Biomedical subjects

W W Blessing

Publications and source records attributed to W W Blessing.

At least 73 records · Page 4Linked to original sources

PubMed1993

Galanin-containing fibers innervate substance P-containing neurons in the pedunculopontine tegmental nucleus in humans.

Galanin is a putative peptide transmitter distributed widely in the central nervous system. Galanin shows potent inhibitory effects on neuronal activity and learning behaviors induced or mediated by acetylcholine. Here, we demonstrate that in humans there are abundant galanin-containing fibers in the pedunculopontine tegmental nucleus, the lateral dorsal tegmental nucleus and the oral pontine reticular nucleus. These neurons contain both acetylcholine and substance P (SP). Using a double-immunostaining method, we show that galanin-containing terminals from pericellular baskets around many SP-positive neurons in these nuclei. Our results suggest galanin may influence brain functions via inputs to the ascending mesopontine acetylcholine-containing nuclei.

Aged↗

PubMed1993

Abdominal vagal afferents excite A1 area neurons antidromically activated from the region of the supraoptic nucleus in the rabbit.

We made extracellular recordings from 113 spontaneously active neurons in the A1 area, after identifying the cells by antidromically activating them from the region of the supraoptic nucleus in urethane-anesthetized rabbits. We tested the response of these neurons to inputs from abdominal vagal, renal and somatic nerves. Electrical stimulation of the abdominal vagus nerve activated 64/85 neurons tested (75%), and had no effect on the remaining 25%. Latency was 195 +/- 25 ms, (conduction velocity 0.7 m/s). Stimulation of renal afferents had no effect on the discharge rate of 4 neurons tested. Stimulation of branches of the sciatic nerve inhibited 7/17 A1 area neurons tested, excited 4 and had no effect on 6 neurons. Stimulation of the central ear nerve inhibited 4/17 neurons tested, excited 6 and had no effect on 7 neurons. Gastric distension had no effect on 20/24 neurons tested. Lightly touching the animals back and legs had no effect on the discharge of 45/49 neurons tested. Similarly, painful stimuli failed to affect 44/49 neurons tested. Our results indicate that A1 area neurons, with projections to the region of the supraoptic nucleus, receive excitatory inputs from the abdominal vagus nerve. The visceral information transmitted to A1 cells by these abdominal vagal afferents is not yet determined, but acute gastric distention does not appear to be a physiological stimulus. A1 area neurons seem not to be involved in transmitting somatic information to the hypothalamus.

Abdomen↗

PubMed1993

Loss of C1 and C3 epinephrine-synthesizing neurons in the medulla oblongata in Parkinson's disease.

We used immunohistochemical analysis to determine whether medulla oblongata neurons containing phenylethanolamine N-methyltransferase (PNMT) are affected in patients who died with idiopathic Parkinson's disease (n = 7) compared with age-matched control subjects who died with nonneurological diseases (n = 8). Transverse sections (50 microns) of medulla were prepared either for conventional neuropathological examination or for the immunohistochemical demonstration of PNMT. Immunopositive neurons at approximately 30 rostrocaudal levels, evenly spaced throughout the whole medulla, were mapped and cells in each section were counted with a camera lucida system linked to a computer. In the ventrolateral medulla, from the level of the obex to 11 mm rostral to the obex where the C1 group of neurons is located, there were 7,631 +/- 844 PNMT-positive neurons in control brains and 3,604 +/- 1,051 in brains affected by Parkinson's disease (47% of control). Many PNMT-positive neurons contained Lewy bodies. We observed a previously undescribed midline (C3) group of PNMT-positive neurons in normal brains, and this group was also severely affected (12% of control) in parkinsonian brains. Neither the C2 group nor the small PNMT-positive neurons in the nucleus tractus solitarii were significantly reduced in numbers but there was a reduction in the numbers of melanin-pigmented cells in both the ventrolateral (50% of control) and the dorsomedial (79% of control) region. Our results demonstrate a selective loss of C1 and C3 PNMT-positive neurons, providing the first quantitative evidence for damage to these presumed brainstem sympathetic premotor neurons in Parkinson's disease. These changes may underlie some of the autonomic symptoms occurring in this condition.

