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PubMed1993

Potentiation of nerve growth factor-induced alterations in cholinergic fibre length and presynaptic terminal size in cortex of lesioned rats by the monosialoganglioside GM1.

The effect of monosialoganglioside GM1 and/or nerve growth factor treatment on the cholinergic innervation of the rat cortex was studied using both light- and electron-microscopic techniques assisted by image analysis. Adult male Wistar rats were unilaterally decorticated and received continuous infusions, via minipump, of vehicle, GM1 (1.5 mg/day) and/or nerve growth factor (12 micrograms/day) into the cerebroventricular space. Treatments were initiated immediately post-lesion and ended after seven days. Thirty days post-lesion (i.e. 23 days after the end of drug administration) brains were processed for choline acetyltransferase immunocytochemistry for either light- or electron-microscopic analysis. At this time-point choline acetyltransferase-immunoreactive neurons in the ipsilateral nucleus basalis magnocellularis were significantly reduced in size especially in the mid portion of this nucleus, in lesion vehicle-treated rats. Moreover, decreases in choline acetyltransferase immunoreactive fibre length (ranging from 31 to 50%) and varicosity number (ranging from 26 to 39%) occurred in all cortical layers within a portion of the remaining cortex of these animals. Monosialoganglioside GM1 or nerve growth factor treatment equally attenuated deficits in nucleus basalis magnocellularis cell size and cortical choline acetyltransferase immunoreactive fibre length. However, nerve growth factor, but not monosialoganglioside GM1 treatment also increased choline acetyltransferase-immunoreactive varicosity number above control levels. In lesioned rats which received both nerve growth factor and the monosialoganglioside GM1, the mean cross-sectional area of nucleus basalis magnocellularis cholinergic neurons did not differ significantly from control values. By contrast, cortical choline acetyltransferase-immunoreactive fibre length and varicosity number were significantly increased above control values and that induced by nerve growth factor treatment alone. Quantitative electron-microscopic analysis showed that cholinergic boutons in cortical layer V were considerably shrunken in lesioned vehicle-treated rats and that GM1 treatment failed to significantly attenuate this deficit. However, exogenous nerve growth factor provoked a significant increase (35% above control values) in cortical cholinergic presynaptic terminal size which was even further augmented by concurrent GM1 treatment (69% above control values). This trophic factor-induced increase in bouton size was confirmed using serial electron microscopy and computer-assisted three-dimensional reconstruction of the cholinergic varicosities. The number of synaptic contacts in cortical layer V was also found to be significantly reduced (45% of control values) in lesioned vehicle-treated rats but was maintained at control levels by exogenous GM1 treatment. In addition, a significant increase (95% above control levels) in the number of choline acetyltransferase-immunoreactive boutons with synaptic differentiations was noted in lesioned nerve growth factor-treated rats.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1989

The cytoskeletal architecture of the presynaptic terminal and molecular structure of synapsin 1.

We have examined the cytoskeletal architecture and its relationship with synaptic vesicles in synapses by quick-freeze deep-etch electron microscopy (QF.DE). The main cytoskeletal elements in the presynaptic terminals (neuromuscular junction, electric organ, and cerebellar cortex) were actin filaments and microtubules. The actin filaments formed a network and frequently were associated closely with the presynaptic plasma membranes and active zones. Short, linking strands approximately 30 nm long were found between actin and synaptic vesicles, between microtubules and synaptic vesicles. Fine strands (30-60 nm) were also found between synaptic vesicles. Frequently spherical structures existed in the middle of the strands between synaptic vesicles. Another kind of strand (approximately 100 nm long, thinner than the actin filaments) between synaptic vesicles and plasma membranes was also observed. We have examined the molecular structure of synapsin 1 and its relationship with actin filaments, microtubules, and synaptic vesicles in vitro using the low angle rotary shadowing technique and QF.DE. The synapsin 1, approximately 47 nm long, was composed of a head (approximately 14 nm diam) and a tail (approximately 33 nm long), having a tadpole-like appearance. The high resolution provided by QF.DE revealed that a single synapsin 1 cross-linked actin filaments and linked actin filaments with synaptic vesicles, forming approximately 30-nm short strands. The head was on the actin and the tail was attached to the synaptic vesicle or actin filament. Microtubules were also cross-linked by a single synapsin 1, which also connected a microtubule to synaptic vesicles, forming approximately 30 nm strands. The spherical head was on the microtubules and the tail was attached to the synaptic vesicles or to microtubules. Synaptic vesicles incubated with synapsin 1 were linked with each other via fine short fibrils and frequently we identified spherical structures from which two or three fibril radiated and cross-linked synaptic vesicles. We have examined the localization of synapsin 1 using ultracryomicrotomy and colloidal gold-immunocytochemistry of anti-synapsin 1 IgG. Synapsin 1 was exclusively localized in the regions occupied by synaptic vesicles. Statistical analyses indicated that synapsin 1 is located mostly at least approximately 30 nm away from the presynaptic membrane. These data derived via three different approaches suggest that synapsin 1 could be a main element of short linkages between actin filaments and synaptic vesicles, and between microtubules and synaptic vesicles, and between synaptic vesicles in the nerve terminals.(ABSTRACT TRUNCATED AT 400 WORDS)

