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M B Shaikh

Publications and source records attributed to M B Shaikh.

33 records · Page 2Linked to original sources
PubMed1987

The pathways mediating affective defense and quiet biting attack behavior from the midbrain central gray of the cat: an autoradiographic study.

The purpose of this study was to describe the pathways which mediate feline affective defense and quiet biting attack behavior elicited from the midbrain central gray. In these experiments, methods of [3H]leucine and 2-deoxy-[14C]glucose (2-DG) radioautography were utilized in concert with the technique of electrical and chemical brain stimulation. Affective defense behavior elicited from the midbrain central gray is characterized by marked vocalization such as hissing and growling, pupillary dilatation, urination and piloerection. In contrast, quiet biting attack elicited from the midbrain central gray lacks overt autonomic signs observed with affective defense response as well as the stalking component which is typically associated with stimulation of the lateral hypothalamus. Nevertheless, central gray-elicited attack resulted in a directed bite of the neck of an anesthetized rat in a manner similar to that observed from the hypothalamus. Affective defense was elicited from the dorsal half of the midbrain central gray, while quiet biting attack was obtained following stimulation of the ventral half of the midbrain central gray, thus indicating a functional differentiation of the central gray with respect to these two forms of aggression. In a separate series of experiments, affective defense or quiet biting attack response was identified by electrical stimulation through a cannula electrode situated in the midbrain central gray. The affective defense responses were subsequently elicited following microinjections of D,L-homocysteic acid through the same cannula electrode in order to demonstrate that these responses were the result of direct stimulation of cell bodies within the central gray. Then, one of the following autoradiographic tracing procedures was utilized: (1) [3H]leucine was injected through a cannula electrode and the animal was sacrificed after a 4- to 14-day survival period; or (2) a 2-DG solution was systemically injected and electrical stimulation was applied through the cannula electrode in order to metabolically activate the pathways associated with each of these responses. In general, the pattern of labelled target regions as indicated by 3H-amino acid radioautography was similar to that obtained from the 2-DG autoradiographic analysis. The principal ascending pathway associated with affective defense was traced to the anteromedial hypothalamus and medial thalamus. Concerning descending projections, label was traced into the central tegmental fields of the midbrain and pons, locus coeruleus and motor and main sensory nuclei of the trigeminal complex.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗
PubMed1987

The effects of intrahypothalamic injections of norepinephrine upon affective defense behavior in the cat.

The effects of norepinephrine microinjected into the anterior hypothalamus were examined in feline affective defense behavior elicited by electrical stimulation of the region of the ventromedial nucleus. Anterior hypothalamic sites from which affective defense behavior could also be elicited by electrical stimulation and which are known to receive inputs from both the ventromedial nucleus and brainstem noradrenergic neurons were selected for pharmacological analysis. Intracerebral injections of 250 ng (1 nM) and 500 ng (2 nM) quantities of norepinephrine placed into the anterior hypothalamus resulted in a significant lowering of the attack thresholds. These reductions in response thresholds which were reversed by either pre- or post-treatment with yohimbine, indicate that the noradrenergic system may play an important role in the regulation of affective defense behavior.

Aggression↗
PubMed1986

Effects of experimental temporal lobe seizures upon hypothalamically elicited aggressive behavior in the cat.

An experiment was performed in order to determine the effects of temporal lobe seizures upon hypothalamically elicited aggressive behavior in the cat. Seizures were induced by electrical stimulation of the pyriform cortex or those subnuclei of the amygdala which had previously been shown to modulate aggressive responses at subseizure current levels. The results clearly indicate that a significant modification of affective defense thresholds following seizures was a direct function of the locus of stimulation. Specifically, seizures generated from the pyriform cortex and medial aspects of the amygdala (sites associated with prior facilitation of affective defense as determined by subseizure electrical stimulation) were followed by a reduction in threshold for this response. In contrast, an elevation in affective defense thresholds occurred when seizures were generated from the central or lateral nuclei of the amygdala (sites associated with prior suppression of affective defense as determined by subseizure electrical stimulation). The primary pathway utilized in the facilitation of affective defense appears to involve the stria terminalis, its bed nucleus, and the anterior medial hypothalamus. Preliminary data suggest that seizures generated from the pyriform cortex or amygdala can also modify quiet biting attack behavior, but in a manner opposite to that demonstrated for affective defense.

Aggression↗
PubMed1986

Regulation of feline aggression by the bed nucleus of stria terminalis.

The purpose of this experiment was to study the possible modulatory role of the bed nucleus of stria terminalis (BNST) in the regulation of affective defense and quiet biting attack reactions in the cat. The experimental paradigm employed concurrent electrical stimulation of the hypothalamic attack sites and of the BNST. The results of the present study demonstrate that concurrent electrical stimulation of the BNST can differentially modulate the two different forms of aggressive behavior by facilitating affective defense and by suppressing quiet biting attack.

