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H Kaba

Publications and source records attributed to H Kaba.

At least 37 records · Page 2Linked to original sources

Influence of dorsal hippocampal stimulation and dorsal fornix lesions on hepatic glucose metabolism in rabbits.

We examined the effects of stimulation of the dorsal hippocampus and lesions of the dorsal fornix on glucose metabolism in liver slices of rabbits. Hippocampal stimulation decreased the 14C transfer rates from 14C-glucose into CO2, ketone bodies, cholesterol ester and free fatty acids, but increased the rates into triglyceride, phospholipids and glycogen. Fornix lesions had various effects on glucose metabolism, and the effects of hippocampal stimulation on glucose metabolism were abolished by fornix lesions. These observations support the hypothesis that the hippocampus is an integral part of the brain regulator system in the hepatic glucose metabolism.

Animals

Influence of microinjection of insulin into the ventromedial hypothalamus on acetate metabolism in rumen epithelium of sheep.

Injections of 50 microU insulin into the ventromedial hypothalamic nuclei (VMH) in intact sheep decreased the rates of 14C transfer from 14C-1-acetate into CO2, glucose, ketone bodies, and increased the rates into triglyceride and phospholipids in rumen epithelium of sheep. Insulin injections into the parietal cortex of intact sheep or into the VMH of sheep with VMH lesions had no effect on the acetate metabolism in rumen epithelium as compared with the control groups which received saline injections into the same brain regions. These results support the view that the VMH serves as an integral part of an insulin-sensitive brain regulatory system in the acetate metabolism of rumen epithelium.

Acetates

Neural basis of olfactory memory in the context of pregnancy block.

In mice, only strange male pheromones block pregnancy; pheromones of the familiar male with which the female has mated have the capacity to block pregnancy but are ineffective with the consort female. Hence, some form of recognition/memory to the stud male is formed at mating. By infusing lignocaine locally into the accessory olfactory bulb and second order olfactory synapses in the medial nucleus of the amygdala, this study localizes changes that occur in the accessory olfactory bulb at mating to be subsequently important in preventing the stud male's pheromones from blocking pregnancy. Further attention is focused on the dendrodendritic synapses between mitral and granule cells in the accessory olfactory bulb. Blockade of the GABA receptors (granule to mitral cell synapse) in the accessory bulb without mating, but in the presence of male pheromones, prevents any male from blocking pregnancy. Conversely inhibition of protein kinase C, a second messenger system activated by excitatory amino acids (mitral to granule cell synapse), in the accessory bulb during a 4-h period after mating permits all male pheromones including the stud's to activate pregnancy block. While blockade of protein kinase C activity during the critical exposure time for memory formation prevents memory formation, infusions of a protein synthesis inhibitor (anisomycin) are without effect. However, protein synthesis inhibition in the accessory olfactory bulb in the late phase of the critical exposure time (3-6 h after mating) does prevent memory formation. These studies show that changes in synaptic plasticity in the accessory olfactory bulb following mating are critical to recognition of the stud male's pheromones, hence preventing these from subsequently blocking pregnancy.

Amygdala

Excitatory influence of the accessory olfactory bulb on tuberoinfundibular arcuate neurons of female mice and its modulation by oestrogen.

The role of the accessory olfactory bulb in conveying pheromonal information to tuberoinfundibular arcuate neurons was examined electrophysiologically in chloral hydrate-anaesthetized, oestrogen (0.5 micrograms in silastic capsules)-treated and untreated ovariectomized Balb/c female mice. Electrical stimulation of the accessory olfactory bulb orthodromically excited part of tuberoinfundibular neurons which were antidromically stimulated from the median eminence and histologically verified as being located within the arcuate nucleus. No inhibitions followed accessory bulb stimulation. The excitatory response to accessory bulb stimulation was reversibly blocked by the local anaesthetic lignocaine infused into the amygdala. The percentage of tuberoinfundibular arcuate neurons responding to accessory bulb stimulation was significantly higher in oestrogen-treated than in untreated animals. There was no difference between the two groups for the antidromic activation threshold, spontaneous firing rate, absolute refractory period or frequency of successful antidromic propagation into the soma of tuberoinfundibular arcuate neurons. In oestrogen-treated preparations, tuberoinfundibular arcuate neurons responsive and unresponsive to accessory bulb stimulation could be distinguished by the frequency of successful antidromic propagation into the soma. These studies demonstrate that olfactory relay neurons in the accessory olfactory bulb act to enhance the activity of a subpopulation of tuberoinfundibular arcuate neurons via the amygdala and that this neural transmission is modulated by oestrogen.

Action Potentials

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

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

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

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

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

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

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

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

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

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

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

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

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

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