Actins↗

PubMed1983

Immunocytochemical evidence for tubulin in the presynaptic terminal of synaptosomes.

Ultrastructural studies of intact tissue rarely show presynaptic microtubules, and immunocytochemical studies on tissue sections have previously been unable to demonstrate tubulin in the nerve terminal. In contrast, a microtubular coil can be readily detected in the presynaptic nerve terminal of synaptosomes. We have developed an immunocytochemical procedure on the synaptosome preparation and demonstrated, using monoclonal antibodies, that in the presynaptic terminal alpha and beta tubulin subunits are specifically restricted to the equatorial microtubular coil.

Animals↗

PubMed1990

Quantitative immunohistochemistry of synaptophysin in human neocortex: an alternative method to estimate density of presynaptic terminals in paraffin sections.

Currently available specific synaptic markers have made it possible to estimate the synaptic density by immunochemical techniques. In the present study we labeled the neocortical presynaptic terminals in histological sections of human autopsy tissue with a monoclonal antibody against synaptophysin. The characteristic granular neuropil reaction was quantified by measuring the average optical density (OD) in the different layers of the parietal cortex with the aid of image analysis equipment. The raw neuropil OD was corrected by subtracting the OD of the white matter in the same section. Our study showed that consistent microdensitometric results can be obtained on 5-microns paraffin sections from specimens with less than 8 hr of post-mortem time before fixation, incubated with 5 micrograms/ml of anti-synaptophysin. The corrected OD measurements were slightly larger in neocortical layers II, III, and V than in layers I, IV, and VI, but the differences were not statistically significant. In area 17, layer IV was denser than the others. We conclude that with certain precautions this method can be used to measure relative amounts of synaptophysin-like immunoreactivity and to infer the density of presynaptic boutons in human situations and in animal models.

Aged↗

PubMed1986

Increased Ca-uptake of presynaptic terminals during long-term potentiation in hippocampal slices.

A combined electrophysiological and neurochemical study was performed on the CA1 area of hippocampal slices in an attempt to identify changes in presynaptic nerve terminal function in long-term potentiation (LTP). After controlled induction of LTP in CA1, the activated region was subjected to subcellular fractionation followed by 45Ca2+ uptake determinations. Synaptosomes prepared from slices in which LTP has been induced showed a faster risetime and a higher level of saturation for K+-induced Ca-uptake than those derived from unstimulated and stimulated control slices. These findings point to a participation of presynaptic terminals in long-term potentiation.

Animals↗

PubMed1999

Two components of transmitter release from the chick ciliary presynaptic terminal and their regulation by protein kinase C.