Aggression↗
PubMed1985

Topographically organized midbrain modulation of predatory and defensive aggression in the cat.

Hypothalamic sites from which quiet biting attack and affective defense were elicited, were concurrently stimulated with others in the midbrain from which modulation of these behaviors was attempted. Stimulation of medial and lateral aspects of the tegmentum differentially modulated quiet biting attack and affective defense behavior. Facilitation of quiet attack and suppression of affective defense resulted from stimulation of the lateral tegmentum, while suppression of quiet attack and facilitation of affective defense followed stimulation of its medial aspect.

Aggression↗
PubMed1985

Differential control of hypothalamically elicited flight behavior by the midbrain periaqueductal gray in the cat.

The purpose of the present study was to determine the role of the midbrain periaqueductal gray (PAG) and thalamic centrum medianum-parafascicular complex (CM-Pf) in the regulation of hypothalamically elicited flight behavior in the cat. The experimental paradigm involved a comparison of the differences in response latencies between single stimulation of the hypothalamus and concurrent stimulation of the hypothalamus and sites in the PAG or the CM-Pf. Dual stimulation of the ventral and dorsal aspects of the PAG resulted in differential modulation of flight behavior. Stimulation of the dorsal PAG suppressed hypothalamically elicited flight behavior while stimulation of the ventral aspects of the PAG facilitated flight behavior. Facilitation of flight behavior was also found from stimulation of ventral portions of the CM-Pf.

Animals↗
PubMed1985

Forebrain structures regulating flight behavior in the cat.

The present study was conducted to determine the role of the bed nucleus of the stria terminalis (BNST) and preoptic region in the regulation of hypothalamically elicited flight behavior in the cat. The general paradigm involved concurrent electrical stimulation of sites in the hypothalamus from which flight responses were elicited and of the BNST or preoptic region from which modulation of flight behavior was attempted. Electrical stimulation of the dorsal and ventral preoptic region modulated flight behavior in opposing ways. Suppression of flight behavior resulted from stimulation of the BNST and ventral aspect of the preoptic region, while facilitation of the behavioral response followed stimulation of the dorsal aspect of the preoptic region.

Animals↗
PubMed1984

An analysis of the mechanisms underlying septal area control of hypothalamically elicited aggression in the cat.

This experiment was performed in order to examine several of the underlying mechanisms by which the septal area and adjacent regions regulate quiet biting attack behavior elicited from electrical stimulation of the hypothalamus in the cat. The results clearly indicate that stimulation of the septal area and anterior cingulate gyrus increased the latency for the occurrence of quiet biting attack behavior. Those sites within the septal area from which inhibition of attack can be produced are linked to sensory mechanisms associated with trigeminal reflexes activated during hypothalamic stimulation. Stimulation of these septal area sites decreased the lateral extent of the 'effective sensory fields' of the lipline established during hypothalamic stimulation, but did not appear to have any affect upon the latency of the hypothalamically elicited jaw-opening response. Deoxyglucose autoradiography revealed that the inhibition resulting from stimulation of the lateral septal area may be due to either the monosynaptic activation of the lateral hypothalamus or the disynaptic activation of this area utilizing a circuit involving the nuclei of the diagonal band of Broca.

Aggression↗
PubMed1984

A [14C]2-deoxyglucose analysis of the functional neural pathways of the limbic forebrain in the rat. IV. A pathway from the prefrontal cortical-medial thalamic system to the hypothalamus.

The present study utilized the [14C]2-deoxyglucose (2-DG) cell labeling procedure to characterize a functional pathway from the prefrontal cortex (Pfc) and mediodorsal thalamic nucleus (MD) to the hypothalamus. Rats were injected with 2-DG prior to a 45 min experimental paradigm consisting of alternating 30 s on-off periods of electrical brain stimulation. Standard procedures were utilized for the removal and processing of brain tissue for X-ray autoradiography. In the first phase of this study, stimulation applied to the prefrontal cortex generally yielded a pattern of 2-DG distribution consistent with the findings of classical anatomical studies. Stimulation of the dorsomedial and ventromedial prefrontal cortex or the infralimbic cortex produced the most effective activation of the diencephalon. This activation was primarily limited to MD, with no involvement of any region of the hypothalamus. In the second phase of this study, brain regions activated following stimulation of sites along the rostro-caudal axis of MD were examined. Stimulation of MD resulted in the activation of the nucleus reuniens and other midline and non-specific thalamic nuclei. Stimulation of this nucleus also activated the ventromedial thalamic nucleus, medial aspects of the nucleus accumbens and the medial and sulcal prefrontal cortices. Again, in each of these cases, labeling within any region of the hypothalamus could not be detected. Since MD stimulation activated the midline thalamus, and the nucleus reuniens in particular, the last phase of this experiment involved stimulation of the nucleus reuniens in order to determine the source of medial thalamic inputs to the hypothalamus. Stimulation of the nucleus reuniens activated fibers which were distributed to both the medial and lateral hypothalamus. In addition, stimulation also activated the descending periventricular system, which could be followed to the level of the midbrain central gray and such limbic structures as the hippocampal formation, septal area, amygdala and prefrontal cortex. These findings indicate that Pfc-MD activation of the hypothalamus is achieved indirectly via interneurons within the nucleus reuniens.

