Biomedical subjects

H Kaba

Publications and source records attributed to H Kaba.

At least 73 records · Page 4Linked to original sources

PubMed1989

Influence of microinjection of glucagon into the amygdala on hepatic acetate metabolism in rabbits.

Glucagon was injected directly into the medial amygdala (AMYG) of rabbits, and changes in hepatic acetate metabolism were studied. The injection of 3 ng glucagon into the AMYG of intact rabbits increased the rates of 14C transfer from 14C-1-acetate into CO2, glucose, ketone bodies, cholesterol ester, free fatty acids and phospholipids but decreased those of 14C transfer into triglyceride. However, the glucagon injection into the AMYG of rabbits with lesions of stria terminals or into the parietal cortex of intact rabbits had no effects on the hepatic acetate metabolism. These observations support the hypothesis that the AMYG is a part of the glucagon-sensitive brain regulator system in the hepatic acetate metabolism.

Acetates↗

PubMed1989

Influence of electrical stimulation of the limbic structure on adrenocortical steroidogenesis in hypophysectomized rats.

The effects of electrical stimulation of the medial amygdala (AMYG) and dorsal hippocampus (DHPC) on the rates of 14C transfer from 14C-1-acetate into adrenocortical steroids in adrenal slices of hypophysectomized rats were investigated. The 14C transfer rates into corticosterone were increased by stimulation of the AMYG and DHPC. The 14C transfer rates into cortisol were increased by the AMYG stimulation but were not altered by the DHPC stimulation. From these results, it might be suggested that these limbic structures were involved in the regulation of adrenocortical steroidogenesis without participation of the pituitary.

Adrenal Cortex Hormones↗

PubMed1988

The effect of microinfusions of drugs into the accessory olfactory bulb on the olfactory block to pregnancy.

Female mice which have mated and are subsequently exposed to the odour (pheromones) of a strange male undergo hormonal changes resulting in a block to their pregnancy. The fact that the stud male's odours can also block pregnancies, that is other than his own, implies the formation of a memory or some form of recognition process by the female for this male's pheromones at the time of mating. The purpose of this study was to evaluate the effect of microinfusions of drugs which interfere with neural transmission, into the accessory olfactory bulbs. This was carried out immediately after mating over a 4-h period during which the "memory" to the stud male's pheromones is formed. Infusions of the alpha-blocker, phentolamine, blocked the formation of the olfactory memory, while the GABA receptor blocker, bicuculline, itself blocked pregnancy, but was without effect on memory formation. Protein synthesis inhibition or calpain inactivation in the accessory bulb was without effect on memory formation at any of the doses used. These studies demonstrate that GABAergic transmitter blockade in the accessory olfactory bulb at the time of mating can prevent subsequent blastocyst implantation some 3 days later, while alpha-noradrenergic blockade can prevent the formation of an olfactory memory to the stud male.

Animals↗

PubMed1988

Hormonal enhancement of neurogenesis and its relationship to the duration of olfactory memory.

On mating with a stud male, virgin female mice from an olfactory memory to this male which is essential to their reproductive success. Failure to form this memory results in the stud male being treated as strange, and hence, his pheromones block pregnancy. This study investigates the duration of the olfactory memory, and the factors which determine this. The results show that a single prolonged exposure to the male during mating forms a life-long olfactory memory trace unless pregnancy ensues. In the event of pregnancy the olfactory memory fades significantly faster, an effect which can be replicated by implants of oestradiol in non-pregnant females. Anatomical studies indicate that neurogenesis of the vomeronasal receptors is enhanced during pregnancy, an event which we interpret as being important for the duration of this olfactory memory.

Animals↗

PubMed1988

Response of medial preoptic/anterior hypothalamic neurones to ventrolateral medulla stimulation and its attenuation by adrenoceptor antagonists.

Extracellular single-unit recordings were made from medial preoptic/anterior hypothalamic (MPOAH) neurones in urethane-anaesthetized female rats, and the responses of these neurones to electrical stimulation of the ventrolateral medulla (VLM) were investigated. Of 189 neurones tested, 20% were excited and 21% were inhibited following VLM stimulation. The latency of inhibitory responses showed a normal distribution and the mean latency was 47 ms, whereas the latency of excitatory responses showed a bimodal distribution with peaks in the ranges of 0-10 ms and 40-50 ms, respectively. Excitatory responses with latencies greater than 15 ms and inhibitory responses were significantly attenuated by intravenous injections of the alpha-adrenoceptor antagonist phenoxybenzamine but not the beta-adrenoceptor antagonist propranolol. In the light of these observations and the known anatomical and electrophysiological findings, it is suggested that A1 noradrenergic and/or C1 adrenergic inputs from the VLM to MPOAH neurones are, at least in part, mediated by alpha-adrenoceptors.

