Histaminergic Transmission in the Brain

Neurophysiology > Intrinsic Regulatory Systems of the Brain > Specific Integrative Regulatory Systems

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Jean‐Charles Schwartz, Monique Garbarg, Héléne Pollard

10.1002/cphy.cp010405

Source: Supplement 4: Handbook of Physiology, The Nervous System, Intrinsic Regulatory Systems of the Brain

Originally published: 1986

Published online: January 2011

Full Article on Wiley Online Library

Abstract
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Abstract

The sections in this article are:

1 Metabolism of Histamine in Brain

1.1 Biosynthesis

1.2 Storage

1.3 Release

1.4 Inactivation

1.5 Turnover

2 Identification of Histaminergic Neuronal Pathways by Lesion Studies

2.1 Evidence for Histaminergic Pathway in Medial Forebrain Bundle

2.2 Studies of Histaminergic Afferents in Hippocampal and Amygdaloid Regions

2.3 Attempts at Localizing Origin of Histaminergic Pathways

3 Immunohistochemical Localization of Histaminergic Neuronal Pathways

3.1 Various Immunohistochemical Tools

3.2 Localization of Immunoreactive Cell Bodies

3.3 Histaminergic Neuronal Projections and Areas of Terminations

4 Histamine Receptors and Actions in Brain

4.1 Pharmacological Tools for Identification of Subclasses of Histamine Receptors

4.2 Radioligand Binding Studies of Histamine Receptors

4.3 Histamine Receptors Linked to cAMP Formation

4.4 Histamine‐Induced Glycogenolysis

4.5 Other Biochemical Responses to Histamine Mediated by H1 Receptors

4.6 Electrophysiological Investigation of Histamine Actions in Brain

4.7 Neuroendocrine Responses to Histamine

4.8 Vegetative Responses to Histamine

4.9 Effects of Histamine on Vascular Regulation in Brain

5 Conclusion

	Figure 1. Main pathways for metabolism of histamine.
	Figure 2. Time course of changes in L‐histidine decarboxylase activity in mouse tissues after systemic administration of α‐fluoromethylhistidine (α‐FMH). Groups of 5–15 mice received intraperitoneal injections of α‐FMH (10 mg/kg) and were killed at indicated time intervals. Control groups of 5–10 mice injected with vehicle solutions were killed at same time intervals. Each value represents percentage of L‐histidine decarboxylase activity remaining as compared with control group killed at same time. Bars, SEM values. Mean histidine decarboxylase activities of controls: 11.1 ± 0.4 dpm · h⁻¹ · μg⁻¹ protein in cerebral cortex; 52.3 ± 2.1 dpm · h⁻¹ · μg⁻¹ protein in hypothalamus; 96.0 ± 9.0 dpm · h⁻¹ · μg⁻¹ protein in glandular portion of stomach. From Garbarg et al. 107
	Figure 3. Regional distribution of histamine N‐methyltransferase (H.M.T.) in rat brain as compared with that of histamine and L‐histidine decarboxylase (H.D.). From Schwartz et al. 273
	Figure 4. Developmental patterns of histidine decarboxylase and histamine N‐methyltransferase activities as compared with that of histamine content in rat brain. From Martres et al. 190
	Figure 5. Developmental pattern of subcellular distribution of L‐histidine decarboxylase (H.D.) activity in rat brain. Whole homogenate was fractionated into P₁ (crude nuclear), P₂ (crude mitochondrial including the synaptosomes), P₃ (microsomal), and S₃ (soluble). From Martres et al. 190
	Figure 6. Effect of K⁺‐induced depolarization on synthesis and release of [³H]histamine (³H‐HA) from slices of rat hypothalamus. Synthesis and release of [³H]histamine were measured during 10‐min incubation of 5 mg of hypothalamic slices in presence of 18 × 10⁶ dpm [³H]histidine in 100 μl of medium. Total synthesis is referred to sum of [³H]histamine in tissue and in medium. Results compared with normal conditions were ± SEM of 8–15 experiments. From Verdière et al. 330
	Figure 7. Potassium‐evoked overflow of newly synthesized [³H]histamine and its inhibition by exogenous histamine in rat cortex. [³H]histamine was synthesized by pooled slices from rat cerebral cortex incubated with [³H]histidine. Slices were then distributed in small baskets and washed by successive transfers in Krebs‐Ringer medium at 37°C. First depolarization was induced by a 5‐min incubation in presence of 30 mM K⁺ (S₁). After four 5‐min washings, slices were incubated A, in Krebs‐Ringer solution alone, or B, together with 10⁻⁶ M histamine (HA), before 2nd 5‐min exposure to 30 mM K⁺ in these 2 conditions (S₂). Released ³H‐amine was isolated by ion‐exchange chromatography (see ref. 19). The ratios S₂/S₁ of released [³H]histamine were 0.89 and 0.19 in absence and in presence of unlabeled histamine respectively, indicating a 79% inhibition elicited by addition of exogenous amine.
	Figure 8. Reversal by burimamide of exogenous histamine‐induced inhibition of release of K⁺‐evoked [³H]histamine from slices of rat cerebral cortex. After 30‐min preincubation with [³H]histidine and extensive washing, slices were exposed for 5 min to burimamide (in fixed concentration). Exogenous histamine (in increasing concentrations) was then added, together with 30 mM K⁺, and 2 min after, the incubations were stopped by centrifugation. Tritiated histamine present in tissue and medium was isolated by ion‐exchange chromatography (see ref. 19). Inset: Schild plot of data, which gave pA₂ value of 7.5 for burimamide. From Arrang et al. 361. Reprinted by permission from Nature, vol. 302, no. 5911, p. 832–837. Copyright © 1983 Macmillan Journals Limited
