NEU200: Unit 2 Key Terms

Autonomic Nervous System

Division of the peripheral nervous system that regulates involuntary physiological functions and coordinates the body's internal state in response to different situations. It controls visceral organs, glands, blood vessels, and other targets, helping prepare the body for emotional and motivational states. Its two major divisions are the sympathetic nervous system (fight or flight) and parasympathetic nervous system (rest and digest). It is distinct from the somatic motor system, which controls skeletal muscles.

Parasympathetic Nervous System

Division of the autonomic nervous system responsible primarily for rest, digestion, energy conservation, and routine maintenance of the body. It generally decreases heart rate, stimulates digestive activity and glandular secretion, and promotes bladder emptying. It has long preganglionic neurons originating in the brainstem and sacral spinal cord, which synapse in ganglia located near or within target organs, followed by short postganglionic neurons. It primarily uses acetylcholine (ACh) as its neurotransmitter at both autonomic ganglia and target organs.

Parasympathetic Ganglia

Collections of postganglionic neuron cell bodies located near or within the organs they innervate. They receive signals from long preganglionic parasympathetic neurons, which release acetylcholine (ACh) onto nicotinic receptors. Short postganglionic neurons then typically release ACh onto muscarinic receptors at target organs, producing effects such as decreased heart rate and increased digestive activity. Their location near the target organs distinguishes them from most sympathetic ganglia, which lie closer to the spinal cord.

Neurotransmitter for Parasympathetic System (ACh)

Acetylcholine (ACh) is the neurotransmitter released by all parasympathetic preganglionic neurons and most parasympathetic postganglionic neurons. Preganglionic ACh activates nicotinic receptors on postganglionic neurons in parasympathetic ganglia, while postganglionic ACh generally activates muscarinic receptors on target organs. These interactions mediate parasympathetic effects such as slowing heart rate, stimulating digestion, and promoting glandular secretion.

Sympathetic Nervous System

Division of the autonomic nervous system responsible for mobilizing physiological resources during stressful or demanding situations, commonly called the fight-or-flight system. It generally increases heart rate, dilates airways, mobilizes energy, redirects blood flow toward skeletal muscles, stimulates sweating and piloerection, and suppresses some digestive and urinary functions. It has short preganglionic neurons originating in the thoracic and upper lumbar spinal cord, which synapse in ganglia near the spinal cord, followed by generally long postganglionic neurons that project to target organs. Its preganglionic neurons release acetylcholine (ACh), while most postganglionic neurons release noradrenaline (norepinephrine).

Sympathetic Ganglia

Collections of postganglionic neuron cell bodies that relay signals from sympathetic preganglionic neurons to target organs. They include paravertebral ganglia arranged in paired chains alongside the spinal cord and prevertebral ganglia located near major abdominal arteries. Short preganglionic sympathetic neurons release acetylcholine (ACh) onto nicotinic receptors in these ganglia; postganglionic neurons then generally release noradrenaline onto adrenergic receptors at target organs. Their proximity to the spinal cord distinguishes them from parasympathetic ganglia, which are located near or within target organs.

Neurotransmitters for Sympathetic System (ACh in Ganglia, Noradrenaline in End Organ)

Sympathetic preganglionic neurons release acetylcholine (ACh), which binds to nicotinic receptors on postganglionic neurons in sympathetic ganglia. Most sympathetic postganglionic neurons release noradrenaline (norepinephrine), which binds to adrenergic receptors on target organs and produces sympathetic responses such as increased heart rate and reduced digestive activity. Important exceptions include most sweat glands, which receive postganglionic sympathetic ACh acting on muscarinic receptors, and the adrenal medulla, which releases catecholamines into the bloodstream in response to preganglionic ACh.