Animals↗

PubMed1988

Influence of microinjection of corticosterone into hippocampus on hepatic acetate metabolism in rabbits.

Corticosterone was injected directly into the hippocampus of rabbits, and changes in hepatic acetate metabolism were studied. The microinjection of corticosterone with seasame oil into hippocampus decreased the rates of 14C transfer from 14C-1-acetate into CO2 and free cholesterol, and increased 14C transfer into glucose, ketone bodies, triglyceride, free fatty acids and phospholipids. But after microinjection of corticosterone into the hippocampus of rabbits with lesions of dorsal fornix, hepatic acetate metabolism did not differ from that of control rabbits, which received injection of seasame oil into the same brain region. From these results it might be suggested that the hippocampus is a part of corticosterone-sensitive brain regulator system in the hepatic acetate metabolism.

Acetates↗

PubMed1988

Influence of electrical stimulation of the limbic structure on ovarian steroidogenesis in hypophysectomized and adrenalectomized rats.

The effects of electrical stimulation of the medial amygdala (AMYG) and dorsal hippocampus (DHPC) on the rates of 14C transfer from 14C-1-acetate into ovarian steroids in hypophysectomized and adrenalectomized rats (H-A rats) were investigated. The 14C transfer rates into estrogen were increased by stimulation of AMYG and DHPC. The 14C transfer rates into progesterone and 20 alpha-hydroxy-pregn-4-en-3-one (20 alpha-OH-P) were increased by the AMYG stimulation but decreased by the DHPC stimulation. From these results, it might be suggested that these limbic structures were involved in the regulation of ovarian steroidogenesis without participation of pituitary and adrenal.

17-alpha-Hydroxypregnenolone↗

PubMed1988

Influence of microinjection of corticosterone into ventromedial hypothalamus on hepatic acetate metabolism in rabbits.

Corticosterone was injected into the ventromedial hypothalamus (VMH) of rabbits, and changes in hepatic acetate metabolism were studied. The microinjection of corticosterone with seasame oil into the VMH of intact rabbits increased the rates of 14C transfer from 14C-1-acetate into CO2, glucose, ketone bodies, triglyceride, free cholesterol, free fatty acids and phospholipids but decreased those of 14C transfer into cholesterol ester. However, corticosterone injected into the VMH of rabbits with VMH lesions or the parietal cortex of intact rabbits was without effect on the hepatic acetate metabolism. From these results it might be suggested that the VMH is an integral part of the corticosterone-sensitive brain regulator system in the hepatic acetate metabolism.

Acetates↗

PubMed1988

Electrophysiology of neurones projections from the rat A1 noradrenergic region to the medial preoptic/anterior hypothalamic area: lack of effect of the oestrous cycle on their excitability.

The neuronal excitability of presumed A1 noradrenergic neurones in the ventrolateral medulla (VLM) which directly project to the medial preoptic/anterior hypothalamic area was analysed in pro-oestrous and metoestrous female rats under urethane anaesthesia. No significant difference was detected between the two groups for the antidromic activation threshold, absolute refractory period, frequency of successful antidromic propagation into the somatodendritic membrane, duration of post-stimulus inhibition, or spontaneous firing rate of these neurones. These results do not support the idea that the neuronal somata of A1 noradrenergic neurones in the VLM show a pro-oestrous increase in excitability during the oestrous cycle, although limitations of the methodology employed do not completely rule out this possibility.

Animals↗

PubMed1987

Subfornical organ and hypothalamic paraventricular nucleus connections with median preoptic nucleus neurons: an electrophysiological study in the rat.

The role of pathways from the subfornical organ (SFO) to the hypothalamic paraventricular nucleus (PVN) through the median preoptic nucleus (MnPO) in regulating the activity of putative vasopressin (VP)-secreting neurons in the PVN was examined in urethane-anesthetized male rats. The activity of the majority (79%) of SFO neurons antidromically identified as projecting to the MnPO was excited by microiontophoretically (MIPh) applied angiotensin II (ANG II) and the effect was blocked by MIPh-applied saralasin (Sar), an ANG II antagonist. Identified SFO neurons that were excited by MIPh-applied ANG II were also excited by intravenously administered ANG II. Electrical stimulation of the SFO produced orthodromic excitation (48%) or inhibition (24%) of the activity of MnPO neurons antidromically identified as projecting to the PVN. Identified MnPO neurons that were excited by SFO stimulation were also excited by MIPh-applied ANG II, while the remaining neurons were not affected. The excitatory responses to SFO stimulation and to MIPh-applied ANG II were both blocked by MIPh-applied Sar, whereas the inhibitory responses to SFO stimulation were not affected. ANG II injected into the region of the SFO produced either an excitation (55%) or no effect (45%) on the activity of identified MnPO neurons. Electrical stimulation of the MnPO produced orthodromic excitation (27%) or inhibition (23%) of the activity of putative VP-secreting PVN neurons. ANG II injected into the region of the MnPO produced either an excitation (31%) or no effect (69%) on the activity of putative VP-secreting PVN neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