	Figure 9. Time course of decreases in histamine (HA) level and in histidine decarboxylase (H.D.) and dopa decarboxylase (D.D.) activities in rat cortex after a unilateral interruption of medial forebrain bundle (see ref. 104). Groups of 5–14 rats were killed at each time after either section (2, 4, 8, 12 days) or high‐frequency lesion (24 h, 36 h, 21 days). Each value represents mean percentage of decrease (SEM) in lesioned side as compared with control side of same animal. Mean control values: 38.2 ± 2.3 ng·g⁻¹ for histamine; 1.25 ± 0.66 dpm · μg⁻¹ protein · h⁻¹ for histidine decarboxylase activity; 0.98 ± 0.08 μmol · g⁻¹ · h⁻¹ for dopa decarboxylase activity. From Garbarg et al. 103
	Figure 10. Effect of pargyline, a monoamine oxidase inhibitor, on catabolism of endogenously synthesized [³H]histamine (³H‐HA) and [³H]methylhistamine (³H‐MHA) in rat brain. Pargyline (100 mg/kg ip) was injected 1 h after administration (iv) of L‐[³H]histidine; animals were killed 3 h later. [³H]histamine and [³H]methylhistamine levels were compared with those of 2 control groups: 1st group was killed 1 h after L‐[³H]histidine administration, i.e., at time chosen for pargyline administration; 2nd group received saline instead of pargyline and was killed 3 h later. In pargyline‐treated animals level of ³H‐amines found at 4 h was only slower than for 1‐h controls. ** P < 0.01 when compared with controls (4 h). From Pollard et al. 228
	Figure 11. Kinetics of [³H]histamine accumulation in mouse brain after infusion of L‐[³H]histidine (L‐His) at constant rate. Specific activities of L‐histidine in mouse plasma and brain and histamine (HA) in mouse brain were measured as function of time during infusion (iv) of L‐[³H]histidine at constant rate (20 μCi/min per animal). Each point is ± SEM for groups of 4–7 animals. From Schwartz et al. 268. Reprinted by permission of the publisher from Figure 8, page 200, chapter component:cp010406 in Current Developments in Psycho‐pharmacology, Volume 5, by Walter B. Essman and Luigi Valzelli (eds.). Copyright 1979, Spectrum Publications, Inc., Jamaica, New York
	Figure 12. Schematic diagram of histamine‐synthesizing afferents to amygdaloid complex and bed nucleus of stria terminalis (BST). Present in medial forebrain bundle (MFB), these afferents project massively to BST, in particular to its ventral part. Histamine‐synthesizing afferents also project via ventral route to pyriform cortex (PYR) and nuclei of amygdaloid complex, in particular the more medially located nuclei (thin arrow). These afferents also innervate the pyriform cortex via another—yet unknown—nonamygdalopetal route (thick, broken line). 1–3, Types of lesion performed in this study. HIP, hippocampal formation; HYP, hypothalamus; CAE, external capsule. From Ben‐Ari et al. 21
	Figure 13. Localization of “efficient lesion areas” responsible when destroyed for significant decreases in histidine decarboxylase activity in occipital cortex (A) and striatum (B). Selective lesions were performed at various sites in hypothalamus and upper midbrain of rats. Animals were killed 1–2 wk after surgery; for each animal, volume and placement of lesion were reconstituted by mapping damaged areas in serial histological slices. Then topographic data were correlated by computer program with modification in histidine decarboxylase activity induced by lesions, to determine efficient lesion areas responsible for decrease >30% with an efficiency >75% in target areas. Dotted areas, efficient lesion areas responsible for significant decrease in histidine decarboxylase activity in occipital cortex and striatum; hatched areas, “inefficient lesion areas.” Topographic and biochemical data from 80 rats combined. From Garbarg et al. 105. Reprinted by permission of the publisher from Figure 2, page 185 in Neurotransmitters, Receptors, and Drug Action, by Walter B. Essman (ed.). Copyright 1980, Spectrum Publications, Inc., Jamaica, New York
	Figure 14. Hypothetical mapping of disposition of ascending histaminergic pathways in rat brain as suggested by a variety of lesion experiments. Posterior plane, most anterior section performed in brain stem, which fails to affect histidine decarboxylase activity in telencephalon. From Garbarg et al. 105. Reprinted by permission of the publisher from Figure 3, page 187 in Neurotransmitters, Receptors, and Drug Action, by Walter B. Essman (ed.). Copyright 1980, Spectrum Publications, Inc., Jamaica, New York