Aged↗

PubMed1993

Blockade of excitatory amino acid receptors in the ventrolateral medulla does not abolish the cardiovascular actions of L-glutamate.

Injection of L-glutamate into the caudal ventrolateral medulla reduces arterial pressure while injection of L-glutamate into the rostral ventrolateral medulla increases arterial pressure. The present experiments were undertaken to determine whether blockade of excitatory amino acid receptor subtypes in the ventrolateral medulla affects the excitatory action of L-glutamate. In the rabbit and rat caudal ventrolateral medulla, injection of either DL-2-amino-5-phosphonovaleric acid (APV), an N-methyl-D-aspartic acid (NMDA) antagonist, or 6,7-dinitroquinoxaline-2,3-dione (DNQX), an alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptor antagonist, increased arterial pressure. Conversely, in the rostral ventrolateral medulla these agents decreased arterial pressure. In the rabbit caudal ventrolateral medulla, injection of APV totally blocked the depressor response to NMDA, and injection of DNQX totally blocked the depressor response to either kainic acid or AMPA. Injection of both APV and DNQX abolished the effects of NMDA, kainic acid and AMPA. However caudal ventrolateral medulla injection of either APV or DNQX, or combined injection of both antagonists, did not affect the relationship between the dose of L-glutamate and the fall in arterial pressure. Similarly, in the rat, combined excitatory amino acid receptor blockade failed to reduce the depressor effect of injected L-glutamate to the caudal ventrolateral medulla. The pressor effect of L-glutamate in the rabbit rostral ventrolateral medulla, when expressed as percentage of baseline level, was unchanged by combined excitatory amino acid receptor blockade.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Amino-5-phosphonovalerate↗

PubMed1993

Transneuronal labelling of neurons in rabbit brain after injection of herpes simplex virus type 1 into the renal nerve.

We mapped the distribution of virus-labelled neurons in the brain after injection of Herpes simplex virus type 1 (HSV1) into the rabbit renal nerve. Seven days after injection, labelled neurons were observed in four brain regions, the rostral ventrolateral medulla (47 +/- 3% of neurons), the A5 area of the lower pons (38 +/- 4%), the caudal raphe nuclei and the parapyramidal area of the medulla (13 +/- 2%), and the paraventricular nucleus of the hypothalamus (1 +/- 1%). In the rostral ventrolateral medulla approximately one half of the HSV1-labelled neurons also contained tyrosine hydroxylase, characterizing them as C1 neurons. In the A5 area virtually all HSV1-labelled neurons also contained tyrosine hydroxylase. In the raphe nuclei and the parapyramidal area 47% of HSV1-positive neurons contained serotonin. The distribution of labelled neurons was similar to that observed after injection of HSV1 into the adrenal gland.

Adrenal Glands↗

PubMed1993

Renal sympathetic preganglionic neurons demonstrated by herpes simplex virus transneuronal labelling in the rabbit: close apposition of neuropeptide Y-immunoreactive terminals.

Renal sympathetic preganglionic neurons in the spinal cord of rabbits were transneuronally retrogradely labelled by injection of Herpes simplex virus type 1 into the renal nerve and immunohistochemical demonstration of viral antigen. The morphology of the labelled neurons was examined, particularly with respect to the shape and extent of their dendritic trees. Double-labelling immunohistochemical studies were performed to determine the relationship of neuropeptide Y-immunoreactive axons to virus-labelled perikarya and dendrites. The shape of the renal sympathetic preganglionic neurons differed according to whether the neurons were located in the intermediolateral cell column or in other sympathetic areas. The neurons in the intermediolateral cell column had very long dendrites, extending in the rostrocaudal and mediolateral directions. The medially oriented processes extended towards and beyond the central canal. The laterally oriented dendritic processes projected within the dorsolateral funiculus, towards the edge of the spinal cord. Neuropeptide Y-immunoreactive fibres were concentrated in regions containing renal sympathetic preganglionic neurons of the spinal segments examined (T7-L2). Immunoreactive varicose terminals were closely opposed to individual preganglionic neurons, especially to the dendritic processes of these neurons. Our findings indicate that neurotransmitter candidates such as neuropeptide Y are likely to influence renal preganglionic neurons by an input to dendritic processes at some distance from the perikarya. Electrophysiological and other functional studies utilizing applications of neurotransmitter candidates onto these neurons should take this into account.

