal made a goal-directed attempt to escape through an escape route. Increasing the current strength to 500 microA in the dorsomedial regions changed the flight response to violent flight, which involved vigorous running with unsheathed claws and attacking objects if obstructed. Similar increase in current strength at loci producing affective attack only led to a decrease in the latency of response and made the attack more vigorous. Microinfusion of carbachol in graded doses of 2-15 microgram at all these loci produced a profound affective display. At lower doses of 2 and 5 microgram, only some components of affective display like alertness, pupillary dilation and ear flatness were exhibited. Increasing the dose to 10 micrograms and 15 micrograms led to the recruitment of other affective components like piloerection, salivation, hissing and baring of teeth. Microinfusion of carbachol at all loci producing affective attack on electrical stimulation produced a prononced affective display while microinfusion of carbachol at loci producing flight response led to the development of defence posture. At six loci a typical flight response was obtained while violent flight was never exhibited at any of these sites. Microinfusion of atropine (10 microgram in 1.0 microliter saline) at these loci completely blocked the carbachol induced response. Both somatomotor and affective components were completely inhibited. However, the responses obtained on electrical stimulation were not totally blocked following atropine infusion and some of the somatomotor and affective components could be elicited with higher current strength. These studies indicate the involvement of cholinoceptive mechanisms in the elicitation of hypothalamically induced aggresive behaviour. Microinfustion of hexamethonium bromide, a nicotinic blocker in 50 micrograms doses did not affect the aggressive response.

Aggression↗
PubMed1995

Predatory aggression induced by hypothalamic stimulation: modulation by midbrain periaqueductal gray (PAG).

Adequate electrical stimulation of extreme lateral hypothalamic regions of healthy, non-aggressive male cats was employed to produce aggression on live but anaesthetized rats. Stimulus response (S-R) curves based on scoring systems for both somatic and affective display components of behaviour were used to assess how manipulation of midbrain PAG by electrocoagulative lesions or drug microinjections affected the sensitivity of attack producing hypothalamic loci. Anodal lesions of dorsal PAG and adjoining tectum increased the excitability of hypothalamic loci producing predatory attack. Microinjection of 250 ng of delta-alanine-methionine enkephalin (DAME) in dPAG completely suppressed the somatomotor components of attack behaviour and markedly inhibited the affective display components. Administration of naloxone, an opioid antagonist (1 microgram) at the same sites facilitated the hypothalamically induced attack behaviour and annulled the inhibitory effect of DAME. These findings indicate the involvement of midbrain enkephalinergic mechanisms in the modulation of predatory attack behaviour elaborated by hypothalamic stimulation.

Aggression↗
PubMed1994

Meditation improves clinicoelectroencephalographic measures in drug-resistant epileptics.

Eleven adults suffering from drug-resistant epilepsies were given meditation practice, while another nine adults acted as waiting list controls. All patients were on antiepileptic drugs and their serum drug levels were monitored regularly. Patients in the intervention group were given training in meditation, and they practiced meditation 20 minutes a day for one year. They showed a significant reduction in seizure frequency and duration, an increase in the dominant background EEG frequency, a reduction in mean spectral intensity of the 0.7-7.7 Hz segment, and an increment in mean spectral intensity in the 8-12 Hz segment of the EEG. All changes were statistically significant. Control patients did not show significant changes in seizure frequency and duration during the observation period of one year. The results indicate that continued meditation practice is of substantial help in improving the clinicoelectrographic picture in drug-resistant epileptics.

Adolescent↗
PubMed1994

Sensory modulation of the medial preoptic area neuronal activity by dorsal penile nerve stimulation in rats.