Animals↗
PubMed1984

Differential control of aggression by the midbrain.

Electrical stimulation of the midbrain tegmentum can produce differential modulation of quiet biting attack and affective defense behavior elicited from the hypothalamus of the cat. Stimulation of the lateral half of the tegmentum facilitated quiet biting attack and suppressed affective defense. Conversely, stimulation of the medial tegmentum suppressed quiet biting attack and facilitated affective defense. These results clearly indicate a topographic organization of modulatory sites controlling hypothalamic aggression within the midbrain tegmentum.

Affect↗
PubMedDate not supplied

Opioid peptides within the midbrain periaqueductal gray suppress affective defense behavior in the cat.

The effects of the methionine-enkephalin analog [D-Ala2-Met5]-enkephalinamide (DAME) upon the threshold for affective defense behavior were determined following microinjections placed into midbrain periaqueductal gray sites from which this response was elicited. Affective defense behavior was elicited by electrical stimulation through a cannula electrode situated in the dorsal aspect of the midbrain periaqueductal gray. Dose-response curves characterizing the effects of DAME upon affective defense behavior were determined utilizing the following doses: 0.25, 0.5 and 1.0 microgram in 0.5 microliter saline, pH = 7.4 or vehicle control (saline). Response thresholds were tested 10-30, 30-60, 60-90, 120-150, 180-210, 1440-1470 and 2880-2910 min postinjection. The results obtained indicated that injections of DAME at a dose of 1.0 microgram/0.5 microliter produced significant, long duration elevations in affective defense thresholds, lasting up to 1440-1470 min postinjection. Lower doses of DAME (0.25 and 0.5 microgram/0.5 microliter) also resulted in significant increases in affective defense thresholds, but these effects were of shorter durations (60-90 and 120-150 min) postinjection, respectively. The suppressive effects of DAME were blocked when animals were pretreated with naloxone (10 micrograms/0.5 microliter) microinjected into the same midbrain periaqueductal gray site into which 0.25 microgram DAME was injected and affective defense behavior was elicited.

Affect↗
PubMedDate not supplied

Ethanol enhances medial amygdaloid induced inhibition of predatory attack behaviour in the cat: role of GABAA receptors in the lateral hypothalamus.

The present study tested the hypothesis that the suppressive effects of ethanol upon predatory attack behaviour in the cat involve a pathway from the medial amygdala to the lateral hypothalamus, and that these suppressive effects are mediated by gamma-aminobutyric acid (GABAA) receptors located in the lateral hypothalamus. Cannula electrodes were implanted into the lateral hypothalamus for elicitation of predatory attack behaviour and for microinjections of the GABAA receptor antagonist, bicuculline. Monopolar stimulating electrodes were implanted into the medial amygdala from which subseizure levels of electrical stimulation suppressed predatory attack behaviour. In the first phase of the study, we compared response latencies for predatory attack behaviour following single stimulation of the lateral hypothalamus alone with those following paired trials of dual stimulation of the medial amygdala plus lateral hypothalamus. Dual stimulation significantly suppressed predatory attack. In the second phase of the study, peripheral ethanol administration (in doses of 0.01, 0.5 and 1.0 g/kg, i.p.) enhanced the suppressive effects of medial amygdaloid stimulation in a dose- and time-dependent manner in which peak effects were obtained 60 min post-injection. In the third phase of the study, bicuculline (0.15 nmol) was microinjected into the lateral hypothalamus both prior to and following paired trials of dual stimulation. Drug infusion blocked the suppressive effects of medial amygdaloid stimulation upon predatory attack behaviour elicited from the lateral hypothalamus, indicating the importance of GABAA receptors in mediating this suppression. In the fourth phase of the study, bicuculline, microinjected into the lateral hypothalamus at the time when ethanol's effects were maximal (i.e. 60-80 min post-ethanol administration), totally blocked the suppressive effects of medial amygdaloid stimulation as well as the enhancing effects of ethanol upon medial amygdaloid suppression of this form of aggressive behaviour. In the last phase of the study, bicuculline (0.15 nmol) infusion into the lateral hypothalamus significantly reduced the suppressive effects of ethanol (1.0 g/kg, i.p.) upon predatory attack behaviour elicited from the lateral hypothalamus. These results support the hypothesis that ethanol's suppressive effects upon predatory attack behaviour in the cat are mediated, at least in part, by GABAA receptors in the lateral hypothalamus. The present and recent findings in our laboratory support the view that GABAA receptors in the lateral hypothalamus are activated, in turn, by a GABAergic pathway which arises from the medial hypothalamus whose neurons receive inputs from the medial amygdala.

Amygdala↗