Animals↗

PubMed1992

Effect of nucleus tractus solitarius lesions on cardiovascular responses elicited from the caudal ventrolateral medulla.

Neurons in the caudal ventrolateral medulla (CVLM) which inhibit sympathetic vasomotor tone may have reciprocal connections with the nucleus tractus solitarius (nTS). This study determined whether changes in arterial pressure elicited by chemical excitation or inhibition of neurons in the vasodepressor region of the rabbit CVLM depend on the integrity of the nTS. Unilateral injections of L-glutamate (10 pmol to 100 nmol), or bilateral injections of GABA (1 nmol to 125 nmol), were made into the CVLM, and dose-response effects on arterial pressure determined. The nTS was then bilaterally cauterized, or inhibited by local injections of muscimol, and the dose-response curves were repeated. Neither cauterization nor injection of muscimol significantly altered the slope of the log dose-response curves for L-glutamate, but nTS muscimol increased the fall in arterial pressure for each dose of L-glutamate (P less than 0.01). Cauterization of the nTS significantly (P less than 0.01) increased the slope of the curve relating dose of GABA to rise in arterial pressure observed, after injection of GABA into the CVLM. This increase in slope was similar to the increase observed when GABA is injected into the CVLM in baroreceptor-denervated rabbits. We conclude that neither the depressor nor the pressor response evoked by stimulation or inhibition of the CVLM is dependent on the integrity of the nTS. Inactivation of the nTS tends to increase the magnitude of the CVLM responses, possibly by removal of baroreceptor-mediated buffering of the responses.

Animals↗

PubMed1992

Characteristics of caudal ventrolateral medullary neurons antidromically activated from rostral ventrolateral medulla in the rabbit.

We made extracellular recordings from 107 spontaneously active neurons in the caudal ventrolateral medulla, after identifying the cells by antidromically activating them from the rostral ventrolateral medulla, in urethane-anesthetized rabbits. We tested the response of these neurons to inputs from baroreceptors and chemoreceptors. The median conduction velocity for antidromically activated neurons was 0.84 m/s. Raising blood pressure with intravenous noradrenaline excited 22% of 96 neurons tested, inhibited 61%, and had no effect on the remaining 17%. The spontaneous discharge rate of neurons excited by an increase in blood pressure was 1.6 +/- 0.3 spikes/s, lower than the discharge rate of neurons inhibited by this procedure (4.9 +/- 0.5 spikes/s). Excitation of chemoreceptors by hypoxia increased the discharge rate of 14/16 neurons tested in the group excited by baroreceptor inputs. In the group inhibited by baroreceptor inputs 21/35 neurons tested were excited and 12/35 neurons were inhibited by chemoreceptor inputs. Neurons excited by an increase in blood pressure were located in the previously defined caudal vasodepressor region and in a region just rostral to the obex, intermediate between the vasodepressor region and the rostral sympathoexcitatory region. These neurons may form part of the central inhibitory link in the baroreceptor-vasomotor pathway. Other antidromically activated neurons in the vasodepressor region may be inhibitory vasomotor cells with a function relatively independent of baroreceptor inputs, or they may be A1 catecholamine neurons, with axons passing through the rostral medulla en route to the forebrain.

Animals↗

PubMed1992

Projections from rabbit caudal medulla to C1 and A5 sympathetic premotor neurons, demonstrated with phaseolus leucoagglutinin and herpes simplex virus.