PubMed1987

The A1 noradrenergic region enhances the responsivity of hypothalamic paraventricular neurohypophyseal neurons to inputs from the subfornical organ in the rat.

The action of the A1 noradrenergic neurons of the ventrolateral medulla on the responsiveness of neurohypophyseal neurons in the rat hypothalamic paraventricular nucleus (PVN) to inputs from the subfornical organ (SFO) was examined in antidromically identified PVN neurons that respond to electrical stimulation of both the SFO and A1 region. In both putative vasopressin (VP)-and oxytocin (OXY)-secreting PVN neurons that were classified according to their spontaneous firing patterns and their responsivity to baroreceptor activation, prior stimulation of the A1 region did not affect the short latency brief duration excitatory response induced by SFO stimulation. Simultaneous stimulation of the A1 region significantly enhanced the long latency prolonged excitatory response induced by SFO stimulation and the enhancement was blocked by microiontophoretically applied phentolamine, and alpha-adrenoceptor antagonist, but not by timolol, a beta-adrenoceptor antagonist. Simultaneous stimulation of the A1 region also significantly enhanced the inhibitory response induced by SFO stimulation and the enhancement was blocked by microiontophoretically applied timolol, but not by phentolamine. These results suggest that the A1 region may act to enhance the partial excitatory (via an alpha-adrenoceptor mechanism) and inhibitory SFO inputs (via a beta-adrenoceptor mechanism) to the PVN neurohypophyseal neurons as a modulatory action.

Animals↗

PubMed1987

Lateral hypothalamic region excites the activity of vasopressin neurons in the supraoptic nucleus through subfornical organ neurons.

In urethane-anesthetized male rats, microinjection of angiotensin II into the lateral hypothalamic area excited the activity of about half (N = 7) of subfornical organ neurons (N = 15) antidromically identified as projecting to the hypothalamic supraoptic nucleus. Microinjection of angiotensin II also excited the activity of approximately one-quarter (N = 8) of putative vasopressin-secreting neurons (N = 28) in the hypothalamic supraoptic nucleus and these excitatory responses of putative vasopressin-secreting neurons were blocked (N = 3) or attenuated (N = 3) by pretreatment with the angiotensin II antagonist saralasin, but not by isotonic saline (N = 2), in the subfornical organ.

Action Potentials↗

PubMed1987

Subfornical organ neurons act to enhance the activity of paraventricular vasopressin neurons in response to intravenous angiotensin II.

The effects of pretreatment of the angiotensin II (ANGII) antagonist, saralasin (Sar), in the subfornical organ (SFO) on intravenous ANGII-induced responses of the activity of phasically firing paraventricular nucleus (PVN) neurons (n = 23) antidromically identified as projecting to the posterior pituitary were examined in urethane-anesthetized rats. The activity of the majority (n = 18) of identified PVN neurons was excited by intravenously administered ANGII, whereas the remaining neurons (n = 5) were not affected. The excitatory responses (n = 13) to ANGII were prevented by pretreatment with Sar, but not by isotonic saline (n = 3), in the SFO. These results suggest that ANGII-sensitive SFO neurons may act to enhance the excitability of putative vasopressin (VP)-secreting neurons in the PVN in response to circulating ANGII.

Action Potentials↗

PubMed1987

Influence of microinjection of glucagon into ventromedial hypothalamus on acetate metabolism in liver slices of rabbit.

Glucagon was injected directly into the ventromedial hypothalamic nuclei (VMH) of rabbits, and changes in hepatic acetate metabolism were studied. The injection of 3 ng glucagon into the VMH of intact rabbits increased the rates of 14C transfer from 14C-1-acetate into CO2, glucose and ketone bodies but decreased those into cholesterol ester, triglyceride, free cholesterol, free fatty acids and phospholipids. However, after glucagon injection into the VMH of rabbits with VMH lesions and the parietal cortex of intact rabbits, hepatic acetate metabolism did not differ from that of the control rabbits, which received saline injection into the same brain regions. These observations support the hypothesis that the VMH are parts of a glucagon-sensitive brain regulator system in the hepatic acetate metabolism.