1. A study was made of the effects of phorbol ester (phorbol 12-myristate 13-acetate, PMA, 0.1 microM) on the two components of evoked transmitter release, namely the fast synchronous and the slow asynchronous components, from the giant presynaptic terminal of the chick ciliary ganglion. The excitatory postsynaptic currents (EPSCs) were recorded under whole-cell voltage clamp of the postsynaptic neuron. 2. The decay time constant of the slow component was prolonged by replacing Ca2+ with Sr2+. In 5 mM [Sr2+]o the fast component decayed with a time constant of 2.6 +/- 1.4 ms whereas the slow component decayed with a time constant of 19 +/- 7 ms. 3. When stimulated with twin pulses with a short interpulse interval, the fast component of the second EPSC was often depressed whereas the slow component was usually facilitated. Both components were positively dependent on [Sr2+]o in a saturable manner, but the fast component approached its maximum at a lower [Sr2+]o than the slow component. 4. PMA potentiated both the fast and slow components to a similar extent and with a similar time course. For each component, the effect of PMA was less potent at high [Sr2+]o than at low [Sr2+]o. For either the fast or the slow component the PMA-induced potentiation was accompanied by a reduction in the paired-pulse ratio (PPR). 5. Despite the different dissociation constant for dextran-conjugated fura-2, the fluorescent ratio for intraterminal [Sr2+] ([Sr2+]i) decayed to the baseline after the nerve-evoked increment with a time course similar to that for [Ca2+]i, suggesting that intraterminal Sr2+ is buffered less efficiently than Ca2+. PMA did not increase the [Sr2+]i transients produced by stimulation of the presynaptic oculomotor nerve. 6. It is suggested that protein kinase C (PKC) modulates both the fast and slow components through common molecular mechanisms that upregulate the Sr2+ sensitivity of the vesicle fusion probability.

Algorithms↗

PubMed1981

Morphological alterations of Purkinje cell axons and presynaptic terminals in organotypic cerebellar cultures exposed to ionizing irradiation.

Ionizing irradiation induced marked morphological alterations in the Purkinje cell axons and axonic terminals in vitro. The myelinated segments demonstrated a very poor development of the myelin sheath. The axoplasm demonstrated various alterations of the mitochondria, and the smooth endoplasmic reticulum and the numerous elongated presynaptic terminals contained large aggregates of tubulovesicular structures and neurofilaments arranged in parallel and reticular array.

Animals↗

PubMed2000

Location of calcium transporters at presynaptic terminals.

The plasma membrane ATP-driven Ca2+ pump (PMCA) and the Na+/Ca2+ exchanger (NCX) are the major means of Ca2+ extrusion at presynaptic nerve terminals, but little is know about the location of these transporters relative to the major sites of Ca2+ influx, the transmitter release sites. We used immunocytochemistry to identify these transport proteins in a calyx-type presynaptic nerve terminal from the ciliary ganglion of the chick. The PMCA clusters were localized to the transmitter release sites, as identified by staining for the secretory vesicle-specific protein synaptotagmin I. This colocalization was not due to the presence of the pump on the secretory vesicle itself because membrane fractionation of chick brain synaptosomes demonstrated comigration of the pump with surface membrane and not vesicle markers. In contrast, the NCX did not colocalize with synaptotagmin but tended to be located at nonsynaptic regions of the terminal. The PMCA location, near the transmitter release sites, suggests that it plays a role in priming the release site by maintaining a low free Ca2+ level, facilitating the dissociation of the ion from its binding sites. The PMCA may also replenish external Ca2+ in the synaptic cleft following periods of synaptic activity. In contrast, the NCX location suggests a role in the rapid emptying of cytoplasmic Ca2+ uptake organelles which serve as the main line of defence against high free Ca2+.

Animals↗

PubMed2002

Calcium signaling at single mossy fiber presynaptic terminals in the rat hippocampus.

We investigated internal Ca(2+) release at mossy fiber synapses on CA3 pyramidal neurons (mossy fiber terminals, MFTs) in the hippocampus. Presynaptic Ca(2+) influx was induced by giving a brief train of 20 stimuli at 100 Hz to the mossy fiber pathway. Using Ca(2+) imaging techniques, we recorded the Ca(2+) response as DeltaF/F, which increased rapidly with stimulation, but was often accompanied by a delayed peak that occurred after the train. The rise in presynaptic [Ca(2+)] could be completely blocked by application of 400 microM Cd(2+). Furthermore, the evoked Ca(2+) signals were reduced by group II mGluR agonists. Under the same experimental conditions, we investigated the effects of several agents on MFTs that disrupt regulation of intracellular Ca(2+) stores resulting in depletion of internal Ca(2+). We found that ryanodine, cyclopiazonic acid, thapsigargin, and ruthenium red all decreased both the early and the delayed increase in the Ca(2+) signals. We applied D,L-2-amino-5-phosphonovaleric acid (D,L-APV; 50 microM) and 6,7-Dinitroquinoxaline-2,3-dione (DNQX; 20 microM) to exclude the action of N-methyl-D-aspartate (NMDA) and non-NMDA receptors. Experiments with alternative lower affinity indicators for Ca(2+) (fura-2FF and calcium green-2) and the transient K(+) channel blocker, 4-aminopyridine were performed to control for the possible saturation of fura-2. Taken together, these results strongly support the hypothesis that the recorded terminals were from the mossy fibers of the dentate gyrus and suggest that a portion of the presynaptic Ca(2+) signal in response to brief trains of stimuli is due to release of Ca(2+) from internal stores.