We combined Phaseolus vulgaris leucoagglutinin anterograde tracing and Herpes simplex virus transneuronal retrograde tracing to determine whether neurons in the vasodepressor region of the rabbit caudal ventrolateral medulla project to brainstem neurons containing the virus after its transneuronal transport from the adrenal medulla. Five days after adrenal injection of virus, 764 +/- 159 virus-positive neurons were found bilaterally in the brainstem: 61% in the C1 sympathoexcitatory region of the rostral ventrolateral medulla, 30% in the A5 region, 5% in the parapyramidal region, and 3% in the paraventricular nucleus of the hypothalamus. Many of the virus-positive neurons in the C1 and A5 areas also contained tyrosine hydroxylase and, in the parapyramidal area, many contained 5-hydroxytryptamine. After iontophoretic deposit of leucoagglutinin into the vasodepressor region of the caudal ventrolateral medulla, brain regions containing varicose processes labeled with leucoagglutinin included the regions containing virus-positive neurons. We examined the C1 and A5 regions following injections of both tracers in the same rabbits, leucoagglutinin into the caudal ventrolateral medulla and virus into the adrenal gland. Varicosities containing leucoagglutinin were seen in contiguity with perikarya and dendritic branches of neurons containing HSV1, in both the C1 and A5 regions. Studies also revealed labeled varicosities in contiguity with TH-containing C1 and A5 neurons. The projection from the caudal medulla to presumed sympathetic premotor neurons in the C1 area, including some C1 cells, represents a potential pathway whereby activity of neurons in the caudal medulla could reduce blood pressure by inhibiting sympathoexcitatory neurons in the rostral medulla.

Adrenal Medulla↗

PubMed1992

Renal and adrenal sympathetic preganglionic neurons in rabbit spinal cord: tracing with herpes simplex virus.

We mapped sympathetic renal preganglionic neurons in the rabbit spinal cord using Herpes simplex virus retrograde transneuronal tracing after application of the virus to the renal nerve. Virus-positive neurons were found in the spinal cord from T7 to L2, principally in the ipsilateral intermediolateral cell column. Renal and adrenal preganglionic neurons are largely separate populations. Extensive nonspecific spread of virus from infected cells to neighboring neurons does not appear to occur.

Adrenal Glands↗

PubMed1992

Medullary pathways for adrenocorticotropic hormone and vasopressin secretion in rabbits.

We determined, in urethan-anesthetized rabbits, whether pharmacological alteration of neuronal function in the ventrolateral medulla oblongata, including the A1 area, and in the nucleus tractus solitarii (NTS), alters plasma adrenocorticotropic hormone (ACTH) and vasopressin and whether inhibition of neuronal function in the ventrolateral medulla impairs the secretion of ACTH normally observed in response to hemorrhage or constriction of the inferior vena cava. We also tested whether the increase in plasma ACTH and vasopressin after pharmacological inhibition of neuronal function in the NTS is dependent on a pathway that synapses in the A1 area of the ventrolateral medulla. Activation of the A1 area with bicuculline increased both ACTH and vasopressin. Inhibition of the NTS with muscimol increased levels of both hormones, as did hemorrhage and constriction of the inferior vena cava. Inhibition of neuronal function within the A1 area with muscimol eliminated the secretion of vasopressin but did not significantly alter the secretion of ACTH, obtained by injecting muscimol into the NTS. Injection of muscimol into the A1 area eliminated the secretion of both ACTH and vasopressin in response to constriction of the inferior vena cava and, in the case of vasopressin, in response to hemorrhage. Although hemorrhage-initiated secretion of ACTH was significantly reduced by injection of muscimol into the A1 area, it was not completely eliminated by these injections or by injections of muscimol into a more rostrocaudally extensive region of the medulla oblongata. We conclude that the net output from the NTS tonically inhibits secretion of both ACTH and vasopressin, reflecting tonic baroreceptor tone. For vasopressin, the pathway from the NTS to the hypothalamus is dependent on a synapse in the A1 area. For ACTH, there are pathways to the hypothalamus that do not synapse in the A1 area, but neurons in this region do have an excitatory effect on secretion of ACTH.

