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T Smock

Publications and source records attributed to T Smock.

At least 19 recordsLinked to original sources
PubMed1998

The medial amygdaloid nucleus modifies social behavior in male rats.

Electrical stimulation of the medial amygdaloid nucleus (AME) produces a behavioral state in male rats that resembles the postejaculatory interval, but electrical recording from cells in the AME shows that they become active earlier in sexual behavior, around the time that the male first appears to become aware of estrus in the female. In an attempt to resolve which feature of sexual behavior was mediated by the AME, we stimulated the structure bilaterally in freely behaving males using voltage levels too low to produce the postejaculatory interval. We found that electrical activation of this kind facilitated sexual behavior when it would not otherwise occur (i.e., in the presence of a nonestrous female). However, the stimuli suppressed sexual behavior when it would normally occur (i.e., in the presence of a nonestrous female). We discuss alternative interpretations of the results in the context of a general model for the central organization of sexual behavior in males.

Amygdala↗
PubMed1998

A peptidergic basis for sexual behavior in mammals.

Vasopressin (VP) is a peptide neurotransmitter in the limbic system of rats. It is synthesized in the medial amygdaloid nucleus in the presence of sex steroids, transported to other limbic structures such as the hippocampus and septum and secreted there by a calcium-dependent process. In the hippocampus, VP acts on cerebral microvessels and local circuit interneurons. Its excitatory action on the inhibitory interneurons produces near-total shutdown of electrical activity of the efferent fibers of pyramidal cells, the projection neurons of the hippocampus. Stimulation of the medial amygdala and release of the endogenous VP duplicates these effects and, since they are blocked by ventricular application of a VP antagonist, the effects are almost certainly mediated by endogenous VP. Recording from the VP-containing cell bodies or of the hippocampal action of the peptide indicates that the system is selectively involved with the early stages of sexual behavior, specifically those appetitive behaviors that anticipate coitus. Stimulation of the VP cells produces alterations in sexual behavior in a manner consistent with the hypothesis that the medial amygdala organizes the appetitive phase of recognition of an appropriate partner and sexual arousal. This role for the medial amygdala complements the proposed role of nearby structures in the consummatory, reward and learned aspects of sexual behavior. Association between VP, oxytocin (OT) and homologs with sexual behavior is very widespread among vertebrates, including amphibians, reptiles, primates and humans. Humans and other primates display a phenomenon called 'concealed ovulation' that may have played a role in the evolution of social structures. The review concludes with a discussion of possible experimental strategies for evaluating the possible role of VP in concealed ovulation and other conditions in which sexual behavior occurs outside of estrus.

Animals↗
PubMed1997

Orthodromic activation of peptidergic cells in the medial amygdala.

Electrical recordings from vasopressin-containing cells in the medial amygdala were obtained. Electrical stimulation of one major afferent structure, the accessory olfactory bulb, invariably elicited single unit discharge in the peptidergic cells and set up a field potential indicating widespread excitation in the structure. Pheromonal stimuli, normally borne into the brain by the accessory olfactory bulb, were ineffective in activating the medial amygdala. These results in combination with preexisting research suggest that the accessory olfactory bulb is an important influence, but not the only influence, on the activity of the peptidergic cells.

Action Potentials↗
PubMed1996

The output of the hippocampus is inhibited during social behavior in the male rat.

During sexual behavior in the male rat, peptidergic cells in the medial amygdaloid nucleus become active and release a vasopressin-like peptide. The present experiments were designed to examine hippocampal changes as a result of this peptide's action during sexual behaviors. Chronic field-potential recordings from the hippocampus of male rats were acquired in a wide variety of social and nonsocial circumstances. Hippocampal responses that resemble the known action of the vasopressin-like peptide were seen only with social stimuli such as sexual stimuli and stimuli that led to aggressive behavior between males. The results show that the occasions of peptide action in the hippocampus correlate with the occasions of peptide release as determined by recording from the peptidergic cell bodies. The results are interpreted to indicate that the amygdala projection to the hippocampus has a special role to play in social behavior.

Animals↗
PubMed1995

Interaction between long-term potentiation and the action of a peptide transmitter.

The interaction between long-term potentiation (LTP) and the action of a peptide transmitter was examined with evoked field potential recording in the CA1 region of the hippocampus in anesthetized male rats. The peptide transmitter transiently reversed and opposed the effects of LTP, and LTP reversed the action of the peptide transmitter. Because the peptide transmitter is released and has action particularly during sexual behaviors, the results are interpreted to mean that any memory trace encoded by potentiating mechanisms in the rat hippocampus is probably not accessible in the 20-30-min period of time surrounding reproductive activity in male rats.

Afferent Pathways↗
PubMed1994

Activity of peptidergic neurons in the amygdala during sexual behavior in the male rat.