2-Amino-5-phosphonovalerate↗

PubMed1990

Linear feedback control of acetylcholine level in the presynaptic terminal.

A dynamic analysis of acetylcholine (ACh) level during nervous signal transmission was performed by means of computer simulation. The rate equation expressed in a system of non-linear ordinary differential equations represents the dynamic aspects of the fundamental metabolic processes in the chemical transmission at the synapse in terms of the relevant metabolite fluxes and the reactions of choline acetyltransferase, ACh receptor and acetylcholinesterase functioning in two putative homogeneous and open compartments. After a transmitter release, the ACh level in the presynaptic terminal cannot be restored by supplying the substrates of acetyl-CoA (AcCoA) and choline (Ch) at constant influx rates for ACh synthesis. A simple regulatory mechanism of linear feedback of the ACh level for variation of the substrate influx rates can accomplish the desired replenishment of ACh, in which the influx rate of AcCoA characterizes the response speed and its ratio to that of Ch governs the maintenance of the ACh level. The CoA level is ineffective for this regulatory mechanism.

Acetylcholine↗

PubMed1969

An effect of postsynaptic neurons upon presynaptic terminals.

Centrifugal ("antidromic") discharges in cat sensory fibers are observed consistently in a variety of experimental preparations and with many different surgical and recording techniques. As is well known, they can be either "spontaneous" or induced by afferent volleys in other sensory fibers. In addition, it is shown here that they can be elicited by antidromic motoneuron activation when the latter is conditioned by natural sensory stimuli or by shocks to the dorsal roots. The latency of the centrifugal dorsal root response to ventral root stimulation is shorter than that of the monosynaptic reflex mediated by the same fibers. An "antidromic" coupling, probably of an electrical nature, between motoneurons and presynaptic terminals is postulated.

Animals↗

PubMed1986

Presynaptic terminals persist following degeneration of "flight" muscle during development of a flightless grasshopper.

We have studied the development of a neuromuscular system for which mature function has been lost through evolution in the grasshopper, Barytettix psolus (Cohn and Cantrall, 1974). Barytettix is flightless throughout life and has only vestigial wings that are incapable of active movement. Adult Barytettix lack muscles homologous to the indirect flight muscles of locusts and grasshoppers that fly, while other thoracic muscles are similar. We have found, using light and electron microscopic examination of tissues from various developmental stages, that the metathoracic dorsal longitudinal muscle is present and is innervated during nymphal life but is absent in adults. Yet its nerve persists and, in the adult, contains axonal presynaptic specializations opposite inappropriate targets such as glial processes and basal lamina. Our findings indicate that selective muscle death during development is one mechanism underlying the reduction of the flight system of Barytettix through evolution. The finding that presynaptic terminals persist in the absence of the muscle indicates that the muscle and its innervation follow programs of development that are at least partially independent and reinforces the concept that in insects motorneurons, and perhaps neurons in general, are not dependent upon trophic influences from their targets for survival and maintenance of their differentiated phenotype.

Animals↗

PubMed2002

High-resolution localization of clathrin assembly protein AP180 in the presynaptic terminals of mammalian neurons.

Synaptic vesicles (SVs) assemble at the presynaptic compartment through a clathrin-dependent mechanism that involves one or more assembly proteins (APs). The assembly protein AP180 is especially efficient at facilitating clathrin cage formation, but its precise ultrastructural localization in neurons is unknown. Using immunoelectron microscopy, we demonstrate the presynaptic localization of AP180 in axon terminals of rat cerebellar neurons. In contrast, the assembly protein AP2 was associated with both the presynaptic plasma membrane and the cytosolic side of the membrane at postsynaptic and extrasynaptic sites. Furthermore, ultrastructural analysis of primate retina showed that AP180 immunoreactivity was preferentially and highly enriched at ribbon synapses, where glutamate is released tonically at high levels and rapid vesicle turnover is essential. To maintain functional synaptic transmission, neurotransmitter-filled SVs must be readily available, and this requires proper reassembly of new vesicles. The expression of AP180, in addition to AP-2, in the clathrin-mediated endocytic pathway might add another level of control to SV reformation for efficient assembly of clathrin, effectively controlling the size of assembled vesicles and faithfully recovering SV-specific components.