Anterior Pituitary

Glandular portion of the pituitary gland, also called the adenohypophysis, located beneath the hypothalamus. It synthesizes and secretes hormones in response to hypothalamic releasing and inhibiting hormones transported through the hypophyseal portal circulation. Its major hormones include thyroid-stimulating hormone (TSH), growth hormone (GH), adrenocorticotropic hormone (ACTH), prolactin, luteinizing hormone (LH), and follicle-stimulating hormone (FSH). Unlike the posterior pituitary, the anterior pituitary produces its own hormones rather than simply storing and releasing hormones synthesized by hypothalamic neurons.

Posterior Pituitary

Neural portion of the pituitary gland, also called the neurohypophysis, connected to the hypothalamus by the pituitary stalk. It stores and releases vasopressin (antidiuretic hormone, ADH) and oxytocin, which are synthesized by hypothalamic magnocellular neurons and transported down their axons to the posterior pituitary. When these neurons become active, their axon terminals release the hormones into the bloodstream. Unlike the anterior pituitary, the posterior pituitary does not synthesize its own principal hormones.

Pituitary Hypophyseal Portal Vein

Part of the specialized vascular system connecting the hypothalamus to the anterior pituitary. Hypothalamic parvocellular neurosecretory neurons release regulatory hormones into capillaries at the median eminence; these hormones travel through hypophyseal portal veins to a second capillary network in the anterior pituitary, where they regulate hormone-secreting glandular cells. This system allows hypothalamic hormones to reach the anterior pituitary efficiently and regulate endocrine activity. It is distinct from the neural axonal pathway connecting magnocellular neurons to the posterior pituitary.

Hypothalamic Magnocellular Cells

Large neurosecretory neurons located primarily in the supraoptic and paraventricular nuclei of the hypothalamus. They synthesize the peptide hormones vasopressin and oxytocin, transport them along their axons through the pituitary stalk, and release them from terminals in the posterior pituitary into the bloodstream. Vasopressin contributes to water balance and blood pressure regulation, while oxytocin contributes to uterine contractions, milk ejection, and aspects of social behavior. Their direct axonal projections to the posterior pituitary distinguish them from parvocellular neurosecretory neurons, which regulate the anterior pituitary through the portal circulation.

Hypothalamic Parvocellular Cells

Smaller neurosecretory neurons located in several hypothalamic nuclei, including the paraventricular nucleus. They synthesize releasing and inhibiting hormones and project primarily to the median eminence, where their secretions enter the hypophyseal portal circulation and travel to the anterior pituitary. Examples include thyrotropin-releasing hormone (TRH) and growth hormone-releasing hormone (GHRH), which regulate the secretion of thyroid-stimulating hormone and growth hormone, respectively. Unlike magnocellular neurons, which release hormones through the posterior pituitary, parvocellular neurons primarily regulate anterior pituitary hormone secretion through the portal vascular system.

Vasopressin

Peptide hormone, also called antidiuretic hormone (ADH), synthesized primarily by magnocellular neurons in the hypothalamic supraoptic and paraventricular nuclei and released into the bloodstream from the posterior pituitary. It acts on V2 receptors in the kidney's collecting ducts to increase water reabsorption, helping regulate blood osmolality and blood volume, and on V1a receptors in blood vessels to promote vasoconstriction. The lecture also discusses vasopressin's proposed involvement in social bonding and pair-bonding behavior, including studies in voles. These behavioral effects vary by species, sex, receptor distribution, and context and should not be treated as a simple determinant of human monogamy.

Oxytocin

Peptide hormone synthesized primarily by magnocellular neurons in the hypothalamic paraventricular and supraoptic nuclei and stored and released by the posterior pituitary. It stimulates uterine contractions during labor and milk ejection during breastfeeding by acting on smooth muscle and mammary myoepithelial cells, respectively. The lecture also associates oxytocin release with physical touch, intimacy, and social bonding. Oxytocin additionally acts as a neuromodulator in the brain, influencing social behavior, although its effects depend on context and are not universally associated with increased trust or bonding.