2-Amino-5-phosphonovalerate↗

PubMed1992

Chemoreceptor and baroreceptor responses of A1 area neurons projecting to supraoptic nucleus.

Extracellular recordings were made from 127 neurons, identified by antidromic activation from the supraoptic nucleus, in the A1 area of urethan-anesthetized rabbits. The median axonal conduction velocity was 0.7 m/s, and the median discharge rate was 3.9 spikes/s. Raising arterial pressure decreased the discharge rate in 94 of 101 neurons tested. Lowering arterial pressure increased the discharge rate in 50 of 64 neurons tested. Of 70 neurons inhibited by baroreceptor activation, 40 were excited and 25 inhibited by hypercapnic hypoxia. Of 23 neurons excited by hypercapnic hypoxia, all were excited by hypoxia but only 2 were affected by hypercapnia. Of 16 neurons inhibited by hypercapnic hypoxia, 15 were inhibited by hypoxia and 1 was inhibited by hypercapnia. Of 14 neurons excited by hypoxia, 13 were excited by injection of sodium cyanide into the common carotid artery. Of five neurons inhibited by hypoxia, four were inhibited by sodium cyanide. Our results provide electrophysiological evidence that neurons projecting from the A1 area to the supraoptic nucleus increase their discharge rate in response to baroreceptor unloading and decrease their discharge rate in response to baroreceptor activation. These neurons may form part of the central pathway mediating secretion of vasopressin in response to hemorrhage. A high proportion of the neurons also receive peripheral chemoreceptor inputs, and these A1 cells may also be part of the central pathway whereby chemoreceptor stimulation modifies the secretion of vasopressin.

Animals↗

PubMed1992

Age-related loss of dorsal vagal neurons in Parkinson's disease.

Older patients who die with Parkinson's disease (PD) have fewer pigmented neurons in the locus coeruleus and fewer substance P-containing neurons in mesopontine tegmental nuclei. We analyzed two other medullary nuclei, the dorsal vagal nucleus and the hypoglossal nucleus, in eight PD patients and six normal controls by counting neurons in serial Nissl stained sections to determine the relationship between age at death and cell loss in these nuclei. PD-related neurodegenerative changes (Lewy bodies and neuronal loss) were present only in the dorsal vagal nucleus (13,637 +/- 1,323 neurons in PD, 24,885 +/- 1,157 in normal controls). Cells in the intermediate rostrocaudal part of the nucleus were most severely affected. There was a significant correlation between loss of vagal neurons and age at death in PD patients. No age-related cell loss was present in the dorsal vagal nucleus of normal brains, or in the hypoglossal nucleus in either PD or normal brains. These results confirm that age-related cell death depends on whether or not there is coexistent PD.

Aged↗

PubMed1991

Transneuronal labeling of neurons in rabbit brain after injection of herpes simplex virus type 1 into the aortic depressor nerve.

Herpes simplex virus type 1 (HSV1) was injected into either the aortic depressor nerve or the vagus nerve in the rabbit. Four or 5 days after injection of virus, the rabbit brain was processed immunohistochemically to demonstrate viral antigen. After injection into the aortic nerve HSV1 positive cells were found principally ipsilaterally within the nucleus tractus solitarius, area postrema, caudal and rostral ventrolateral medulla oblongata, the spinal trigeminal complex, raphe nuclei, A5 area, locus coeruleus, parabrachial nucleus, periaqueductal gray, ventrolateral hypothalamic area, paraventricular nucleus, amygdala, bed nucleus of the stria terminalis and insular cortex. Double labeling studies indicated that approximately 85% of the virus-containing neurons in the ventrolateral medulla, and virtually all the HSV-positive neurons in the A5 area and locus coeruleus also contained tyrosine hydroxylase. In the raphe nuclei and parapyramidal region approximately 33% of virus-containing cells reacted positively with PH8 antibody, a marker for serotonin synthesis. After injection of HSV1 into the vagus nerve labeled cells were found in similar brain areas, with a more bilateral distribution. The HSV-positive neurons may be involved in the processing of baroreceptor-derived information.