Adaptor Protein Complex 2↗

PubMed1986

Synaptic transmission in amphibian retinae during conditions unfavourable for calcium entry into presynaptic terminals.

Toad (Bufo marinus) retinae were peeled from the pigment epithelium and superfused over the photoreceptor surface with a calcium-poor, cobalt-rich medium. The shape of the electroretinogram indicated that post-synaptic neurones received synaptic input. Adding the putative transmitters glutamate and N-acetylhistidine changed the shape of the electroretinogram. The change suggests that an excess of the putative transmitters blocked a component of synaptic transmission that persisted when a retina was bathed in cobalt. Salamander (Ambystomatigrinum) retinae in hemisected eye cups were superfused over their vitreal surface. Intracellular responses were recorded from photoreceptors. Reducing the calcium concentration in the superfusing medium from 1 mM to less than 10 microM slowly changed responses produced by light. The change indicates that the calcium concentration in the extracellular space surrounding photoreceptors fell to less than 100 microM. When retinae were superfused with a medium containing 1 mM-calcium, 3 mM-barium, and 10 mM-tetraethylammonium (TEA), rods produced action potentials that were later blocked by adding 1 mM-cobalt. Blocking calcium channels with cobalt and lowering the extracellular calcium concentration should together block calcium-dependent synaptic transmission. Intracellular responses were recorded from horizontal cells. After replacing external calcium with cobalt the membrane potential hyperpolarized and responses produced by light became smaller but did not entirely disappear. The responses that remained were less sensitive to light and had an altered shape. The change was reversible. Similar responses could be recorded after prolonged (30-120 min) exposure to cobalt. Electrical synapses between horizontal cells were uncoupled by adding 10 microM-forskolin to the cobalt medium. The polarity of a response could then be reversed if a cell was depolarized by injecting current. The observation of a reversal potential demonstrates that the response was produced by a conductance change. Intracellular responses were recorded from depolarizing and hyperpolarizing bipolar cells while retinae were superfused with cobalt-rich medium. After changing to a cobalt-free medium containing 1 mM-calcium, responses produced by light were slightly smaller. Large responses were recorded after superfusing with cobalt-rich, calcium-poor medium for 30-120 min. The results indicate that synaptic transmission by photoreceptors continues during conditions expected to block the entry of calcium into their presynaptic terminals.

Ambystoma↗

PubMed1969

Tetrodotoxin-resistant electric activity in presynaptic terminals.

1. The electric properties of the giant synapse in the stellate ganglion of the squid have been further investigated.2. During tetrodotoxin (TTX) paralysis, a local response can be elicited from the terminal parts of the presynaptic axons after intracellular injection of tetraethyl ammonium ions (TEA).3. The response is characterized by an action potential of variable size and duration, whose fall is often preceded by a prolonged plateau. The response, especially the duration of the plateau, is subject to ;fatigue' during repetitive stimulation.4. The TTX-resistant form of activity is localized in the region of the synaptic contacts, and shows a marked electrotonic decrement even within less than 1 mm from the synapse. It is found only on the afferent, not on the efferent, side of the synapse.5. During the plateau of the response, the membrane resistance is greatly reduced below its resting value.6. The response depends on presence of external calcium and increases in size and duration with the calcium concentration. Strontium and barium substitute effectively for calcium. Manganese and, to a lesser extent, magnesium, counteract calcium and reduce the response. The response also declines, and ultimately disappears, if sodium is withdrawn for long periods.7. The relation of the local TTX-resistant response to the influx of calcium ions and to the release of the synaptic transmitter is discussed.

Action Potentials↗

PubMed1978

Voltage sensitive calcium channels in the presynaptic terminals of a decrementally conducting photoreceptor.