The medial amygdaloid nucleus (AME) occupies a central position in the circuitry that organizes sexual behavior in the male rat. It receives a projection from olfactory structures that are activated by pheromonal cues indicating receptivity in the female and projects in turn to limbic and hypothalamic structures that are thought to organize aspects of coitus. Electrical stimulation of the AME elicits a behavioral state that is indistinguishable by several measures from the post-ejaculatory interval. We used chronic single-unit recording techniques to determine the behavioral conditions in which the AME is normally active. We found that the cells indeed fired selectively during the presence of a receptive female, but that the discharge considerably anticipated copulation in time. We propose that sexual behavior in the male rat is a reaction chain of fixed action patterns, each one acting as a releaser for the next. The AME mediates an early event in the reaction chain, namely recognition of the receptive female, but electrical activation of the AME causes the reaction chain to proceed to its culminating behavior, the post-ejaculatory interval.

Amygdala↗
PubMed1993

Antidromic activation of a peptidergic pathway in the limbic system of the male rat.

Stimulation of the medial amygdaloid nucleus (AME) produces a long-latency and long-lasting inhibition of pyramidal cells in both the dorsal and the ventral hippocampus. The inhibition is blocked by a specific antagonist to vasopressin, which is a candidate neurotransmitter in the system. Antidromic activation of the AME from the hippocampus occurs with a latency suggestive of the conduction velocity of small diameter unmyelinated fibers. Immunocytochemistry for vasopressin reveals small diameter, unmyelinated immunoreactive fibers in the vicinity of the stimulating electrode in the hippocampus, and immunoreactive cell bodies in the vicinity of the recording electrode in the AME.

Amygdala↗
PubMed1993

An inexpensive microdrive for chronic single-unit recording.

A microdrive and microelectrode costing about $2.67 is described. The assembly is lightweight, compact, and versatile and is ideal for chronic single-unit recording from behaving rats. It is easy to assemble and operate and has been used successfully by undergraduates in the teaching and research laboratory.

Animals↗
PubMed1992

A peptidergic circuit for reproductive behavior.

A projection from the medial amygdaloid nucleus to the hippocampus and septum probably uses vasopressin as a transmitter. The nucleus synthesizes vasopressin and activation of the nucleus has a hippocampal effect that is completely blocked by a vasopressin antagonist. The afferent and efferent projections of this peptidergic nucleus suggest a possible role for the system in sexual behavior. Stimulation of the nucleus inhibits the output of the hippocampus in both genders and reorganizes behavior for a period of 15-20 min. In males, the effect of peptidergic activation is to produce a behavior that resembles the post-ejaculatory interval in coitus. This state is characterized by an EEG that resembles slow-wave sleep and by ultrasonic vocalizations at a characteristic frequency of 22 kHz. Castration in either gender causes depletion of the peptide from the target fields and eliminates the peptidergic signal in the hippocampus after about 15 weeks. The effects of castration in males can be reversed by testosterone replacement. The fluctuation of estrogen levels in rat plasma during the estrus cycle happens too quickly to impact the peptidergic system, and thus there is no significant change in the strength of the peptidergic signal among the proestrus, estrus, metestrus and diestrus stages. This fact permits study of the physiology of the system without concern for stage of estrus but does not permit conclusions regarding its function in females.

Amygdala↗
PubMed1990

Peptidergic transmission in the brain. I. Vasopressin-like signal in the hippocampus.

Studies of the action of arginine vasopressin (AVP) in the rat hippocampal slice have produced a model of the peptide's neural action. AVP excites local circuit inhibitory interneurons and causes consequent inhibition of pyramidal cells that is apparent as a reduction in the amplitude of the evoked population spike in field potential recording. Here we show that applied AVP does the same thing to the evoked population spike in the whole animal. Then we show that stimulation of the source of hippocampampal AVP, the medial amygdaloid nucleus, also inhibits the evoked population spike. Analysis of the synaptic potential indicates that the same mechanisms are employed by exogenously applied and endogenously released peptide. The inhibition can only be obtained by stimulating those brain structures known to project vasopressin fibers to the hippocampus. The stimulus-response characteristics and kinetics of the endogenous signal correspond to the properties of peptidergic signals in simple systems. The results are taken to support a transmitter role for AVP in the rat hippocampus.

Action Potentials↗
PubMed1990

Peptidergic transmission in the brain. II. Mediation by a vasopressin-like peptide.

The medial amygdaloid nucleus (AME) sends a projection of fibers containing a peptide similar to arginine vasopressin (AVP) to the rat hippocampus. Electrical stimulation of the AME has an impact on evoked hippocampal field potentials that is identical to the effect obtained by applied AVP in vitro or in vivo. Here we show that the AVP-like peptide released by AME stimulation has action that is blocked by a structural AVP analog. The antagonist specificity suggests that the native transmitter is a peptide similar, but not identical, to AVP. We conclude that the AME projection to the hippocampus satisfies all the criteria for recognition as a central peptidergic system important in the generation of behavior.

Amygdala↗
PubMed1989

Microvascular spasm is mediated by vasopressin fibers in the rat hippocampal slice.