	Figure 15. Localization of histamine‐immunoreactive cells in rat brain. A: photomicrograph of transverse section at caudal level of median eminence after incubation with antibody to histamine. Histamine‐positive fibers are demonstrated in lateral aspects of median eminence by use of indirect fluorescence technique. Relatively large number of histamine‐positive mast cells are seen in leptomeninges. Bars, 50 μm. B: histamine‐immunoreactive cells in nucleus caudalis magnocellularis postmamillaris of rat as revealed by use of peroxidase‐antiperoxidase method. × 25. C: histamine‐immunoreactive varicose fibers in periaqueductal gray dorsomedial to nucleus raphe dorsalis. × 40. A from Steinbusch and Mulder 465; B and C, photomicrographs courtesy of Dr. H. W. M. Steinbusch
	Figure 16. Localization of histidine decarboxylase‐immunoreactive cells in rat brain by use of monoclonal antibody. Photomicrographs of frontal‐freeze microtome section through posterior hypothalamus of rat after incubation with monoclonal antibody to histidine decarboxylase and immunostaining by peroxidase‐antiperoxidase method. A: histidine decarboxylase‐immunoreactive neurons in caudate magnocellular nucleus. × 100. B: group of immunoreactive cells in basal hypothalamus at level of posterior caudal magnocellular nucleus. × 40. C: histidine decarboxylase‐immunoreactive fibers in premammillary region of rat hypothalamus. × 40.
	Figure 17. Activity of histamine agonists and antagonists on reference biological systems. Relative agonist potency, EC₅₀ histamine/EC₅₀ agonists × 100.
	Figure 18. Saturation curve of [³H]mepyramine binding to guinea pig cerebellum. Particulate fraction from guinea pig cerebellum was incubated with increasing concentrations of [³H]mepyramine alone or together with 0.2 μM of mianserin or 0.2 μM of triprolidine. By use of an iterative computing method a K_d value of 0.7 nM and a maximal capacity of 205 fmol · mg⁻¹ protein were found.
	Figure 19. Autoradiogram of sagittal section from guinea pig brain generated with [¹²⁵I]iodobolpyramine. Total binding shown was achieved by incubation with 0.1 nM [¹²⁵I]iodobolpyramine. Nonspecific binding obtained in presence of 0.2 μM mianserin gave uniform pale gray sections. M. Körner, M. L. Bouthenet, C. R. Ganellin, M. Garbarg, C. Gros, R. J. Ife, N. Sales, and J.‐C. Schwartz, unpublished data
	Figure 20. Autoradiographic localization of H₁ receptors in guinea pig cerebellum. A, C: dark‐field photomicrographs showing autoradiographic grains. B, D: the same respective areas with bright‐field illumination. As shown in A and B, after mounted tissue sections were incubated with [³H]‐mepyramine, high densities of autoradiographic grains were found over molecular layer (M) of cerebellum. Very low levels were found over granule cell layer (G), and negligible densities were found in white matter areas (W). Underlying brain stem (BS) areas showed low but significant levels of grain densities. As shown in C and D, addition of 2 μM triprolidine to block specific binding eliminated grains in molecular layer and elsewhere. From Palacios et al. 440
	Figure 21. Binding of [³H]mepyramine in cortex of mice as function of nonradioactive mepyramine. Groups of mice received 1 μCi of [³H]mepyramine (iv) together with nonradioactive mepyramine in increasing dosage. Cerebral cortex was dissected out 3 min later and specific binding of [³H] mepyramine was determined. Nonsaturable binding that was substracted represented ∼50% of total at highest dosages. Results expressed in fmol · mg⁻¹ protein, based on specific activity of injected material. Hill plot of same data (inset) gives straight line with slope not different from unity (n_H = 0.96). B, [³H]mepyramine bound; B_M, maximal binding of [³H]mepyramine. From Quach et al. 233
	Figure 22. Inhibition by cimetidine of stimulation of cAMP accumulation elicited by impromidine in hippocampal slices from guinea pig. Pooled slices were incubated for 30 min at 37°C in Krebs‐Ringer bicarbonate medium (40 ml/g tissue) under constant stream of 95% O₂:5% CO₂. At end of preincubation they were washed with same fresh medium and aliquots were incubated, with cimetidine when required, for 15 min. Impromidine was then added for an additional 15 min of incubation. Reaction was stopped by sonication and heating the homogenates at 95°C for 8 min. Levels of cAMP were determined by protein binding assay method (see ref. 38). Maximal stimulation of cAMP accumulation elicited by impromidine alone was 17.5 ± 1.1 pmol · mg⁻¹ protein. Apparent dissociation constant of cimetidine was calculated according to the equation K_i = A/[(EC₅₀¹/EC₅₀) − 1] where A is concentration of antagonist and EC₅₀ and EC₅₀¹, the concentrations of agonist required for half‐maximal response in absence or in presence of antagonist. Value of K_i, for cimetidine was 0.95 μM.
	Figure 23. Accumulation of cAMP in slices from guinea pig hippocampus induced by 2‐thiazolylethylamine (TEA), an H₁ agonist, in presence of dimaprit (DIM), an H₂ agonist. The various agonists were added together at beginning of 15‐min incubation. Accumulation of cAMP elicited by TEA in various concentrations was checked alone or together with 10⁻⁴ M DIM. Mepyramine (MEP) was added 10 min before the 2 agonists. In presence of DIM, EC₅₀ of TEA is 60 μM, which corresponds to a potency relative to histamine that is close to that found in peripheral H₁ receptor systems. From Palacios et al. 207