1. Intracellular recordings were made from the presynaptic regions of the photoreceptors of the median ocellus of the giant barnacle, Balanus nubilus.2. Millivolt changes in membrane potential near the dark resting level in the terminals elicit post-synaptic activity and consequently must be sufficient to modulate transmitter release from these endings.3. In normal saline the terminal voltage usually changes in a graded manner to increasing intensities of illumination of the cell. When the terminal region is superfused with saline containing TEA, 3-AP or high concentrations of K, an all-or-none action potential can be elicited consistently by light or injected current.4. The peak value of this action potential depends on the Ca concentration in the saline. The action potential can be generated if Sr or Ba ions replace Ca, but is reduced or blocked if Mg, Co, or Mn ions are added to the saline. It is virtually unaffected by TTX or replacement of Na with TMA ions in the saline. These results suggest that Ca carries most or all of the inward current during the action potential.5. The action potential is followed by a large undershoot which can last several seconds. The amplitude and duration of the action potential and the duration of the undershoot all grow in increasing concentrations of TEA up to 400 mM, the highest concentration tested. The threshold for the action potential decreases as the concentration of TEA is increased to 10 mM; increasing the concentration further has no effect on the threshold. These observations suggest that TEA blocks a voltage-sensitive potassium conductance at low concentrations but has less effect on the current responsible for the undershoot.6. Electrophysiological and pharmacological evidence suggests that the Ca channels are concentrated in the presynaptic terminals of this photoreceptor.

Action Potentials↗

PubMed2002

A metabotropic glutamate receptor regulates transmitter release from cone presynaptic terminals in carp retinal slices.

The role of group III metabotropic glutamate receptors (mGluRs) in photoreceptor-H1 horizontal cell (HC) synaptic transmission was investigated by analyzing the rate of occurrence and amplitude of spontaneous excitatory postsynaptic currents (sEPSCs) in H1 HCs uncoupled by dopamine in carp retinal slices. Red light steps or the application of 100 microM cobalt reduced the sEPSC rate without affecting their peak amplitude, which is consistent with hyperpolarization or the suppression of Ca(2+) entry into cone synaptic terminals reducing vesicular transmitter release. Conversely, postsynaptic blockade of H1 HC AMPA receptors by 500 nM CNQX reduced the amplitude of sEPSCs without affecting their rate. This analysis of sEPSCs represents a novel methodology for distinguishing between presynaptic and postsynaptic sites of action. The selective agonist for group III mGluRs, l-2-amino-4-phosphonobutyrate (L-APB or L-AP4; 20 microM), reduced the sEPSC rate with a slight reduction in amplitude, which is consistent with a presynaptic action on cone synaptic terminals to reduce transmitter release. During L-APB application, recovery of sEPSC rate occurred with 500 microM (s)-2-methyl-2-amino-4-phosphonobutyrate (MAP4), a selective antagonist of group III mGluR, and with 200 microM 4-aminopyridine (4-AP), a blocker of voltage-dependent potassium channels. Whole-cell recordings from cones in the retinal slice showed no effect of L-APB on voltage-activated Ca(2+) conductance. These results suggest that the activation of group III mGluRs suppresses transmitter release from cone presynaptic terminals via a 4-AP-sensitive pathway. Negative feedback, operating via mGluR autoreceptors, may limit excessive glutamate release from cone synaptic terminals.

Animals↗

PubMed1995

Potentiation of Ca2+ transients in the presynaptic terminals of goldfish retinal bipolar cells.

1. To study a possible contribution of intracellular Ca2+ stores to the presynaptic Ca2+ regulation, the Ca2+ current (ICa) and the intracellular free Ca2+ concentration ([Ca2+]i) were simultaneously monitored in isolated goldfish retinal bipolar cells using the whole-cell voltage clamp procedure and fura-2 fluorimetry. 2. The Ca2+ transient triggered by the activation of ICa was potentiated when [Ca2+]i was increased by applying either a prepulse or a small steady depolarization. The potentiation seemed to be partly due to the release of Ca2+ from intracellular Ca2+ stores. 3. The intracellular Ca2+ release was reversibly inhibited by caffeine but was not affected by ryanodine, suggesting that Ca2+ is released through intracellular Ca2+ channels which differ from ryanodine receptor channels. 4. These results suggest that the intracellular Ca2+ release may contribute to the facilitation of transmitter release.

Animals↗