Microvessels in the rat hippocampal slice can be used as an in vitro model for the study of cerebral vasospasm. Serum from coagulated blood causes prompt and long-lasting microvascular constriction that is neurogenic in nature. Here we show that a candidate spasmogen, thromboxane B2, has excitatory action on neural elements in the slice. However, spasmogenic serum lacks this excitatory effect. Instead, it is inhibitory for a major population of slice neurons. Thus, neurogenic microvascular spasm is produced by a subpopulation of slice neurons or projection fibers, not all neurons acting in concert. Arginine vasopressin (AVP) is contained in fibers that project to the hippocampus, and hippocampal microvessels contain pressor (V1) receptors for the peptide. AVP causes vasoconstriction in the slice, and a specific V1 antagonist for the peptide blocks the microvascular spasm induced by blood serum. The results are interpreted to mean that neurogenic microvascular spasm is mediated by locally released AVP.

Animals↗
PubMed1988

A mechanism for vasopressin action in the hippocampus.

The action of arginine vasopressin (AVP) in the rat hippocampal slice has been extensively studied. Extracellular recording indicates that the peptide excites spontaneously active neurons in the slice, though uncertainty exists regarding the identity of this cell type. Intracellular recording from pyramidal cells also reveals an excitatory action of the peptide, but these results are confounded by simultaneous constriction of small blood vessels that surround each pyramidal cell. Here we use field potential recordings to show that AVP inhibits pyramidal cell discharge and employs a pressor-type (V1) receptor to bring about its action. The results resolve issues regarding the identity of AVP targets in the slice. Each reported result is consistent with a model that posits direct AVP excitation of inhibitory interneurons and direct AVP constriction of slice microvessels. Inhibition of pyramidal cells recorded extracellularly and excitation of pyramidal cells recorded intracellularly are respective indirect consequences of the two direct effects.

Animals↗
PubMed1987

Neurogenic mediation of serum-induced microvascular constriction.

We have used the rat hippocampal slice preparation as a model system for the study of microvascular vasospasm. Penetrating cerebral microvessels in the slice constrict in response to a variety of stimuli, including serum from coagulated blood. Microvascular responses to many stimuli are associated with changes in the activity of nearby neurons, and in some cases can be shown to be neurogenically mediated. Here we use the selective neurotoxin, tetrodotoxin (TTX), to show that serum-induced constriction is also neurogenically mediated. This neural regulation of microvessel caliber may participate in pathological vasoconstriction mechanisms in the whole animal.

Action Potentials↗
PubMed1987

Blood-borne factors regulating microvascular constriction in the rat hippocampal slice.

Previous work shows that blood serum contains a factor that elicits constriction of large cerebral arteries and may be responsible for cerebral vasospasm in subarachnoid hemorrhage patients. However, few studies have considered the action of potential spasmogens on intraparenchymal resistance vessels. We used a common preparation for neurophysiology, the rat hippocampal slice, to study penetrating arterioles and their response to a variety of potential vasoconstrictors. Dilute serum from clotted rat blood evoked profound microvascular constriction when applied to the slice, but plasma incubated with heparin to prevent coagulation was unable to do so. A variety of potential vasoconstrictor substances were tested to see if they could duplicate the effects of serum. Norepinephrine (10 microM), serotonin (one microM) and prostaglandin E2 (one nM) were ineffective in this regard. However, when a stable eicosanoid, thromboxane B2, was applied at a concentration achieved in the cerebrospinal fluid of subarachnoid hemorrhage patients, it duplicated a portion of the vasoconstriction produced by serum. It is concluded that thromboxane B2 may account for part of the spasmogenic property of serum and that unidentified molecules in the coagulation pathway may also play a role.

Animals↗
PubMed1987

Vasoconstriction and neural excitation in response to transient hypoxia in the rat hippocampal slice.

The vascular and neural responses to transient hypoxia in the rat hippocampal slice were studied. Neural hyperexcitability produced by tissue hypoxia was associated with localized decreases in the diameter of precapillary arterioles. Vasoconstriction occurred periodically along the length of vessels observed. The mean percent decrease in vessel diameter in these narrowed regions was 10.25%. Population spikes recorded in the cell body layer of the dentate gyrus showed a mean increase in amplitude of 71.3%. The mean latency to peak response was similar for both the vessels and neurons. The results suggest mechanisms by which autoregulatory influences on microvessel caliber may be counteracted in conditions of hypoxia and hypotension in the whole animal.

Animals↗
PubMed1987

Action of vasopressin on neurons and microvessels in the rat hippocampal slice.

Arginine vasopressin is reported to have an excitatory effect on hippocampal neurons in the slice preparation. However, vasopressin also has a classic vasopressor action on mammalian blood vessels. We used the rat hippocampal slice to examine the effects of this peptide on central neural and vascular targets. The hippocampus is densely vascularized and pyramidal cells are enmeshed in a network of microvessels. Vasopressin increased the excitability of impaled neurons without substantially altering membrane potential or resistance. The peptide also caused pronounced vasoconstriction in penetrating microvessels when applied at micromolar concentrations. The concerted action of vasopressin on neurons and blood vessels and the physical proximity of these cell types suggest mechanisms whereby these responses may be associated.

Action Potentials↗