	Figure 24. Restoration of H₁ receptor‐mediated effect by addition of Ca²⁺ in guinea pig hippocampal slices. Slices were prepared in normal Krebs‐Ringer solution, preincubated 30 min at 37°C and then washed 4 times with a Ca²⁺‐free Krebs‐Ringer solution. Aliquots were then incubated 15 min with increasing concentrations of Ca²⁺, and a further 15‐min incubation was performed in presence of 100 μM dimaprit (DIM) and 1 μM 2‐thiazolylethylamine (TEA).
	Figure 25. Time course of [³H]glycogen synthesis and histamine‐induced hydrolysis in slices from mouse cortex. Slices were incubated in presence of [³H]glucose. After 30 min (arrow) 10⁻⁴ M histamine was added to incubation medium. From Quach et al. 232
	Figure 26. Inhibition by mepyramine (MEPY), an H₁ receptor antagonist, of histamine‐induced glycogenolysis in slices from mouse cortex. After 30‐min preincubation in presence of [³H]glucose, slices were incubated with increasing concentrations of histamine (HA) alone, or with mepyramine at various concentrations. Results are expressed as percentages of basal [³H]glycogen level. Inset, Schild plot of same data. From Quach et al. 232
	Figure 27. Effect of histamine preincubation on histamine‐induced hydrolysis of [³H]glycogen in slices from mouse cortex. Slices were preincubated without (controls) or with 50 μM histamine for 20 min and washed 3 times; [³H]glycogen hydrolysis induced by histamine at indicated concentrations was then determined. Results expressed as percentages of basal [³H]glycogen levels: 20.2 ± 1.0 × 10³ dpmmg‐1 protein for controls and 20.9 ± 1.0 × 10³ dpm · mg⁻¹ protein for histamine‐incubated slices. From Quach et al. 234
	Figure 28. Intracellular recording from dentate granule cell. A: membrane potential (68 mV) replayed from magnetic tape with increased speed so that fast voltage deflections are not visible. Histamine was applied by pressure ejection from micropipette in dendritic region ∼250 μM from soma layer. Bar above trace indicates 20‐ and 50‐mmHg ejection pressure. B‐D: expanded traces taken before, during, and after histamine action as indicated in A. Voltage deflections produced by constant‐current injection of ±0.5 nA or −0.1 to −2.0 nA and +0.1 to +0.5 nA. b‐d: Such deflections at an even more expanded time base (±0.5 nA and −2.0 nA). From Haas 131
	Figure 29. Hypersensitivity to microiontophoretic applications of histamine and norepinephrine (noradrenaline) in cortical neurons of guinea pig brain after electrolytic lesion of medial forebrain bundle (MFB). Animals were anesthetized with urethan for iontophoresis experiments 8–20 days after unilateral lesion of MFB. Dose‐response curves were constructed by measuring change in firing levels effected by different ejecting currents as it reached plateau. Data shown were obtained from plateau responses of 2 neurons to histamine (left) and norepinephrine (right) in guinea pig sensorimotor cortex, which were recorded in immediate succession and with same micropipette on intact and lesioned side. Abscissa, ejecting current intensity in nA, except for negative values, which refer to retaining currents. From Haas et al. 138
	Figure 30. Intracellular recording of neurosecretory neuron from paraventricular nucleus (PVN) in rat hypothalamic slice. Left: records illustrate spontaneous excitatory postsynaptic potentials (EPSPs) before, during, and after perfusion with histamine (10⁻⁵ M). Increased size and frequency of EPSPs indicates action of histamine on nearby interneurons rather than direct action on this cell membrane. Right: schematic drawing of experimental situation and response to injection of ±0.25 nA through recording electrode. Membrane potential and resistance were unchanged. From Haas and Geller 134. Reprinted with permission from Advances in the Biosciences, edited by B. Uvnäs and K. Tasaka. Copyright 1982 by Pergamon Press
	Figure 31. Actions of histamine and impromidine on pyramidal neurons intracellularly recorded in CA1 area of rat hippocampal slices. Left: block of firing accommodation by 1 μM histamine, bath applied. In presence of histamine (lower left) same depolarizing current as in upper left (during time indicated by black bar) evokes many more action potentials, in absence of changes in basic membrane properties. Middle: Ca²⁺ spikes evoked by depolarizing current injection in absence (upper middle) and/or in presence (lower middle) of 1 μM impromidine in tetrodotoxin‐poisoned slice. Right: afterhyperpolarizations following these Ca²⁺ spikes. Long‐lasting component is markedly reduced by 1 μM impromidine. Results indicate that histamine (through H₂ receptors) blocks a Ca²⁺‐dependent K⁺ current without altering Ca²⁺ current. Photomicrographs courtesy of Dr. H. Haas