The study was aimed at finding out the influence exerted by the genital afferents on the medial preoptic area (mPOA), which plays a pivotal role in the regulation of male sex behavior. To fulfil this objective, the effects of stimulation of the dorsal penile nerve (DPN) on the activity of 82 mPOA neurons were studied. The base line firing rates of the mPOA neurons, studied by extracellular recording, ranged between 0.5 and 38.5 Hz (mean 7.18 +/- 7.91). The stimulation of the DPN (20 Hz, 0.4 msec. 70 microA) influenced 79.69% of the neurons studied. Though increased firing was the predominant influence produced (50%), decreased firing was also seen in a few (29.69%). The excited and inhibited neurons were randomly distributed within the mPOA. Neurons located in the lateral and posterior hypothalamus were not affected by the DPN stimulation. The stimulation parameters used in this study did not produce any change in the systemic arterial pressure and heart rate. The results provide electrophysiological evidence of afferent inputs from the male sex organ to the mPOA, which is an important area controlling male sex behavior.

Action Potentials↗
PubMed1993

Sleep-inducing function of noradrenergic fibers in the medial preoptic area.

The aim of the investigation was to find out the role of noradrenergic (NE) terminals of the medial preoptic area (mPOA), in the regulation of sleep-wakefulness. Studies were conducted on free-moving adult male rats with chronically implanted cannulae in the mPOA. Sleep-wakefulness was assessed on the basis of EEG, EMG, and EOG recordings along with behavioral observations. Lesioning of catecholamine terminals (with 6-hydroxydopamine) in the mPOA produced an increase in quiet wakefulness. Prevention of NE fiber destruction, by pretreating the rats with imipramine, prevented this effect. This demonstrated that the increased quiet wakefulness produced by 6-OHDA was the result of NE fiber destruction. Changes in sleep-wakefulness were also assessed after microinjection of NE into the mPOA, in normal and ventral noradrenergic bundle (VNA)-lesioned rats. NE administration induced sleep in VNA-lesioned rats, and arousal in normal rats. The findings suggest that the NE terminals in the mPOA, projecting via VNA, play a role in the induction of sleep.

Animals↗
PubMed1993

Midbrain adrenergic mechanism modulating predatory attack behaviour induced by hypothalamic stimulation.

The present study was carried out in ten cats which did not attack the rats spontaneously. Predatory attack on a rat was produced by lateral hypothalamic stimulation using mean current strength of 340-690uA. This attack was accompanied by minimal affective display and culminated in neck biting. It was found that norepinephrine (NE) when microinjected into dorsal periaqueductal gray (dPAG) region in doses of 2, 4 and 10ug significantly lowered the mean current strength required for the elicitation of predatory attack by hypothalamic stimulation. Microinjection of propranolol (Prop), a beta-blocker, within the same region in similar doses significantly blocked the response as indicated by the increase in current strength required to produce the response. Control injections of normal saline and propylene glycol failed to produce any change. These findings indicate that hypothalamically induced aggressive responses involves beta adrenoceptive mechanisms located in the dPAG.

Adrenergic alpha-Agonists↗
PubMed1993

Midbrain adrenergic mechanisms modulating flight behaviour induced by hypothalamic stimulation.

The present study was carried out in ten cats of either sex. Flight response was obtained by electrical stimulation of dorsomedial regions of preoptic area (A13-14.5, L3.5 V-3.5 to -3.7) and lateral hypothalamic regions (A12.5, L2.5-3.5, V-3.7). It consisted of a goal directed attempt to get out of the cage with a vigorous leaping to foot. Norepinephrine when microinjected in 10 micrograms doses into pretectal area of midbrain (A3.5, 3.0, V+1.0 to +1.5 mm) significantly lowered the mean current strength from 640uA to 420uA; clonidine, an alpha-2 agonist in 5 micrograms dose when microinjected into the same locus also significantly lowered the mean current strength to the same level. On the other hand yohimbine, an alpha-2 blocker in 5 micrograms dose when microinjected in to the same locus significantly increased the mean current strength from 640 to 970 uA. These results indicate that hypothalamically induced flight response is mediated via the alpha-2 adrenoceptive mechanism operating at the midbrain level. Control microinjection of normal saline and propylene glycol in similar volumes failed to produce any changes in current strength.