Acetates↗

PubMed1987

Influence of electrical stimulation of the limbic structure on glucagon level in rabbit's plasma.

Amygdala (AMYG) stimulation caused marked increase in the circulating level of glucagon and these stimulatory effects were abolished by lesions of stria terminalis (ST). Stimulation of dorsal hippocampus (DHPC), on the other hand, greatly decreased the glucagon level and lesions of dorsal fornix (DFX) abolished these stimulatory effects. These results suggested that the reciprocal influence of AMYG and DHPC on plasma level of glucagon played some role in the regulation of glucagon release and these limbic structure had hypothalamic-mediated effects on glucagon release.

Amygdala↗

PubMed1986

Lateral hypothalamic area stimulation excites neurons in the region of the subfornical organ with efferent projections to the hypothalamic paraventricular nucleus in the rat.

Fifteen neurons in the region of the subfornical organ (SFO) were antidromically activated by electrical stimulation of the paraventricular nucleus (PVN) in the rat. Electrical stimulation of the lateral hypothalamic area (LHA) excited the activity of 9 of the identified units, but did not affect the remaining units. The excitatory response of the identified units was blocked by microiontophoretically (MIPh) applied saralasin (Sar), an angiotensin II (ANGII) antagonist, but not by atropine (Atr), a muscarinic antagonist. These results suggest that the LHA has an excitatory influence on the activity of neurons in the region of the SFO with efferent projections to the PVN and that the influence may be mediated by ANGII receptors.

Angiotensin II↗

PubMed1986

Experimental study on the relationship between cardiac arrhythmias and sleep states by ambulatory ECG-EEC monitoring.

The relationship between cardiac arrhythmias and sleep states was investigated in rats using the ambulatory ECG-EEG monitoring system under the 14/10 light-dark illumination schedule. Records of 14 rats obtained over 94 days were analyzed. Bradyarrhythmias (SA block and AV block) and ventricular arrhythmias [ventricular premature contraction (VPC) and short run of VPCs (ventricular tachycardia, VT)] were observed. Average number of episodes of bradyarrhythmia per day was 7.5, and the ratio of SA block to AV block was 34.9% to 65.1%. Average VPC or VT occurrence per day was 0.9 or 0.1 times, respectively. Sleep states were divided into alertness, slow-wave sleep, and paradoxical sleep, and the relationship between sleep states and arrhythmias was investigated. Bradyarrhythmias appeared predominantly during paradoxical sleep, while ventricular arrhythmias appeared during alertness as well as paradoxical sleep. Bradyarrhythmic episodes decreased by right or left vagotomy 78% or 70%, respectively. Sinus bradyarrhythmias disappeared almost completely by the right vagotomy, while the occurrence of AV block decreased by the right or left vagotomy. Circadian rhythms in arrhythmias were also analyzed by the cosine-fitting technique, and significant circadian rhythms were demonstrated in both bradyarrhythmias and ventricular arrhythmias. Acrophases were 9:56 A.M. and 1:47 A.M., respectively. Occurrence of VT was rare, but the most frequent incidental time zone was immediately following transition from light effects (rest) to dark (activity). This knowledge of circadian rhythm effects in arrhythmias must be incorporated into improved treatment of arrhythmias.

Animals↗

PubMed1986

Efferent pathways from the region of the subfornical organ to hypothalamic paraventricular nucleus: an electrophysiological study in the rat.

Twenty-three neurons in the region of the subfornical organ (SFO) were antidromically activated by electrical stimulation of the hypothalamic paraventricular nucleus (PVN) in male rats under urethane anesthesia. Microiontophoretically (MIPh) applied angiotensin II (AII) excited the activity of all units in the region of the SFO and the effect of AII was blocked by MIPh applied saralasin (Sar), an AII antagonist, but not by atropine (Atr), a muscarinic antagonist. In these units, 12 were also excited by MIPh applied acetylcholine (ACh) while 11 were not affected and the effect of ACh was attenuated by not only MIPh applied Atr, but also Sar, suggesting that not only neurons specific for AII, but also neurons sensitive to both AII and ACh project to the PVN in the region of the SFO. Intravenously administered AII excited the activity of both types of units in the region of the SFO. Microinjected AII or ACh into the region of the SFO excited the activity of putative vasopressin (VP)-secreting units in the PVN. These results suggest that neurons projecting to the PVN in the region of the SFO may act to enhance the activity of putative VP-secreting neurons in the PVN in response to circulating AII.

Acetylcholine↗