Figure 1.

Main pathways for metabolism of histamine.

Figure 2.

Time course of changes in L‐histidine decarboxylase activity in mouse tissues after systemic administration of α‐fluoromethylhistidine (α‐FMH). Groups of 5–15 mice received intraperitoneal injections of α‐FMH (10 mg/kg) and were killed at indicated time intervals. Control groups of 5–10 mice injected with vehicle solutions were killed at same time intervals. Each value represents percentage of L‐histidine decarboxylase activity remaining as compared with control group killed at same time. Bars, SEM values. Mean histidine decarboxylase activities of controls: 11.1 ± 0.4 dpm · h⁻¹ · μg⁻¹ protein in cerebral cortex; 52.3 ± 2.1 dpm · h⁻¹ · μg⁻¹ protein in hypothalamus; 96.0 ± 9.0 dpm · h⁻¹ · μg⁻¹ protein in glandular portion of stomach.

From Garbarg et al. 107

Figure 3.

Regional distribution of histamine N‐methyltransferase (H.M.T.) in rat brain as compared with that of histamine and L‐histidine decarboxylase (H.D.).

From Schwartz et al. 273

Figure 4.

Developmental patterns of histidine decarboxylase and histamine N‐methyltransferase activities as compared with that of histamine content in rat brain.

From Martres et al. 190

Figure 5.

Developmental pattern of subcellular distribution of L‐histidine decarboxylase (H.D.) activity in rat brain. Whole homogenate was fractionated into P₁ (crude nuclear), P₂ (crude mitochondrial including the synaptosomes), P₃ (microsomal), and S₃ (soluble).

From Martres et al. 190

Figure 6.

Effect of K⁺‐induced depolarization on synthesis and release of [³H]histamine (³H‐HA) from slices of rat hypothalamus. Synthesis and release of [³H]histamine were measured during 10‐min incubation of 5 mg of hypothalamic slices in presence of 18 × 10⁶ dpm [³H]histidine in 100 μl of medium. Total synthesis is referred to sum of [³H]histamine in tissue and in medium. Results compared with normal conditions were ± SEM of 8–15 experiments.

From Verdière et al. 330

Figure 7.

Potassium‐evoked overflow of newly synthesized [³H]histamine and its inhibition by exogenous histamine in rat cortex. [³H]histamine was synthesized by pooled slices from rat cerebral cortex incubated with [³H]histidine. Slices were then distributed in small baskets and washed by successive transfers in Krebs‐Ringer medium at 37°C. First depolarization was induced by a 5‐min incubation in presence of 30 mM K⁺ (S₁). After four 5‐min washings, slices were incubated A, in Krebs‐Ringer solution alone, or B, together with 10⁻⁶ M histamine (HA), before 2nd 5‐min exposure to 30 mM K⁺ in these 2 conditions (S₂). Released ³H‐amine was isolated by ion‐exchange chromatography (see ref. 19). The ratios S₂/S₁ of released [³H]histamine were 0.89 and 0.19 in absence and in presence of unlabeled histamine respectively, indicating a 79% inhibition elicited by addition of exogenous amine.

Figure 8.

Reversal by burimamide of exogenous histamine‐induced inhibition of release of K⁺‐evoked [³H]histamine from slices of rat cerebral cortex. After 30‐min preincubation with [³H]histidine and extensive washing, slices were exposed for 5 min to burimamide (in fixed concentration). Exogenous histamine (in increasing concentrations) was then added, together with 30 mM K⁺, and 2 min after, the incubations were stopped by centrifugation. Tritiated histamine present in tissue and medium was isolated by ion‐exchange chromatography (see ref. 19). Inset: Schild plot of data, which gave pA₂ value of 7.5 for burimamide.

Figure 9.