Thyrotropin Releasing Hormone, Thyrotropin, Thyroxine

Thyrotropin-releasing hormone (TRH) is produced by hypothalamic parvocellular neurons and released into the hypophyseal portal circulation, where it stimulates anterior pituitary thyrotrophs to secrete thyroid-stimulating hormone (TSH), also called thyrotropin. TSH travels through the bloodstream to the thyroid gland and stimulates the synthesis and release of thyroid hormones, primarily thyroxine (T4) and also triiodothyronine (T3). Thyroid hormones regulate metabolic activity, growth, development, and thermogenesis. Circulating thyroid hormones provide negative feedback to the hypothalamus and anterior pituitary to regulate TRH and TSH secretion.

Growth Hormone Releasing Hormone, Growth Hormone

Growth hormone-releasing hormone (GHRH) is secreted by hypothalamic neurons and transported through the hypophyseal portal circulation to the anterior pituitary, where it stimulates somatotroph cells to release growth hormone (GH). GH enters the bloodstream and promotes growth, protein synthesis, and metabolic regulation, partly by stimulating the production of insulin-like growth factor 1 (IGF-1) in the liver and other tissues. GH secretion is also regulated by hypothalamic somatostatin, which inhibits its release, and by negative feedback involving GH and IGF-1.

Dorsolateral Hypothalamus

Region of the hypothalamus that the lecture associates with feeding motivation. In the animal stimulation experiments described, electrical stimulation of this region induced eating, and eating stopped when stimulation ceased. Lesions of the region reduced feeding and motivation to eat. The lecture emphasizes that hypothalamic stimulation generates a motivational state or drive to eat rather than directly producing the motor movements involved in eating. These findings are based on classical animal experiments and should be distinguished from the more complex neural circuits regulating human hunger.

Ventromedial Hypothalamus

Hypothalamic region associated in classical animal experiments with satiety and the suppression of feeding. Electrical stimulation of this region was reported to make animals stop eating and produce aversive responses to food, while lesions were associated with impaired satiety, excessive eating, and weight gain. The lecture presents it as functionally opposing the feeding-promoting effects of dorsolateral hypothalamic stimulation, illustrating how hypothalamic circuits contribute to the regulation of food intake. Modern research identifies additional roles in energy balance, glucose regulation, and defensive behavior, so it is not exclusively a satiety center.

Preoptic Nucleus

Group of nuclei in the anterior hypothalamus, including the medial preoptic area, associated with reproductive behavior, thermoregulation, and neuroendocrine regulation. The lecture emphasizes its role in sexual motivation and mating behavior, particularly findings from classical animal stimulation experiments, with some effects differing between males and females. The preoptic area also contains neurons involved in regulating body temperature and reproductive hormone secretion. Historical studies of anatomical variation and sexual behavior should be interpreted cautiously and do not establish a simple neural explanation of human sexual orientation.

Sham Rage

Pattern of exaggerated, apparently unprovoked rage-like behavior observed in classical animal experiments following particular forebrain lesions or disconnections that left hypothalamic and lower brain circuits intact. In the lecture's example, electrical stimulation of the posterior hypothalamus in cats elicited aggressive and defensive behaviors, which stopped when stimulation ended. These experiments suggested that hypothalamic and brainstem circuits can organize the physiological and behavioral components of rage, while intact forebrain circuits normally modulate or inhibit their expression. Sham rage demonstrates the distinction between generating an emotional or motivational state and executing the specific motor actions associated with it.

Amygdala

Collection of interconnected nuclei located in the medial temporal lobe, anterior to the hippocampus, involved in processing emotionally significant information, emotional learning, and coordinating behavioral and physiological responses. It receives sensory and cortical information and communicates with the hypothalamus and brainstem to influence autonomic and behavioral responses. The basolateral amygdala is particularly important in associative learning, including fear conditioning, while central amygdala circuits contribute to organizing defensive and autonomic responses. The lecture describes the amygdala as an emotional switchboard that helps recruit hypothalamic circuits to generate different emotional states. It participates in both positive and negative emotional processing and is not exclusively a fear center.