Animals↗

PubMed1991

Transneuronal transport of herpes simplex virus from the cervical vagus to brain neurons with axonal inputs to central vagal sensory nuclei in the rat.

The recent introduction of live viruses as intra-axonal tracing agents has raised questions concerning which central neurons are transneuronally labelled after application of the virus to peripheral organs or peripheral nerves. Since the central connections of the vagus nerve have been well described using conventional neuronal tracing agents, we chose to inject Herpes Simplex Virus Type 1 into the cervical vagus of the rat. After survival times of up to 3 days the rat brains were processed immunohistochemically using a polyclonal antiserum against herpes simplex virus. Two days after injection of the virus we observed viral antigen in the area postrema and in the nucleus tractus solitarius and the dorsal motor nucleus of the vagus (dorsal vagal complex), principally ipsilaterally. At this survival time the viral antigen in the dorsal vagal complex was largely confined to glial cells. After 3 days the viral antigen was localized both in glia and in nerve cells within the dorsal vagal complex and in brain regions previously demonstrated, using conventional tracing procedures, to contain neurons with axonal projections to the dorsal vagal complex. This was true for medullary, pontine, midbrain and hypothalamic regions and for telencephalic regions including the amygdala, the bed nucleus of the stria terminalis, and the insular and medial frontal cortices. Many of the nerve cells containing viral antigen were displayed in a Golgi-like manner, with excellent visualization of the dendritic tree. Axonal processes, in contrast, were not visualized. We used co-localization studies to confirm previous findings concerning monoamine neurotransmitter-related antigens present in medullary and pontine neurons projecting to the dorsal vagal complex. After 3 days there were many Herpes Simplex Virus Type 1-containing glial cells along the intra-medullary course of the vagal rootlets. However, no viral antigen was found in brain regions containing neurons whose axons pass through the region of glial cell-labelled rootlets. Glial cells containing viral antigen were particularly numerous in brain regions known to receive an input from neurons in the area postrema and the dorsal vagal complex. Taken together with our observation concerning the early appearance of viral antigen within glial cells in the dorsal vagal complex, this suggests that when the virus reaches the axon terminal portion it is transferred to nearby glial cells and possibly enters central neurons by way of these structures.

Amidines↗

PubMed1991

Substance P-containing neurons in the mesopontine tegmentum are severely affected in Parkinson's disease.

Substance P immunoreactive (SP+) neurons were analysed quantitatively in serial sections of the mesopontine tegmentum in 6 patients with idiopathic Parkinson's disease and 5 age-matched normal controls. In the tegmentum of the Parkinson's disease brains many SP+ neurons contained swollen, twisted neuronal processes as well as Lewy bodies. There were significant reductions in the total number of SP+ neurons in the pedunculopontine tegmental nucleus (loss 43%), in the laterodorsal tegmental nucleus (loss 28%), in the oral pontine reticular nucleus (loss 41%) and in the median raphe nucleus (loss 76%). It was the large SP+ (greater than 20 microns) neurons that were particularly affected. In our control group we did not document a significant relationship between age at death and number of SP+ neurons in these tegmental nuclei or between age at death and number of pigmented neurons in the locus coeruleus. In contrast, in patients with Parkinson's disease, there was a strong inverse relationship between age at death and numbers of SP+ and pigmented neurons. Our findings suggest an interaction between the pathophysiological mechanisms initiated by Parkinson's disease and other processes related to ageing. Since tegmental SP+ neurons are affected by the primary pathological processes underlying Parkinson's disease as severely as catecholamine-synthesizing neurons are affected, theories of pathogenesis and therapeutic strategies in Parkinson's disease will need to take into account the involvement of these SP+ neurons.

Aged↗

PubMed1991

Neurons in rabbit caudal ventrolateral medulla inhibit bulbospinal barosensitive neurons in rostral medulla.