Adrenergic alpha-Agonists↗
PubMed1993

A computer programme for recording male sex behaviour in rats.

An accurate method of recording the frequencies of copulatory events, the latencies of initiation to copulation and the time spent in different behavioural categories is described. A microcomputer (IBM-PC) based data collection system for acquisition and analysis of male rodent sex behaviour has been developed. This software features ease of data entry and operation, using single key presses by assigning a preset code to each. Internal clock of the computer is made to function as a timer for accurate recording of latencies and intervals. A print out of the frequency or duration of data can be obtained either concurrently or after the completion of the experiment, as required. The least count of the technique is about 10(-4) min and this precludes its use for extremely rapidly changing behaviour.

Animals↗
PubMed1991

Ontogeny of phenylalanine (endogenous cholecystokinin) induced modulation of food intake in normal and undernourished rats.

1. The development of endogenous cholecystokinin (CCK) effects on food intake was studied in normal and undernourished growing rats of postnatal day 1-22. 2. Food intake was estimated by recording the gain in body weight before weaning. 3. l-phenylalanine, a potent stimulant of endogenous CCK release, suppressed 30 min food intake in normally nourished pups of day 7-15 or more but not of day 1-6 rats. 4. However, l-phenylalanine did not affect 24 hr gain in body weight day 1-6 or more, rat pups. 5. l-phenylalanine neither suppressed 30 min food intake nor affected 24 hr body weight in day 16-19 or 20-22 undernourished rat pups. 6. The study suggests that the endogenous CCK satiety effects appear early in the second week of postnatal life in normally nourished rats, whereas in undernourished rat pups it does not appear till day 20-22.

Animals↗
PubMed1991

Role of opioid receptors in self-aggression in rats.

Self-aggression is a behavioural disorder in which an individual damages its own body parts by intense biting or scratching. Self aggression has been reported in human patients in Lesch-Nyhan syndrome and in cases of schizophrenia, depression, and congenital analgesia. In human patients as well as in experimental animals some kind of dysesthesia of the part of the body that is mutilated has been suggested. This study was conducted to find out the underlying pain mechanisms in self-aggressive behaviour arising out of stereotypy. The study was performed in 40 adult male rats. In all these animals, self-aggression was produced as part of amphetamine induced stereotyped behaviour. A predetermined scale was used for quantifying this behaviour. Reserpine and phenoxybenzamine pretreatment led to an increase in the incidence of self-aggression. Naloxone administration in reserpine pretreated animals led to a further significant increase in the incidence of self biting as compared to controls. From these studies it appears that self-aggressive behaviour may be associated with increased pain sensation.

Aggression↗
PubMed1990

Coitus induced changes in oviductal motility & effect of progesterone.

Motility of different oviductal segments of conscious rabbits was recorded through permanently implanted sensors using the technique of impedance plethysmography. The implants were around the oviductal wall and therefore did not obstruct its lumen. Pre-ovulatory ampullary motility was always less than the isthmic motility. Coitus induced ovulation produced a characteristic oviductal motility pattern consisting of (i) initial relaxation of both isthmus and ampulla (4-12 h) followed by (ii) increased isthmic motility in the face of a continually relaxed ampulla (36-48 h), and finally phase (iii) leading to restitution of both ampullary and isthmic motility to the base-line at 72-96 h. Estimation of ova positions indicated the presence of fertilized eggs in the ampulla and ampullo-isthmic junction at 48 h and the ova could come to the end of the isthmic segment only at 72 h or after. Increased isthmic motility thus served to counter the transportation of ova and their retention in the ampulla. Rabbits in which oviducts were not taken out for ova positioning achieved normal pregnancy. Administration of progesterone (im, 2.5 mg) produced complete relaxation of both isthmus and ampulla, did not produce increased isthmic contractility on coitus, accelerated the ovum transport rate and inhibited pregnancy, again emphasising the ova retentive role of oviductal motility.

Animals↗