Kluver-Bucy Syndrome

Neurobehavioral syndrome classically observed in monkeys following bilateral removal or damage of the anterior temporal lobes, including the amygdala. The original experiments produced behavioral changes including psychic blindness (difficulty recognizing or assigning significance to visually perceived objects despite preserved basic vision), reduced fear and emotional reactivity, hyperorality (excessive oral exploration), altered feeding behavior, and hypersexuality. The findings demonstrated that temporal lobe structures contribute to visual recognition, emotional significance, and behavioral regulation. Later research helped identify the amygdala's role in emotional processing, although the full syndrome results from damage to a broader temporal lobe network rather than necessarily from isolated amygdala damage.

Fear Conditioning

Form of associative learning in which a previously neutral conditioned stimulus (CS), such as a light or tone, is repeatedly paired with an aversive unconditioned stimulus (US), such as a mild electric foot shock in animal experiments. Following learning, the conditioned stimulus alone can elicit a defensive response, such as freezing, even when the aversive stimulus is absent. The amygdala, particularly the basolateral complex, is important for acquiring and forming many conditioned fear associations, while central amygdala circuits help coordinate the resulting behavioral and autonomic responses. Classical experiments demonstrated that disrupting relevant amygdala circuits can impair fear conditioning. The lecture uses this phenomenon to illustrate how repeated associations can modify neural connections and produce learned emotional responses.

Capgras Syndrome

Delusional misidentification syndrome in which an individual believes that a familiar person, often a close family member, has been replaced by an identical-looking impostor. The lecture presents a proposed explanation involving disrupted communication between visual recognition systems in the temporal cortex and emotional processing circuits involving the amygdala. Under this account, the person can visually recognize a familiar face but fails to experience the normal emotional sense of familiarity associated with that person, contributing to the belief that the individual is an impostor. This illustrates the distinction between conscious visual recognition and emotional familiarity. The disconnection hypothesis is influential but is not a universal explanation; Capgras syndrome can arise in several neurological and psychiatric conditions.

Toxoplasmosis

Infection caused by Toxoplasma gondii, a protozoan parasite whose definitive hosts are felids, including domestic cats. The parasite can infect rodents and establish persistent cysts in the central nervous system. The lecture discusses animal research in which infected rodents showed altered avoidance of cat-associated odors, potentially increasing the probability of transmission to feline hosts. These behavioral changes have been associated with alterations in fear-related neural processing, including amygdala-related circuits, although the underlying mechanisms are complex and not attributable to a single brain structure. Human studies have investigated associations between T. gondii infection and behavioral or psychiatric outcomes, but such associations do not establish causation or demonstrate that the parasite reliably reduces human inhibition.

Nucleus Accumbens (and its Relation to Dopamine, Reward, and Addiction)

Structure within the ventral striatum of the basal forebrain, located near the ventral junction of the caudate nucleus and putamen. It receives dopaminergic projections from the ventral tegmental area (VTA) and glutamatergic inputs from regions including the prefrontal cortex, amygdala, and hippocampus. It is involved in reward-related learning, motivation, reinforcement, and assigning incentive salience to reward-predictive stimuli. Dopamine signaling modulates nucleus accumbens activity and synaptic plasticity, helping encode motivational significance and reinforcement-related information. Addictive drugs can alter dopamine signaling and synaptic function in this circuit, contributing to learned drug-seeking behavior and persistent responses to drug-associated cues. The nucleus accumbens is not simply a pleasure center; dopamine is especially important for motivation, reinforcement learning, and incentive salience rather than pleasure alone.

Ventral Tegmental Area

Region of the ventral midbrain, located in the ventral tegmentum, medial to the substantia nigra, containing dopamine-producing neurons and other neuronal populations. Dopaminergic neurons in the VTA project to the nucleus accumbens and other limbic structures through the mesolimbic pathway and to cortical regions, including the prefrontal cortex, through the mesocortical pathway. These projections contribute to reward-related learning, motivation, reinforcement, and cognitive functions. The VTA is a major source of dopamine involved in the neural circuitry affected by addictive drugs. Its projections to the nucleus accumbens are particularly important for understanding the relationship between dopamine, reward, motivation, and addiction.