We made extracellular recordings from 104 spinally projecting neurons in the rostral ventrolateral medulla of urethan-anesthetized rabbits to test whether inhibitory vasomotor neurons in the caudal ventrolateral medulla act by inhibiting rostral sympathoexcitatory neurons. The median conduction velocity was 8.3 m/s, and the median discharge rate was 2.9 spikes/s. Raising arterial pressure with intravenous phenylephrine inhibited 88% of 77 neurons tested. The remaining units were excited. Lowering arterial pressure with nitroprusside excited 90% of 30 neurons tested. Remaining units were unaffected. Ninety-one percent of 58 rostral neurons inhibited by phenylephrine were also inhibited by injection of L-glutamate into the caudal ventrolateral medulla and 81% of 43 tested were excited by caudal injection of gamma-aminobutyric acid. These results confirm our suggestion [Brain Res. 253: 161-171, 1982; Am. J. Physiol. 254 (Heart Circ. Physiol. 23): H686-H692, 1988] and the findings of S. K. Agarwal, A. J. Gelsema, and F. R. Calaresu [Am. J. Physiol. 257 (Regulatory Integrative Comp. Physiol. 26): R265-R270, 1989]. The depressor neurons in the caudal medulla act substantially by inhibition of spinally projecting sympathoexcitatory neurons in the rostral medulla. All rostral units excited by phenylephrine were also excited by injections of L-glutamate into the caudal ventrolateral medulla, suggesting that some sympathoinhibition of baroreceptor and caudal medullary origin may take place in the spinal cord and be mediated by a subpopulation of rostral sympathoinhibitory neurons.

Animals↗

PubMed1990

Galanin immunoreactive neurons in the human hypothalamus: colocalization with vasopressin-containing neurons.

Galanin (GA) is a recently described neuropeptide that has been demonstrated to be widely distributed in the hypothalamus of experimental animals. So far there is no immunohistochemical description of GA in the human hypothalamus and, in particular, no studies of the colocalization of this neuropeptide with other transmitter candidates in the human hypothalamus. We have now investigated this question immunohistochemically by using human brains fixed by vascular perfusion within 24 hours of death. Nerve cell bodies and fibers stained for GA were observed throughout the hypothalamus. Major populations of GA-ir cell bodies were found in the suprachiasmatic, intermediate, supraoptic, paraventricular, arcuate, tuberomammillary, and supramammillary nuclei. Scattered positive neurons were found in the periventricular preoptic area, the posterior hypothalamic nucleus, the lateral hypothalamic area, and zona incerta. A few positive cells were located in the dorsomedial and ventromedial hypothalamic nuclei. The number of GA-ir neurons estimated from three brains was 11,100 +/- 2,400 for the intermediate nucleus, 57,800 +/- 9,100 for the supraoptic nucleus and 47,400 +/- 13,900 for the paraventricular nucleus. GA-ir fibers were widely distributed in the hypothalamus. They were more dense in the periventricular and medial hypothalamic zones, whereas the lateral tuberal nuclei and the dorsolateral part of the supraoptic nucleus contained sparse positive fibers. The mammillary complex contained almost no GA-ir fibers. In the ventromedial tuberal region, GA-ir axons formed bundles travelling down in the infundibular stem. In the median eminence the vascular plexus was wrapped by GA-ir fiber networks. The coexistence of GA with arginine vasopressin (AVP), oxytocin (OXY), and tyrosine hydroxylase (TH) was examined in the supraoptic, paraventricular, and suprachiasmatic nuclei in adjacent paraffin sections. Neurons containing both GA and AVP were very common in the supraoptic nucleus and also occurred in the paraventricular and suprachiasmatic nuclei. The supraoptic and paraventricular nuclei also contained some neurons immunoreactive for both GA and OXY. Neurons positive for GA and TH were rare. The topographic distribution of GA-ir neuronal structures in the hypothalamus and the colocalization of GA, principally with AVP and to a lesser extent with OXY, in some hypothalamic nuclei constitute anatomical evidence that this neuropeptide may be involved in the regulation of endocrine, autonomic, and behavioural homeostatic responses.

Aged↗