Time course of decreases in histamine (HA) level and in histidine decarboxylase (H.D.) and dopa decarboxylase (D.D.) activities in rat cortex after a unilateral interruption of medial forebrain bundle (see ref. 104). Groups of 5–14 rats were killed at each time after either section (2, 4, 8, 12 days) or high‐frequency lesion (24 h, 36 h, 21 days). Each value represents mean percentage of decrease (SEM) in lesioned side as compared with control side of same animal. Mean control values: 38.2 ± 2.3 ng·g⁻¹ for histamine; 1.25 ± 0.66 dpm · μg⁻¹ protein · h⁻¹ for histidine decarboxylase activity; 0.98 ± 0.08 μmol · g⁻¹ · h⁻¹ for dopa decarboxylase activity.

From Garbarg et al. 103

Figure 10.

Effect of pargyline, a monoamine oxidase inhibitor, on catabolism of endogenously synthesized [³H]histamine (³H‐HA) and [³H]methylhistamine (³H‐MHA) in rat brain. Pargyline (100 mg/kg ip) was injected 1 h after administration (iv) of L‐[³H]histidine; animals were killed 3 h later. [³H]histamine and [³H]methylhistamine levels were compared with those of 2 control groups: 1st group was killed 1 h after L‐[³H]histidine administration, i.e., at time chosen for pargyline administration; 2nd group received saline instead of pargyline and was killed 3 h later. In pargyline‐treated animals level of ³H‐amines found at 4 h was only slower than for 1‐h controls. ** P < 0.01 when compared with controls (4 h).

From Pollard et al. 228

Figure 11.

Kinetics of [³H]histamine accumulation in mouse brain after infusion of L‐[³H]histidine (L‐His) at constant rate. Specific activities of L‐histidine in mouse plasma and brain and histamine (HA) in mouse brain were measured as function of time during infusion (iv) of L‐[³H]histidine at constant rate (20 μCi/min per animal). Each point is ± SEM for groups of 4–7 animals.

From Schwartz et al. 268. Reprinted by permission of the publisher from Figure 8, page 200, chapter component:cp010406 in Current Developments in Psycho‐pharmacology, Volume 5, by Walter B. Essman and Luigi Valzelli (eds.). Copyright 1979, Spectrum Publications, Inc., Jamaica, New York

Figure 12.

Schematic diagram of histamine‐synthesizing afferents to amygdaloid complex and bed nucleus of stria terminalis (BST). Present in medial forebrain bundle (MFB), these afferents project massively to BST, in particular to its ventral part. Histamine‐synthesizing afferents also project via ventral route to pyriform cortex (PYR) and nuclei of amygdaloid complex, in particular the more medially located nuclei (thin arrow). These afferents also innervate the pyriform cortex via another—yet unknown—nonamygdalopetal route (thick, broken line). 1–3, Types of lesion performed in this study. HIP, hippocampal formation; HYP, hypothalamus; CAE, external capsule.

From Ben‐Ari et al. 21

Figure 13.

Localization of “efficient lesion areas” responsible when destroyed for significant decreases in histidine decarboxylase activity in occipital cortex (A) and striatum (B). Selective lesions were performed at various sites in hypothalamus and upper midbrain of rats. Animals were killed 1–2 wk after surgery; for each animal, volume and placement of lesion were reconstituted by mapping damaged areas in serial histological slices. Then topographic data were correlated by computer program with modification in histidine decarboxylase activity induced by lesions, to determine efficient lesion areas responsible for decrease >30% with an efficiency >75% in target areas. Dotted areas, efficient lesion areas responsible for significant decrease in histidine decarboxylase activity in occipital cortex and striatum; hatched areas, “inefficient lesion areas.” Topographic and biochemical data from 80 rats combined.

From Garbarg et al. 105. Reprinted by permission of the publisher from Figure 2, page 185 in Neurotransmitters, Receptors, and Drug Action, by Walter B. Essman (ed.). Copyright 1980, Spectrum Publications, Inc., Jamaica, New York

Figure 14.

Hypothetical mapping of disposition of ascending histaminergic pathways in rat brain as suggested by a variety of lesion experiments. Posterior plane, most anterior section performed in brain stem, which fails to affect histidine decarboxylase activity in telencephalon.

From Garbarg et al. 105. Reprinted by permission of the publisher from Figure 3, page 187 in Neurotransmitters, Receptors, and Drug Action, by Walter B. Essman (ed.). Copyright 1980, Spectrum Publications, Inc., Jamaica, New York

Figure 15.

Localization of histamine‐immunoreactive cells in rat brain. A: photomicrograph of transverse section at caudal level of median eminence after incubation with antibody to histamine. Histamine‐positive fibers are demonstrated in lateral aspects of median eminence by use of indirect fluorescence technique. Relatively large number of histamine‐positive mast cells are seen in leptomeninges. Bars, 50 μm. B: histamine‐immunoreactive cells in nucleus caudalis magnocellularis postmamillaris of rat as revealed by use of peroxidase‐antiperoxidase method. × 25. C: histamine‐immunoreactive varicose fibers in periaqueductal gray dorsomedial to nucleus raphe dorsalis. × 40.

A from Steinbusch and Mulder 465; B and C, photomicrographs courtesy of Dr. H. W. M. Steinbusch

Figure 16.

Localization of histidine decarboxylase‐immunoreactive cells in rat brain by use of monoclonal antibody. Photomicrographs of frontal‐freeze microtome section through posterior hypothalamus of rat after incubation with monoclonal antibody to histidine decarboxylase and immunostaining by peroxidase‐antiperoxidase method. A: histidine decarboxylase‐immunoreactive neurons in caudate magnocellular nucleus. × 100. B: group of immunoreactive cells in basal hypothalamus at level of posterior caudal magnocellular nucleus. × 40. C: histidine decarboxylase‐immunoreactive fibers in premammillary region of rat hypothalamus. × 40.

Figure 17.

Activity of histamine agonists and antagonists on reference biological systems. Relative agonist potency, EC₅₀ histamine/EC₅₀ agonists × 100.

Figure 18.

Saturation curve of [³H]mepyramine binding to guinea pig cerebellum. Particulate fraction from guinea pig cerebellum was incubated with increasing concentrations of [³H]mepyramine alone or together with 0.2 μM of mianserin or 0.2 μM of triprolidine. By use of an iterative computing method a K_d value of 0.7 nM and a maximal capacity of 205 fmol · mg⁻¹ protein were found.

Figure 19.

Autoradiogram of sagittal section from guinea pig brain generated with [¹²⁵I]iodobolpyramine. Total binding shown was achieved by incubation with 0.1 nM [¹²⁵I]iodobolpyramine. Nonspecific binding obtained in presence of 0.2 μM mianserin gave uniform pale gray sections.

M. Körner, M. L. Bouthenet, C. R. Ganellin, M. Garbarg, C. Gros, R. J. Ife, N. Sales, and J.‐C. Schwartz, unpublished data

Figure 20.

Autoradiographic localization of H₁ receptors in guinea pig cerebellum. A, C: dark‐field photomicrographs showing autoradiographic grains. B, D: the same respective areas with bright‐field illumination. As shown in A and B, after mounted tissue sections were incubated with [³H]‐mepyramine, high densities of autoradiographic grains were found over molecular layer (M) of cerebellum. Very low levels were found over granule cell layer (G), and negligible densities were found in white matter areas (W). Underlying brain stem (BS) areas showed low but significant levels of grain densities. As shown in C and D, addition of 2 μM triprolidine to block specific binding eliminated grains in molecular layer and elsewhere.

From Palacios et al. 440

Figure 21.

Binding of [³H]mepyramine in cortex of mice as function of nonradioactive mepyramine. Groups of mice received 1 μCi of [³H]mepyramine (iv) together with nonradioactive mepyramine in increasing dosage. Cerebral cortex was dissected out 3 min later and specific binding of [³H] mepyramine was determined. Nonsaturable binding that was substracted represented ∼50% of total at highest dosages. Results expressed in fmol · mg⁻¹ protein, based on specific activity of injected material. Hill plot of same data (inset) gives straight line with slope not different from unity (n_H = 0.96). B, [³H]mepyramine bound; B_M, maximal binding of [³H]mepyramine.

From Quach et al. 233

Figure 22.

Inhibition by cimetidine of stimulation of cAMP accumulation elicited by impromidine in hippocampal slices from guinea pig. Pooled slices were incubated for 30 min at 37°C in Krebs‐Ringer bicarbonate medium (40 ml/g tissue) under constant stream of 95% O₂:5% CO₂. At end of preincubation they were washed with same fresh medium and aliquots were incubated, with cimetidine when required, for 15 min. Impromidine was then added for an additional 15 min of incubation. Reaction was stopped by sonication and heating the homogenates at 95°C for 8 min. Levels of cAMP were determined by protein binding assay method (see ref. 38). Maximal stimulation of cAMP accumulation elicited by impromidine alone was 17.5 ± 1.1 pmol · mg⁻¹ protein. Apparent dissociation constant of cimetidine was calculated according to the equation K_i = A/[(EC₅₀¹/EC₅₀) − 1] where A is concentration of antagonist and EC₅₀ and EC₅₀¹, the concentrations of agonist required for half‐maximal response in absence or in presence of antagonist. Value of K_i, for cimetidine was 0.95 μM.

Figure 23.

Accumulation of cAMP in slices from guinea pig hippocampus induced by 2‐thiazolylethylamine (TEA), an H₁ agonist, in presence of dimaprit (DIM), an H₂ agonist. The various agonists were added together at beginning of 15‐min incubation. Accumulation of cAMP elicited by TEA in various concentrations was checked alone or together with 10⁻⁴ M DIM. Mepyramine (MEP) was added 10 min before the 2 agonists. In presence of DIM, EC₅₀ of TEA is 60 μM, which corresponds to a potency relative to histamine that is close to that found in peripheral H₁ receptor systems.

From Palacios et al. 207

Figure 24.

Restoration of H₁ receptor‐mediated effect by addition of Ca²⁺ in guinea pig hippocampal slices. Slices were prepared in normal Krebs‐Ringer solution, preincubated 30 min at 37°C and then washed 4 times with a Ca²⁺‐free Krebs‐Ringer solution. Aliquots were then incubated 15 min with increasing concentrations of Ca²⁺, and a further 15‐min incubation was performed in presence of 100 μM dimaprit (DIM) and 1 μM 2‐thiazolylethylamine (TEA).

Figure 25.

Time course of [³H]glycogen synthesis and histamine‐induced hydrolysis in slices from mouse cortex. Slices were incubated in presence of [³H]glucose. After 30 min (arrow) 10⁻⁴ M histamine was added to incubation medium.

From Quach et al. 232

Figure 26.

Inhibition by mepyramine (MEPY), an H₁ receptor antagonist, of histamine‐induced glycogenolysis in slices from mouse cortex. After 30‐min preincubation in presence of [³H]glucose, slices were incubated with increasing concentrations of histamine (HA) alone, or with mepyramine at various concentrations. Results are expressed as percentages of basal [³H]glycogen level. Inset, Schild plot of same data.

From Quach et al. 232

Figure 27.

Effect of histamine preincubation on histamine‐induced hydrolysis of [³H]glycogen in slices from mouse cortex. Slices were preincubated without (controls) or with 50 μM histamine for 20 min and washed 3 times; [³H]glycogen hydrolysis induced by histamine at indicated concentrations was then determined. Results expressed as percentages of basal [³H]glycogen levels: 20.2 ± 1.0 × 10³ dpmmg‐1 protein for controls and 20.9 ± 1.0 × 10³ dpm · mg⁻¹ protein for histamine‐incubated slices.

From Quach et al. 234

Figure 28.

Intracellular recording from dentate granule cell. A: membrane potential (68 mV) replayed from magnetic tape with increased speed so that fast voltage deflections are not visible. Histamine was applied by pressure ejection from micropipette in dendritic region ∼250 μM from soma layer. Bar above trace indicates 20‐ and 50‐mmHg ejection pressure. B‐D: expanded traces taken before, during, and after histamine action as indicated in A. Voltage deflections produced by constant‐current injection of ±0.5 nA or −0.1 to −2.0 nA and +0.1 to +0.5 nA. b‐d: Such deflections at an even more expanded time base (±0.5 nA and −2.0 nA).

From Haas 131

Figure 29.

Hypersensitivity to microiontophoretic applications of histamine and norepinephrine (noradrenaline) in cortical neurons of guinea pig brain after electrolytic lesion of medial forebrain bundle (MFB). Animals were anesthetized with urethan for iontophoresis experiments 8–20 days after unilateral lesion of MFB. Dose‐response curves were constructed by measuring change in firing levels effected by different ejecting currents as it reached plateau. Data shown were obtained from plateau responses of 2 neurons to histamine (left) and norepinephrine (right) in guinea pig sensorimotor cortex, which were recorded in immediate succession and with same micropipette on intact and lesioned side. Abscissa, ejecting current intensity in nA, except for negative values, which refer to retaining currents.

From Haas et al. 138

Figure 30.

Intracellular recording of neurosecretory neuron from paraventricular nucleus (PVN) in rat hypothalamic slice. Left: records illustrate spontaneous excitatory postsynaptic potentials (EPSPs) before, during, and after perfusion with histamine (10⁻⁵ M). Increased size and frequency of EPSPs indicates action of histamine on nearby interneurons rather than direct action on this cell membrane. Right: schematic drawing of experimental situation and response to injection of ±0.25 nA through recording electrode. Membrane potential and resistance were unchanged.

Figure 31.

Actions of histamine and impromidine on pyramidal neurons intracellularly recorded in CA1 area of rat hippocampal slices. Left: block of firing accommodation by 1 μM histamine, bath applied. In presence of histamine (lower left) same depolarizing current as in upper left (during time indicated by black bar) evokes many more action potentials, in absence of changes in basic membrane properties. Middle: Ca²⁺ spikes evoked by depolarizing current injection in absence (upper middle) and/or in presence (lower middle) of 1 μM impromidine in tetrodotoxin‐poisoned slice. Right: afterhyperpolarizations following these Ca²⁺ spikes. Long‐lasting component is markedly reduced by 1 μM impromidine. Results indicate that histamine (through H₂ receptors) blocks a Ca²⁺‐dependent K⁺ current without altering Ca²⁺ current.

Photomicrographs courtesy of Dr. H. Haas

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Jean‐Charles Schwartz, Monique Garbarg, Héléne Pollard. Histaminergic Transmission in the Brain. Compr Physiol 2011, Supplement 4: Handbook of Physiology, The Nervous System, Intrinsic Regulatory Systems of the Brain: 257-316. First published in print 1986. doi: 10.1002/cphy.cp010405

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